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Diamox (Acetazolamide)

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Diamox is an FDA-approved medication used to treat certain types of glaucoma, congestive heart failure, certain types of seizures. Diamox also prevents altitude sickness.

Other names for this medication:

Similar Products:
Lasix, Topomax, Topiragen, Trokendi XR, Zonegran, Qudexy XR, Topamax Sprinkle


Also known as:  Acetazolamide.


Diamox contains an active ingredient Acetazolamide, which belongs to class of drugs called carbonic anhydrase inhibitors.

Diamox effectively treats certain types of glaucoma (excessive pressure in the eyes) by reducing the amount of fluid in the eye, and thereby decreases pressure inside the eye.

Acetazolamide acts also as a diuretic ("water pill") and inhibits the protein in the body called carbonic anhydrase. This leads to reducing the build-up of certain fluids in the body, significantly alleviating the symptoms of congestive heart failure.

Acetazolamide is also used to treat certain types of seizures, and to treat or prevent altitude sickness.


Diamox is available in tablets.

The dosage depends on the disease and its prescribed treatmen.

Glaucoma treatment:

250 mg to 1 gram per 24 hours in 2 or more smaller doses.

In secondary glaucoma and before surgery in acute congestive (closed-angle) glaucoma, the usual dosage is 250 mg every 4 hours or, in some cases, 250 mg twice a day.

Epilepsy treatment:

The daily dosage is 8 to 30 mg per 2.2 pounds of body weight in 2 or more doses. Typical dosage may range from 375 to 1,000 mg per day.

Congestive Heart Failure treatment:

The usual dosage is 250 mg to 375 mg per day or 5 mg per 2.2 pounds of body weight, taken in the morning.

Diamox can be used by children.

If you want to achieve most effective results do not stop taking Diamox suddenly.


If you overdose Diamox and you don't feel good you should visit your doctor or health care provider immediately.


Store at room temperature between 20 and 25 degrees C (68 and 77 degrees F) away from moisture and heat. Throw away any unused medicine after the expiration date. Keep out of the reach of children.

Side effects

The most common side effects associated with Diamox are:

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Side effect occurrence does not only depend on medication you are taking, but also on your overall health and other factors.


Do not take Diamox if you are allergic to Diamox components.

Be careful with Diamox if you're pregnant or you plan to have a baby, or you are a nursing mother.

Do not take Diamox if your sodium or potassium levels are low.

Do not take Diamox if you have kidney or liver disease, including cirrhosis.

Be careful with Diamox if you suffer from or have a history of emphysema or other breathing disorders.

Be careful with Diamox if you take high doses of aspirin.

Be careful with Diamox if you are taking Amitriptyline, Cyclosporine, Lithium, Methenamine, oral diabetes drugs such as Glyburide, Quinidine.

Do not use potassium supplements or salt substitutes.

If you want to achieve most effective results without any side effects it is better to avoid alcohol.

Do not stop taking Diamox suddenly.

diamox dose altitude sickness

All CAIs induced relaxation of contracted ciliary arteries, but the effect of dorzolamide was most pronounced. Dorzolamide-induced relaxation was unaffected by changes in pH and CO(2), and by removal of substrates to the carbonic anhydrase enzyme, but was abolished after inhibition of NO synthase and guanylyl cyclase and after removal of the vascular endothelium.

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In this retrospective study, we found that comorbidity with acute cerebrovascular disease and chronic cerebral diseases (senile dementia, cerebral atrophy and chronic cerebral ischaemia) were more common in patients with XFG than in patients with POAG. Prospective data are needed in order to conclude upon the associations found in this study.

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The presence of an ophthalmic artery pathway may provide the first evidence of disturbed vasomotor reactivity. The use of cerebral angiography to evaluate collateral pathways must be considered carefully since transcranial Doppler ultrasound is a reliable noninvasive alternative.

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As expected, renal clearance (which almost equals total body clearance) was severely decreased in CAPD (1.2 vs 80.3 L/h) and the elimination half-life of total ACTZ was prolonged (20.6 vs 3.4 hours). The protein binding was significantly altered with a mean free fraction 4.2% in HV and 8.6% in CAPD. Moreover protein binding of ACTZ was concentration dependent in both HV and CAPD. Despite a higher free fraction of ACTZ, the Emax was lower in CAPD: 4.4±1.4 vs 7.4±2.8 mmHg.

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Approximately 6% weight loss was associated with resolution of marked papilledema in these authors' patients. The benefit of acetazolamide in IIH is questioned since weight loss, rather than acetazolamide, appeared to have been the catalyst for reducing the severity of papilledema.

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Twenty type 3 patients were enrolled in this prospective, longitudinal cohort study. Hemodynamic and metabolic parameters were quantitatively determined by (15)O-gas PET. All of them were medically treated.

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The cilnical features of patients from HOKPP family were summurized. Techniques of target exon PCR and direct sequencing were used to screen the mutation in CACNA1S and SCN4A genes in all numbers of the family.

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To evaluate whether the effect of acetazolamide on piperacillin's aqueous humor concentrations observed in animals exists also in humans for ceftazidime, cefotaxime, ceftriaxone and aztreonam.

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A prospective, randomized, double-masked, placebo-controlled study.

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During follow-up, seven patients had new strokes (five minor strokes and two major ones), two ipsilateral and four contralateral to the ICA occlusion and one in the posterior circulation. Four patients died, All patients experiencing a new stroke had previous symptoms and pathological flow patterns in the OA, i.e retrograde or isoelectric flow were noted in six of them. One patient with contralateral stroke experienced occlusion of the ICA located above the origin of the OA with anterograde flow; otherwise none of 11 patients with anterograde flow had a new stroke (p<0.05, Fisher exact text). During the follow-up, the initial mean velocity (MV) in the middle cerebral artery (MCA) on the occluded side in six patients with a new stroke in the anterior circulation, was 26.83+/-10.50 cm/s, which was significantly different from that of patients without a new stroke (45.80+/-12.8 cm/s) (p<0.01). MV in the ICA on the non-occluded side at the last examination was greater than that at the first examination (p<0.05) and increased after the use of acetazolamide only on this side (p<0.05), while PI decreased bilateraly (p<0.001 and 0.05). Resting MV both in the MCA on the occluded and ACA on the non-occluded side slightly decreased, while MV in the posterior cerebral artery (PCA) increased on the occluded side (p<0.083) compared with that at the start of the follow-up. VMR in the ACA decreased slightly both on the non-occluded and occluded side (Delta-6.9 and Delta-5.3 respectively), while impaired VMR

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The effects of carbonic anhydrase inhibitors on secretion by macropodine parotid and mandibular glands were investigated using anaesthetized red kangaroos. In the parotid gland, acetazolamide (500 mumol.l-1) reduced a stable acetylcholine-evoked, half-maximal flow rate of 2.02 +/- 0.034 to 0.27 +/- 0.023 ml.min-1 (87% reduction). Concurrently, salivary bicarbonate concentration and secretion fell (129.4 +/- 1.46 to 80.9 +/- 1.63 mmol.l-1 and 264.8 +/- 7.96 to 22.3 +/- 2.30 mumol.min-1, respectively), phosphate and chloride concentrations rose (14.0 +/- 0.79 to 27.6 +/- 0.85 mmol.l-1 and 5.6 +/- 0.25 to 27.5 +/- 1.32 mmol.l-1, respectively), sodium concentration and osmolality were unaltered, and potassium concentration fell (8.8 +/- 0.33 to 6.4 +/- 0.29 mmol.l-1). High-rate cholinergic stimulation during acetazolamide blockade was unable to increase salivary flow beyond 11 +/- 0.9% of that for equivalent unblocked control stimulation. However, superimposition of isoprenaline infusion on the acetylcholine stimulation caused a three-fold increase in the blocked flow rate. These treatments were accompanied by small increases in salivary phosphate and chloride concentrations but not bicarbonate concentration. Methazolamide infusion caused similar changes in parotid secretion. In the mandibular gland, acetazolamide infusion had no effect on salivary flow rate during either low- or high-level acetylcholine stimulation. Acetazolamide caused no alterations in salivary electrolyte secretion at low flow rates, but curtailed the rise in bicarbonate concentration associated with high-level acetylcholine stimulation. Acetazolamide administration did not affect the increase in salivary flow rate associated with isoprenaline infusion, but did block the concomitant increase in bicarbonate concentration and secretion substantially.(ABSTRACT TRUNCATED AT 250 WORDS)

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A young age and concomitant use of carbonic anhydrase inhibitors are associated with an increased risk of hyperammonemia regardless of whether the patient is taking VPA. In patients receiving VPA, concomitant use of phenytoin and/or phenobarbital enhances the risk of hyperammonemia. An increase in ammonia can be caused by multiple factors. Our results may help clinicians to avoid problems of hyperammonemia.

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An organism from a goldfish aquarium, isolated on barbital medium, was found to be a Gram-positive coccus which divided in alternating planes, often appearing as a doublet or as a tetrad with adjacent sides flattened. It grew well, although slowly, on rich solid medium (LB agar) and in liquid brain-heart infusion at room temperature (ca. 22 degrees C); growth was slower and less extensive at 30 degrees C or 37 degrees C. No growth was seen at 4-5 degrees C or at 42 degrees C. It withstands brief exposure to ultraviolet radiation. Its growth was inhibited by low levels (0.1 unit/ml) of penicillin but was unaffected by levels of acetazolamide in excess of 1 mg/ml, indicating that it lacks carbonic anhydrase. Acid was not produced from glucose, maltose, mannose, lactose, or sucrose and only weakly, if at all, from fructose. Its DNA has a G + C mol percent of 59 measured chromatographically and neither the DNA nor rRNA from the organism hybridized with DNA from any organism that seemed related on morphological or other bases. Thin-layer chromatography of chloroform:methanol extracts of the organism show that it contains phosphatidyl choline, phosphatidyl ethanolamine, and phosphatidyl glycerol. Cell-wall preparations contain glutamic acid, serine, histidine, lysine, and alanine in the ratio of 1:1:1:1:8. Colonies were red-orange in color due, in larger measure, to a carotenoid tentatively identified as rhodopin. The organism was named Pelczaria aurantia.

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Studies primarily describing responses in adults were selected. Animal research is described that illustrates findings in humans.

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(1) In improving the endurance of mice in the condition of hypoxia, the survival time of 6.25 mg/(kg x d) and more doses of P-8 groups were (27.38 +/- 4.63, 29.53 +/- 4.43, 29.67 +/- 7.28, 31.55 +/- 6.34, 32.45 +/- 6.65, 36.81 +/- 7.24 and 35.41 +/- 4.20) min, compared with the control group (22.90 +/- 3.19) min , the survival time significantly prolonged (P < 0.05, P < 0.01); compared to the same dose of acetazolamide groups (24.54 +/- 3.17, 22.70 +/- 3.04, 22.67 +/- 2.99, 23.93 +/- 0.96, 27.87 +/- 5.06, 30.79 +/- 5.12 and 35.14 +/- 6.46) min, the survival time significantly prolonged; P-8 groups and Acetazolamide's minimum effective dose were 6.25 and 100 mg/(kg x d), the potency of P-8 is 16 times Acetazolamide. (2) In improving the endurance of mice in the condition of hypoxia, the survival time of middle and high doses of P-8 groups [(24.82 +/- -3.92, 28.27 +/- 5.89) min] were significantly longer than those in control group [(21.96 2.51) min, P < 0.05]; compared with the acetazolamide (23.11 +/- 3.71) min, the survival time of high dose of P-8 group was significantly prolonged. (3) Compared with the normal control group, P-8 [(25 mg/(kg x d), 50 mg/(kg x d), 100 mg/(kg x d), 200 mg/(kg x d)] dose groups inhibited the activity of carbonic anhydrase II (CAII) in the renal (P < 0.05, P < 0.01); P-8 [100 mg/(kg x d) and 200 mg/(kg x d)] dose group significantly inhibited the activity of carbonic anhydrase II (CA II) in the brain (P < 0.05).

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Acetazolamide treatment significantly improves action myoclonus in Ramsay Hunt Syndrome. A family with two brothers and a sister, and a sporadic case with Ramsay Hunt Syndrome and uncontrollable action myoclonus, are described where addition of oral acetazolamide lead to marked improvement in their action myoclonus.

diamox dose altitude sickness prevention

Cerebral blood flow before and after 1 g acetazolamide was analyzed by 99mTc-HMPAO-SPECT in 21 symptomatic patients with documented extracranial obstructions. SPECT findings were correlated with the results of angiography, transcranial Doppler sonography, and computed tomographic scan.

diamox dose acute glaucoma

Isovolemic hemodilution in subjects with normal cerebral perfusion can augment cerebral blood flow efficiently in a rapid fashion, and this effect can last for at least a week. The mechanism of flow augmentation may be partially attributed to vasodilation, which could be manifested as tachycardia, increased cardiac output, and decreased cerebral vascular reactivity.

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The relationship between surface epithelial alkaline secretion and pH at the mucosal cell surface was studied in the duodenum of anesthetized rats. Alkaline secretion was measured by direct titration in situ using perfused segments of duodenum just distal to the Brunner gland area and devoid of pancreatic and biliary HCO3-. Mucosal surface pH was measured by advancing a pH-sensitive antimony microelectrode from the luminal solution to the mucosal cell surface during continuous recording of pH. Acidification of the luminal solution markedly stimulated epithelial alkaline secretion: a change of luminal pH from 7.60 to 5.00 by approximately 100%, and from pH 7.60 to 2.00 by approximately 600%. Maximal pH in the immediate vicinity of the (luminal) cell surface remained at or slightly above neutrality during exposure to both luminal acidities. Prostaglandins (E2, 16,16-dimethyl E2, and F2 alpha, 3-140 microM luminally) increased the rate of alkaline secretion, surface alkalinity, and thickness of the pH gradient. Acetazolamide (40-80 mg/kg, i.v.) was a much more potent inhibitor of prostaglandin or acid-stimulated secretion than of basal alkaline secretion and decreased surface pH in acid-exposed duodenum. Aspirin (30 mg/kg, i.v.) had no effect on basal alkaline secretion (titrated at luminal pH 7.60) but significantly inhibited secretion at luminal pH 2.00, resulting in a decrease of surface pH. These data suggest that endogenous prostaglandins may be involved in mediating the alkaline response to luminal acid. Furthermore, because it is quantitatively sufficient to maintain neutral pH at the mucosal cell surface at luminal acidities normally encountered within the duodenal bulb, epithelial alkaline secretion presumably has an important role in duodenal protection against acid.

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Hyperbaric oxygen (HBO2) causes CO2 retention in the brain that leads to the increase in cerebral blood flow (CBF) by poorly understood mechanisms. We have tested the hypothesis that NO is implicated in CBF-responses to hypercapnia under hyperoxic conditions. Alert rats were exposed to HBO2 at 5 ata and blood flow in the striatum measured by H2 clearance every 10 min. Acetazolamide, the inhibitor of carbonic anhydrase, was used to increase brain PCO2. CBF responses to acetazolamide administration (30 mg/kg, i.p.) were assessed in rats breathing air at 1 ata or oxygen at 5 ata with and without NOS inhibition (L-NAME, 30 mg/kg, i.p.). In rats breathing air, acetazolamide increased CBF by 34 +/- 7.4% over 30 min and by 28 +/- 12% over 3 hours while NOS inhibition with L-NAME attenuated acetazolamide-induced cerebral vasodilatation. HBO2 at 5 ata reduced CBF during the first 30 min hyperoxia, after that CBF increased by 55 +/- 19% above pre-exposure levels. In acetazolamide-treated animals, no HBO, induced vasoconstricton was observed and striatal blood flow increased by 53 +/- 18% within 10 min of hyperbaric exposure. After NOS inhibition, cerebral vasodilatation in response to acetazolamide during HBO2 exposure was significantly attenuated. The study demonstrates that NO is implicated in acetazolamide (CO2)-induced cerebral hyperemia under hyperbaric oxygen exposure.

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Excellent results from multiple burr-hole operations for adult moyamoya disease are reported in this study. Ten patients had between one and four burr holes (mean 2.1) drilled in each hemisphere. In four patients new burr holes were added on the opposite side after depression of cerebral blood flow (CBF) was detected by follow-up single-photon emission computerized tomography imaging of the brain with N-isopropyl-p-[123I]iodoamphetamine. The postoperative follow-up period ranged from 6 to 62 months (mean 34.7 months). Beginning at 6 months postsurgery, angiograms disclosed rich neovascularization at 41 of 43 burr holes, first from the middle meningeal artery, then from the superficial temporal artery. Neovascularization did not occur at two burr holes at which there was subdural effusion and local cerebral atrophy, respectively. Progression of stenosis of the major vessels was seen in six patients. Moyamoya vessels were decreased at six sites in four patients. The CBF study revealed that the reactivity to acetazolamide improved in all six patients tested. Transient ischemic attacks disappeared in all six patients presenting with this symptom, and preoperative symptoms improved in both of the patients who presented with cerebral infarction and in both patients with intraventricular hemorrhage. There was no mortality or morbidity, and no new neurological deficits or rebleeding developed during the follow-up period. The authors strongly recommend the multiple burr- hole operation as the surgical treatment of choice for adult moyamoya disease because of its safety and effectiveness.

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Cerebral blood flow (CBF) is usually decreased in patients with hypertensive putaminal hemorrhage (HPH). However, there are few reports concerning cerebrovascular reserve capacity (CRC) in these cases. This study evaluated cerebral hemodynamics in patients with HPH by measuring CBF and CRC. CBF and CRC were measured by stable xenon enhanced computed tomography (Xe-CT) in 11 patients with HPH (HPH group) and 11 patients with essential hypertension without intracerebral hematoma (non-HPH group). CBFs of the hemisphere and thalamus in the HPH group were lower than those in the non-HPH group. And the CBF of the hemisphere was increased transiently after the surgical evacuation of the hematoma. Thereafter, it fell gradually. The CRCs were also lower in acute stage of the HPH group. The CRC recovered during the chronic stage. Hemodynamics in patients with HPH can be modulated by surgical removal of hematoma. However, some adjunct therapies are necessary to prevent delayed neuronal inactivity, Stable Xe-CT with acetazolamide test is useful to evaluate hemodynamics in the HPH patients.

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Moyamoya disease is a rare, progressive, steno-occlusive disease of the distal branches of the carotid arteries associated with the development of a profuse basal collateral vascular network. In the United States, the disease occurs sporadically and literature on the topic in limited. With data lacking relative to moyamoya epidemiology and management, we report our survey results among a sample of neurovascular surgeons.

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To describe the incidence and characteristics of acute and rapidly progressive visual loss in idiopathic intracranial hypertension (IIH).

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The author presents conservative treatment of glaucoma. Pharmacologic action of antiglaucoma drugs from group of mioties, and adrenergic blockers and other hypothension agents is discussed. Furthermore side effects of these drugs and their synergic action is presented. Personal experience connected with it is also discussed.

diamox 1000 mg a day

Carbonic anhydrase activity (carbonic dehydratase, EC has been detected in the fetal lungs of stillborn human infants and rhesus monkeys, but a role for this enzyme in the fetal lung has not been elucidated. In utero the mammalian lung develops as a liquid-filled structure, the liquid being secreted by the lung. In the fetal lamb this liquid, when compared with plasma, has a high chloride and a low bicarbonate concentration, suggesting a possible role for carbonate dehydratase. Studies on 10 fetal lambs confirmed the presence of carbonate dehydratase in the lung. Levels at 60-66 days were negligible and rose to 0.30 Meldrum Roughton units/mg protein at about 140 days (term 147 days), with little change after birth. In another six fetal lambs at 135-136 days, inhibition of this enzyme with 100 mg acetazolamide suppressed the mean rate of secretion of lung liquid by 64.5% (P less than 0.005), which correlated with a significant drop in chloride concentration (P less than 0.001). This magnitude of changes in secretion after acetazolamide is of the same order as that occurring in the secretion of cerebrospinal fluid when carbonate dehydratase is inhibited. This observation supports the hypothesis that carbonate dehydratase in fetal lung affects the secretion of lung liquid, although its mechanism is as yet unknown.

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Forty-nine patients with unilateral ICA stenosis who underwent CEA were studied. Preoperative blood flow in the poststenotic portion of the extracranial ICA was studied by using TOCU. Regional cerebral blood flow (rCBF) and vasoreactivity to acetazolamide (VR) in the territory of the middle cerebral artery were investigated by using single-photon emission CT (SPECT) before, 2 weeks after, and 3 months after CEA.

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1) During the symptomatic period, Xe-CBF was normal or slightly increased both in and outside the low density lesion. 2) The CBF response to acetazolamide loading was well preserved both in and outside the low density lesions. 3) After the neurological symptoms and low density lesions disappeared, Xe-CBF pattern and vascular response was the same as during the symptomatic period. 4) In the PET study, normal or slightly increased PET-CBF, increased CMRGlu and markedly decreased CMRO2 in comparison to normal control was noted resulting in a marked decrease in OEF and CMRO2/CMRGlu ratio, a characteristic metabolic pattern for MELAS.

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In eight normal rabbits, sodium acetazolamide (5.5 mg per kg of body weight) in 11% solution was injected subconjunctivally daily for about four weeks in the left eye of each rabbit, with the right eye serving as a control. Ocular tension in both eyes was measured by the Perkins hand-held applanation tonometer. Five of the eight rabbits showed a significant difference (P less than 0.05) in ocular tension between treated and untreated eyes, with a decrease in the treated left eye. The ocular tension decrease in the treated left eye began about one week after the beginning of the injections and lasted for about two weeks. Thereafter, ocular tension in the treated left eye returned to base-line levels, despite continued subconjuctival injection of sodium acetazolamide.

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Of 70 patients enrolled (35 in each group), data from 54 were analysed per protocol, while last observation carried forward was used for the remaining 16. During the 5-day treatment, Pa O2 increased on average 0.81 kPa in the placebo group and 1.41 kPa in the acetazolamide group. After adjustment for baseline skewness, the difference was statistically significant (adjusted mean difference 0.55 kPa, 95% confidence interval 0.03-1.06). Pa CO2 decreased in both groups, but the difference was not statistically significant. As expected, pH and BE decreased markedly in the acetazolamide group.

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This prospective randomized double-blind study comprised 60 eyes of 52 patients having phacoemulsification under topical anesthesia. There were no intraoperative complications. Eyes were randomized to receive oral acetazolamide 500 mg 1 hour preoperatively followed by 250 mg acetazolamide every 6 hours, 1 drop of brinzolamide 1% every 12 hours starting immediately after speculum removal, or no ocular hypotensive medication. Intraocular pressure (IOP) was measured using a Perkins tonometer preoperatively and 4 to 6 hours and 18 to 24 hours postoperatively.

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The treatment of choice for moderate to severe obstructive sleep apnoea (OSA) is continuous positive airway pressure (CPAP) via a mask during sleep. However this is not tolerated by all patients and its role in mild OSA is not proven. Drug therapy has been proposed as an alternative to CPAP in some patients with mild to moderate sleep apnoea. The mechanisms by which drugs might reduce OSA include; a reduction in the proportion of rapid eye movement (REM) sleep (during which apnoeas tend to be more frequent), an increase in ventilatory drive or an increase in upper airway muscle tone during sleep.

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Ischaemic stroke is a major complication of cardiac surgery. The optimal strategies for operating on patients with obstructive carotid and/or intracranial artery disease (CIAD) are controversial. We aimed to clarify whether single-photon emission computed tomography (SPECT) with acetazolamide, to quantify the cerebral perfusion reserve, could predict the risk of haemodynamic ischaemic stroke during cardiac surgery.

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We evaluated the buy diamox clinical usefulness of CT perfusion (CTP) with angiography (CTA) as an alternative to digital subtraction angiography (DSA) and acetazolamide (ACZ)-challenged single-photon emission computed tomography (SPECT) in the follow-up evaluation of hemodynamic changes and bypass patency after bypass surgery in chronic cerebral ischemic diseases.

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We report the occurrence of idiopathic intracranial hypertension in a patient treated with ofloxacin, a fluoroquinolone antimicrobial agent, for 16 months. The withdrawal of ofloxacin and acetazolamide therapy were followed by buy diamox a complete recovery of visual function.

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We evaluated evidence for utility of shunting in idiopathic normal pressure hydrocephalus (iNPH) Serevent Inhaler Cost and for predictors of shunting effectiveness.

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It was intended to explore the role of Azulfidine Brand Name alimentary acid-base load and carbonic anhydrase activity for regulatory responses of renal, pulmonary or metabolic origin in rabbits as typical herbivores.

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AMS is a preventable disease about which travellers are frequently uninformed and one which physicians may wrongfully assume is limited to the population of ultra high altitude adventurers. These studies on incidence, while not without flaws, point out the frequency of AMS, as well as its significant incidence at moderate and commonly frequented altitudes. The current literature does not fully answer questions about incidence at moderate altitudes, nor about the full effects of altitude on children. Certainly AMS is not a rare complication of travel to altitudes and may indeed be under-recognized and under-treated. Both acetazolamide and dexamethasone provide adequate prophylaxis, and the choice of medications can be to some extent based on experience and patient profile. The best prophylaxis is a slow stepwise ascent, and the best treatment descent. The availability of medications for the amelioration or prevention of symptoms, and succinct advice on prevention by travel planning Discount Online Viagra will make many of our patients' holidays more enjoyable and business trips more productive.

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Pyrazole carboxylic acid amides of 5-amino-1,3,4-thiadiazole-2-sulfonamide 1 (inhibitor 1) were synthesized from 4-benzoyl-1-(4-nitrophenyl)-5-phenyl-1H-pyrazole- Crestor And 81 Mg Aspirin 3-carbonyl chloride and 4-benzoyl-1-(3-nitrophenyl)-5-phenyl-1H-pyrazole-3-carbonyl chloride compounds. Human carbonic anhydrase isoenzymes (hCA-I and hCA-II) were purified from erythrocyte cells by the affinity chromatography. The inhibitory effects of inhibitor 1, acetazolamide (AAZ), and of 16 newly synthesized amides (8-11, 12a-f, 13a-c, 14a-b, and 15) on hydratase and esterase activities of these isoenzymes have been studied in vitro. The average IC(50) values of the new compounds (8-11, 12a-f, 13a-c, 14a-b, and 15) for hydratase activity ranged from 3.25 to 4.75 microM for hCA-I and from 0.055 to 2.6 microM for hCA-II. The mean IC(50) values of the same inhibitors for esterase activity were in the range of 2.7-6.6 microM for hCA-I (with the exception of inhibitor 10, which did not inhibit the esterase activity of hCA-I) and of 0.013-4.2 microM for hCA-II. The K(i) values for new compounds (8-11, 12a-f, 13a-c, 14a-b, and 15) were observed well below that of the parent compound inhibitor 1 and were also comparable to that of AAZ under the same experimental conditions. The comparison of newly synthesized amides to inhibitor 1 and to AAZ indicated that the new derivatives preferentially inhibit hCA-II and are more potent inhibitors of hCA-II than the parent inhibitor 1 and AAZ.

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Carbonic acid accumulation, which results from CO2 insufflation, can produce visceral and referred pain in the postoperative setting. Acetazolamide inhibits carbonic anhydrase, an enzyme that accelerates carbonic acid formation. We hypothesized that preoperative administration of acetazolamide would decrease postoperative Levitra 40 Mg pain in patients undergoing laparoscopic inguinal herniorrhaphy.

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To determine the effects of urinary pH on fluoride ion Paracetamol Terapia 500 Mg Pret excretion and the resulting plasma fluoride concentration during and after enflurane anesthesia, renal function, plasma inorganic fluoride levels, and fluoride excretion were studied in two groups of patients pretreated with either NH4Cl or acetazolamide to produce acidic or alkaline urine, respectively. During anesthesia, urinary flow rate, inulin clearance (Cin) and para-aminohippurate (PAH) clearance (CPAH) were 7, 61, and 43 per cent of control values in the acidic-urine group and 22, 74, and 57 per cent of control values in the alkaline-urine group, respectively. Fractional fluoride clearances (CF/CIN) during anesthesia and operation were 0.06 +/- 0.05 in the acidic-urine group (urinary pH 5.08) and 0.68 +/- 0.23 in the alkaline-urine group (urinary pH 8.16). Values of total fluoride excretion during the same period were 0.06 +/- 0.04 mg and 0.87 +/- 0.29 mg, respectively. Mean maximal plasma levels of fluoride were 26.3 +/- 7.3 microM in the acidic-urine group and 13.5 +/- 2.4 microM in the alkaline-urine group. The differences between groups in fluoride clearance, fluoride excretion, and plasma fluoride levels were all statistically significant. The data clearly show that renal fluoride clearance is closely related to urinary pH.

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A case report of a 43-year-old man who during convalescence after mumps (parotitis epidemica) developed bilateral glaucoma associated with redness of his eyes but no other ocular manifestations. The chamber angles were open. No signs of scleritis or iritis were present. The best treatment was found to be prednisolone topically and acetazolamide orally. After Prandin User Reviews ten days the intraocular pressure was normalized and after a fortnight all treatment could be discontinued.

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This is a crucial observation for the clinical interpretation of CBF SPECT data and should Viagra 50 Mg Price direct the choice of tracer for a specific examination.

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Hyperperfusion syndrome (HPS) after carotid artery stenting (CAS) may cause hemorrhagic or ischemic events leading to serious sequelae. We previously reported the staged angioplasty (SAP) to prevent HPS. In the present study, we analyzed our treatment results of SAP to know its effectiveness and problems. The study included 43 patients scheduled for SAP in whom preoperative single photon emission computed tomography (SPECT) showed severely impaired cerebral blood flow (CBF). The analyzed subjects were 38 males and 4 females, mean age was 73 ± 8.5 years old. SAP was indicated for the patients whose CBF ratio in the affected/unaffected hemisphere (asymmetry index) was below 0.8, and cerebrovascular reactivity measured Nexium Drug Interactions Side Effects by acetazolamide challenge was below 10%. First, percutaneous transluminal angioplasty (PTA) was performed. If PTA was successful, CAS was performed 2 weeks later. If PTA was not successful due to inadequate dilatation or extensive dissection, a stent was placed. SPECT was performed immediately after PTA and CAS to confirm the presence or absence of hyperperfusion phenomenon (HPP) indicating radiologic hyperperfusion. In 39 of 43 patients (91%), SAP was successfully performed and HPP was not observed. On the other hand, in the other four patients (9%), immediate stent placement was added due to inadequate dilatations in three patients and vascular dissection in one. Among 43 candidates for SAP, 41 patients (95.4%) had favorable course, but one hemorrhagic and one ischemic complications were observed after PTA. SAP was a relatively simple procedure, and its clinical results seemed acceptable.

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Following a timolol and acetazolamide run-in, 105 patients with elevated intraocular pressure (IOP) were randomized Bactrim 800 Mg Side Effects to dorzolamide or acetazolamide, in addition to timolol, for 12 weeks.

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The episodic ataxias are autosomal dominant disorders usually beginning in the first two decades of life. Episodic ataxia type 1 (EA1) is characterized by brief episodes of ataxia, typically lasting seconds, and interictal myokymia, while episodic ataxia type 2 (EA2) is manifested by longer episodes of ataxia (hours) with interictal nystagmus. The EA1 gene (KCNA1) codes for the six transmembrane segments (S1 to S6) of the Kv1.1 potassium channel subunit and the EA2 gene (CACNA1A) encodes for the Ca(v)2.1 subunit of the P/Q calcium channel complex. EA1 mutations are always missense while most EA2 mutations disrupt the reading frame. Studies of the biophysical properties of the mutant Kv1.1 and Ca(v)2.1 channels in Xenopus oocytes and mammalian cell lines demonstrate clear physiologic consequences of the genetic Sinequan Doxepin Dosage Recommendations mutations although no consistent pattern for genotype-phenotype correlation has emerged. Genetic testing for EA1 and EA2 is available, but since no single mutation is prominent for either KCNA1 or CACNA1A, all of the coding regions of the genes need to be screened for mutations. Acetazolamide can be dramatic in controlling episodes of ataxia with EA2 but is typically less beneficial with EA1.

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The effects of the aquaporin-4 (AQP-4) inhibitor TGN-020 on regional cerebral blood flow (rCBF) was examined in wild-type (WT) and AQP-4 knockout (KO) mice in vivo. Although baseline absolute rCBF of WT and KO mice were equivalent (158.9 ± 17.7 and 155.5 ± 10.4 ml/100 g/min, respectively), TGN-020 produced a significant increase in rCBF compared with saline-treated WT mice (control), reaching a plateau 20 min after administration (118.45 ± 8.13%, P<0.01). TGN-020 showed no effect on KO mice, supporting the concept that the observed increase in rCBF in WT mice was AQP-4 dependent. Administration of acetazolamide (positive control) produced an even greater increase in rCBF in WT compared with TGN-020 and a similar response in KO mice as well, reaching a sustained plateau 5 min after administration (138.50 ± 9.75 and 138.52 ± 9.76%, respectively, P<0.01 compared with baseline or saline-treated control mice). The study demonstrated that AQP-4 plays a role Voltaren Dosage Card in regulation of rCBF.

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Patients afflicted by cystine stone disease need an aggressive medical treatment, gentle stone-removing Lexapro Overdose With Alcohol surgery and careful follow-up.

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Over 40 million people travel to high altitude for both work and pleasure each year, and all of them are at risk of the acute effects of hypoxia. This article reviews the prevention, diagnostic features and treatments Cymbalta Vs Lyrica Cost of these illnesses.

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To determine the postoperative morbidity on day Celebrex Food Drug Interactions 1 after uncomplicated phacoemulsification.

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Alteration of the cerebrovascular reserve (CVR) Viagra 0 25 Mg in the frontal lobes has been associated with cognitive dysfunction in adults with moyamoya disease (MMD). Elevation of the apparent diffusion coefficient (ADC) in normal-appearing white matter on conventional MRI may occur as a consequence of chronic haemodynamic failure. In the present study, the authors examined the relation of ADC with CVR and cognitive dysfunction in adults with MMD.

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The performance of color velocity imaging quantification for evaluating cerebral vasoreactivity is comparable to that of transcranial Doppler sonography. Because color velocity imaging quantification is not as limited as transcranial Doppler sonography, it could be an ideal complementary tool to transcranial Doppler sonography. More studies are required to define its clinical value.

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Microdialysis is used in vivo for measuring compounds in brain interstitial fluid. The authors describe another application of this technique to the central nervous system, namely microprobe dialysis in the cisterna magna to study the dynamics of ion transport and cerebrospinal fluid (CSF) formation in the rat. The choroid plexus is the major source of CSF, which is produced by active transport of Na from blood into the cerebral ventricles. Formation of CSF is directly proportional to the blood-to-CSF transport of Na. By injecting 22Na into the systemic circulation and quantifying its movement into CSF by microdialysis, one can reliably estimate alterations in the rate of CSF formation. The sensitivity of this system was determined by administering acetazolamide, a standard inhibitor of CSF production. Because acetazolamide is known to decrease CSF formation by 40% to 50%, the cisternal microdialysis system in animals treated with this drug should detect a corresponding decrease in the amount of 22Na dialyzed. This hypothesis is supported by the 22Na uptake curves for control versus treated animals: that is, by the acetazolamide-induced average diminution of about 45% in both the rate and extent of tracer accession to dialysate. Bumetanide, a loop diuretic, reduced by 30% the 22Na entry into dialysate. Microprobe dialysis of fluid in the cisterna magna is thus a minimally invasive and economical method for evaluating effects of drugs and hormones on the choroid plexus-CSF system.

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The η-carbonic anhydrases (CAs, EC were recently discovered as the sixth genetic class of this metalloenzyme superfamily, and are so far known only in protozoa, including various Plasmodium species, the causative agents of malaria. We report here an inhibition study of the η-CA from Plasmodium falciparum (PfCA) against a panel of sulfonamides and one sulfamate compound, some of which are clinically used. The strongest inhibitors identified were ethoxzolamide and sulthiame, with KIs of 131-132 nM, followed by acetazolamide, methazolamide and hydrochlorothiazide (KIs of 153-198 nM). Brinzolamide, topiramate, zonisamide, indisulam, valdecoxib and celecoxib also showed significant inhibitory action against PfCA, with KIs ranging from 217 to 308 nM. An interesting observation was that the more efficient PfCA inhibitors are representative of several scaffolds and chemical classes, including benzene sulfonamides, monocyclic/bicyclic heterocyclic sulfonamides and compounds with a more complex scaffold (i.e., the sugar sulfamate derivative, topiramate, and the coxibs, celecoxib and valdecoxib). A comprehensive inhibition study of small molecules for η-CAs is needed as a first step towards assessing PfCA as a druggable target. The present work identifies the first known η-CA inhibitors and provides a platform for the development of next generation novel PfCA inhibitors.

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Studies on long-term outcome of subarachnoid hemorrhage (SAH) have been carried out for many years using various neuroimaging techniques, such as e.g.: SPECT, PET, TCD and XeCT. In our study angio-MRI supplemented with the acetazolamide test was used to assess cerebrovascular reserve impairment in 30 patients within 6 months since clipping an intracranial aneurysm. Severity of the SAH course was evaluated using the WFNS (World Federation of Neurosurgical Societies) scale [3]. The patients' clinical status was assessed at follow-up by means of the Glasgow Outcome Scale (GOS) [8]. Cereberovascular reserve evaluated at the follow-up in hypercapneal conditions was found to be insufficient. The degree of vessel reactivity dysfunction as a long-term outcome of SAH turned out to depend on massiveness of hemorrhage from the ruptured aneurysm.

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The effect of timolol, acetazolamide, and the combination of the two drugs on the rate of aqueous formation in 18 healthy human subjects was measured during the day and at night in a placebo-controlled, double-masked, randomized study. In the absence of any drugs, aqueous flow during the day was 2.61 +/- 0.82 (mean +/- SD) microliters/min and at night, 1.08 +/- 0.59, a 59% lower flow rate when compared with the daytime value (P < 0.0001). When compared with these aforementioned control values, timolol alone reduced the rate of aqueous flow by 39% (P < 0.0001) in awake subjects but had no statistically significant effect on the flow rate in sleeping subjects (P = 0.33). Acetazolamide alone reduced aqueous flow during the day by 21% compared with the control flow rate (P = 0.02) and at night by 24% below the nocturnal flow rate in the sleeping eye (P = 0.04). The combination of the two drugs reduced flow during the day by an additional 13% (P = 0.024) compared with the flow rate achieved by timolol alone, and by an additional 32% (P < 0.0001) compared with the flow rate reduction attained by acetazolamide alone. There was no statistically significant difference in the nocturnal flow rates achieved by acetazolamide alone or in combination with timolol (P = 0.37). These data confirm previous studies demonstrating the effect of timolol, acetazolamide, and sleep on the rate of aqueous humor formation. Unlike a previous study, it was found that acetazolamide lowers the aqueous flow below the already low nocturnal flow rate that occurs spontaneously in the sleeping eye.(ABSTRACT TRUNCATED AT 250 WORDS)

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Equivalent-circuit impedance analysis experiments were performed on the urinary bladders of freshwater turtles in order to quantify membrane ionic conductances and areas, and to investigate how changes in these parameters are associated with changes in the rate of proton secretion in this tissue. In all experiments, sodium reabsorption was inhibited thereby unmasking the electrogenic proton secretion process. We report the following: transepithelial impedance is represented exceptionally well by a simple equivalent-circuit model, which results in estimates of the apical and basolateral membrane ionic conductances and capacitances; when sodium transport is inhibited with mucosal amiloride and serosal ouabain, the apical and basolateral membrane conductances and capacitances exhibit a continual decline with time; this decline in the membrane parameters is most likely caused by subtle time-dependent changes in cell volume, resulting in changes in the areas of the apical and basolateral membranes; stable membrane parameters are obtained if the tissue is not treated with ouabain, and if the oncotic pressure of the serosal solution is increased by the addition of 2% albumin; inhibition of proton secretion using acetazolamide in CO2 and HCO3- -free bathing solutions results in a decrease in the area of the apical membrane, with no significant change in its specific conductance; stimulation of proton transport with CO2 and HCO3- -containing serosal solution results in an increase in the apical membrane area and specific conductance. These results show that our methods can be used to measure changes in the membrane electrophysiological parameters that are related to changes in the rate of proton transport. Notably, they can be used to quantify in the live tissue, changes in membrane area resulting from changes in the net rates of endocytosis and exocytosis which are postulated to be intimately involved in the regulation of proton transport.

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The amphibian skin represents an important organ for osmoregulation and, like the mammalian kidney, maintains acid-base balance by secreting protons or base. However, the lack of a reliable and accurate method to measure the contribution of unidirectional fluxes of HCO3- ions to this mechanism has been an obstacle for the determination of the role of bicarbonate in epithelial acid-base homeostasis. Recently, one of us developed a method that allows for the reliable determination of transepithelial fluxes of bicarbonate, and this method was applied to determine unidirectional fluxes of (14)CO2 and H(14)CO3 under a variety of conditions. We report that the combined CO2 and HCO3- mucosal-to-serosal flux under 5% CO2 was 40% larger than the opposing flux, giving a net flux in the mucosal-to-serosal direction. This net flux was inhibited by acetazolamide. In CO2-free conditions, there was no detectable net flux; however, acetazolamide and PGF(2alpha) attenuated the mucosal-to-serosal flux and established an apparent secretion of HCO3-. A model is presented that depicts twelve vectors or components to the CO2 plus HCO3- fluxes in the frog skin. This model can accurately reproduce the experimental values measured from unidirectional fluxes of CO2 and HCO3- under a variety of conditions and can explain the effects of PGF(2alpha) on unidirectional 14C-labeled fluxes as a consequence of inhibition of H+ secretion to the apical bath, similar to what was previously suggested by our laboratory using a different methodological approach. The present method, utilizing radiolabeled HCO3-, may be useful as a means to evaluate the mechanism of action of hormones and drugs that may regulate acid-base homeostasis by altering proton and bicarbonate transport processes.

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The present study examined the relationship between circulatory and metabolic reserve in patients with hemodynamic impairment.

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The mechanism of HCO3- transport was studied applying microelectrodes in "giant" cells fused from single epithelial cells of the diluting segment of frog kidney. A sudden increase of extracellular HCO3- concentration from 10 to 20 mmol/l at constant pH hyperpolarized the cell membrane potential of the fused cell. This cell-voltage response was totally abolished by 10(-3) mol/l SITS and significantly reduced by 10(-4) mol/l acetazolamide or by omission of Na+ from the extracellular perfusate. Removal of Na+ from the perfusate caused a transient depolarization. Reapplication of Na+ induced a transient hyperpolarization. 10(-3) mol/l SITS abolished the cell-voltage response to removal and reapplication of Na+. In the intact diluting segment of the isolated perfused frog kidney peritubular perfusion of 10(-4) mol/l acetazolamide reduced the limiting transepithelial electrochemical gradient for H+ significantly from 30 +/- 4 mV to 14 +/- 3 mV. The results suggest: In the diluting segment of the frog kidney a Na+-dependent rheogenic HCO3- transport system exists across the peritubular cell membrane. This rheogenic peritubular Na+/HCO3- cotransporter cooperates with a Na+/H+ exchanger in the luminal membrane, thus driving HCO3- reabsorption. Reabsorption of HCO3- and secretion of H+ depend upon the presence of carbonic anhydrase.

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The contribution of metabolic bicarbonate to cytosolic pH (pHcyto) regulation was studied on isolated perfused rat liver using phosphorus-31 NMR spectroscopy. Removal of external HCO3- decreased proton efflux from 18.6+/-5.0 to 1.64+/-0.29 micromol/min per g liver wet weight (w.w.) and pHcyto from 7.17+/-0.06 to 6.87+/-0.06. In the nominal absence of bicarbonate, inhibition of carbonic anhydrase by acetazolamide induced a further decrease of proton efflux of 0.69+/-0.26 micromol/min per g liver w.w. reflecting a reduction in metabolic CO2 hydration, and hence a decrease of H+ and HCO3- supplies. Even though 27% of the proton efflux was amiloride-sensitive under bicarbonate-free conditions, amiloride did not change pHcyto, revealing the contribution of additional regulatory processes. Indeed, pH regulation was affected by the combined use of 4-acetamido-4'-isothiocyanostilbene-2,2'-disulfonic acid (SITS) and amiloride since pHcyto decreased by 0.16+/-0.05 and proton efflux by 0.60+/-0.14 micromol/min per g liver w.w. The data suggest that amiloride-sensitive or SITS-sensitive transport activities could achieve, by themselves, pHcyto regulation. The involvement of two mechanisms, most likely Na+/H+ antiport and Na+:HCO3 symport, was confirmed in the whole organ under intracellular and extracellular acidosis. The evidence of Na-dependent transport of HCO3- in the absence of exogenous bicarbonate implies that the amount of metabolic bicarbonate is sufficient to effectively participate to pHcyto regulation.

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In a man with orthostatic and effort syncopes due to primary dysautonomia, we measured cerebral blood flow (CBF)--by the 133-Xenon inhalation method--in supine and in sitting positions, and after the i.v. administration of Acetazolamide, a potent cereal vasodilator. Heart rate (HR) and blood pressure (BP) were monitored over the 24 hours by a non-invasive device. The CBF was normal in supine position and significantly reduced when the patient was sitting. Despite che sympathetic denervation, good response to acetazolamide infusion was seen. BP changed with the position of the subject according to gravity, and HR was unresponsive to orthostatic and effort stimuli.

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We conclude that 99mTc-HMPAO-SPECT with acetazolamide challenge is a useful method for assessment of the adequacy of hemispheric collateral pathways in patients with severe occlusive cerebrovascular disease.

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At first evaluation US showed a significantly enlarged ONSD (.68 cm right; .66 cm left side) and the presence of increased ODE (.1 cm right; .15 cm left side). Post-punctural assessments showed a bilateral decrease of ONSD (.58 cm right; .58 cm left side), without changes in ODE values. After 12 months of treatment with acetazolamide and diet ODE completely normalized (0 cm on both sides). ODE values correlated directly with ONSD, and both ODE and ONSD values correlated directly with BMI. Correlations were statistically significant. ONSD changes occurred rapidly after the lumbar puncture, whereas the papilloedema required longer to reduce.

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1. Intracellular pH (pHi) was measured using pH-sensitive glass micro-electrodes. The effects on pHi of CO2 applied externally and HCO3-, H+ and NH4+ injected iontophoretically, were investigated. 2. The transport numbers for iontophoretic injection into aqueous micro-droples were found by potentiometric titration to be 0-3 for HCO3- and 0-94 for H+. 3. Exposure to Ringer, pH 7-5, equilibrated with 2-2% CO2 caused a rapid, but only transient, fall in pHi. Within 1 or 2 min pHi began to return exponentially to normal, with a time constant of about 5 min. 4. When external CO2 was removed, pHi rapidly increased, and then slowly returned to normal. The pHi changes with CO2 application or removal gave a calculated intracellular buffer value of about 30 m-equiv H+/pH unit per litre. 5. Injection of HCO3- caused a rise in pHi very similar to that seen on removal of external CO2. 6. The pHi responses to CO2 application, CO2 removal and HCO3- injection were slowed by the carbonic anhydrase inhibitor acetazolamide. 7. H+ injection caused a transient fall in pHi. In CO2 Ringer pHi fell less and recovered faster than in CO2-free Ringer. Calculation of the internal buffer value from the pHi responses to H+ and HCO3- injection gave very similar values. 8. The internal buffer value (measured by H+ injection) was greatly increased by exposure to CO2 Ringer. Acetazolamide reduced this effect of CO2, suggesting that the function of intracellular carbonic anhydrase may be to maximize the internal buffering power in CO2. 9. It was concluded that the internal HCO3- was determined primarily by the CO2 level and pHi, that internal HCO3- made a large contribution to the buffering power, and that after internal acidfication pHi was restored to normal by active transport of H+, OH- or HCO3- across the cell membrane. The active transport was much faster in CO2 than in CO2-free Ringer.