The prevalence of primary headaches was 44.72%. There was a predominance of females (71.4%). 31.1% of cases were between 50 and 59 years old. 36.6% had a family history of headaches. Onset of headaches occurred before the age of 15 years in 44.1% of patients. The most frequent location was occipital (45.3% of cases). The most frequent precipitating factors were stress (27.9%) and menstruation (27.3%). The predominant accompanying symptom was dizziness (26.1%). Tension-type headache was the most prevalent, with 92 patients (25.56%), followed by migraine, with 61 diagnoses (16.94%). 78.3% of the patients with tension-type headache and 70.5% of those with migraine tried self-medication with dipyrone and paracetamol. Patients with migraine made more frequent use of prophylactic treatment than those who suffered from tension-type headache (32.8% versus 16.3%; p = 0.01).
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Trace amines including tyramine and β-phenylethylamine (β-PEA) increase blood pressure and cause vasoconstriction which is attributed to indirect sympathomimetic actions. However, there is evidence that they may also have non-sympathomimetic mechanisms. This study examined whether β-PEA causes vasoconstriction of rat aorta by a sympathomimetic action or through the recently described trace-amine-associated receptors (TAAR). Concentration-response curves (CRCs) for β-PEA were constructed either cumulatively or non-cumulatively in rat isolated aortic rings. TAAR-1 and TAAR-4 protein expression was determined in rat aorta by Western blotting and TAAR-1 mRNA by reverse transcriptase polymerase chain reaction (RT-PCR). β-PEA caused concentration-related constriction of rat aorta. The contractions were unaffected by endothelium removal or the nitric oxide synthase inhibitor, N(ω)-nitro-L-arginine methyl ester (L-NAME, 100 μM) or the cyclooxygenase inhibitor, indomethacin (10 μM). Non-cumulative CRCs showed greater contractions and sensitivity to β-PEA than cumulative. The α(1)-adrenoceptor antagonist, prazosin, failed to inhibit either curve. The β-adrenoceptor antagonist, propranolol, the adrenergic neuronal transport inhibitor, cocaine, and the monoamine oxidase inhibitor, pargyline, also failed to alter the CRC. In the combined presence of prazosin, cocaine, pargyline, and the selective β(2)-adrenoceptor antagonist, ICI-118,551, the trace amine contractile potency order was tryptamine > β-PEA > octopamine > D: -amphetamine > tyramine. Western blotting and RT-PCR revealed the presence of TAAR-1 in rat aorta, but TAAR-4 was poorly expressed. Vasoconstriction of rat aorta by β-PEA appears not to be an indirect sympathomimetic action. The presence of TAAR-1 suggests that vasoconstriction may be via these receptors; however, the potency order differed from that reported for transfected cells expressing rat TAAR-1.
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Carvedilol, a selective alpha1 and non-selective beta-adrenoceptor antagonist and antioxidant, has been shown to provide significant cardiac protection in animal models of myocardial ischemia. To further explore the mechanisms contributing to carvedilol cardioprotection efficacy, the effects of carvedilol on hemodynamic variables, infarct size and myeloperoxidase activity (an index of neutrophil accumulation) were compared with a beta1-selective adrenoceptor antagonist, metoprolol. Carvedilol (1 mg/kg) or metoprolol (1 mg/kg or 1 mg/kg + 0.5 mg/kg 90 min later) was given intravenously 5 min before reperfusion. In vehicle-treated rabbits, ischemia (60 min) and reperfusion (180 min) resulted in significant increments in left ventricular end diastolic pressure, large infarcts (59+/-2.6% of area-at-risk) and marked increase in myeloperoxidase activity (0.59+/-0.09 U/100 mg tissue). Carvedilol treatment resulted in sustained reduction of pressure-rate-index and significantly smaller infarcts (22.0+/-2.5%, P < 0.01 vs. vehicle) as well as decreased myeloperoxidase activity (0.186+/-0.056 U/100 mg tissue, P < 0.01 vs. vehicle). The highest dose of metoprolol, 1 mg/kg + 0.5 mg/kg, that resulted in pressure-rate-index comparable to that of 1.0 mg/kg carvedilol, failed to reduce myeloperoxidase activity in the ischemic myocardial tissue, and the infarct size (35+/-3.1%) was significantly larger than in carvedilol-treated animals. Taken together, this study suggests that the superior cardioprotection of carvedilol over metoprolol is not a consequence of hemodynamic variances but possibly the result of the additional pharmacological properties of carvedilol such as the antioxidant and anti-neutrophil effects.
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LV dysfunction occurs after PTCA, as described in animal models after ischemia. Alpha-blockers abolished LV, macrocirculatory and microcirculatory dysfunction, whereas the alpha-blocker effect was prevented by combining alpha- and beta-blockers. The evidence of diffuse rather than regional dysfunction, together with the opposite effects of alpha- and beta-blockade, supports the hypothesis of neural mechanisms eliciting postischemic LV dysfunction.
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Structural and functional changes of the pulmonary circulation, particularly during the pathogenesis of pulmonary arterial hypertension (PAH), remain to be fully elucidated. In this study, we utilized monochromatic synchrotron radiation (SR) microangiography to assess changes in pulmonary arteriole blood flow in the intact-chest rat after 4 wk of chronic hypoxia. Sprague-Dawley rats were exposed to normoxia (N-rats) or chronic hypoxia (10% O(2); CH-rats) for 28 days. Rats were anesthetized, and microangiography was performed on the left lung to assess 1) the branching distribution of pulmonary arteriole blood flow (internal diameter >80 microm) and 2) dynamic changes in vessel lumen diameter during acute hypoxic (8% O(2) for 4 min) pulmonary vasoconstriction (HPV) before and after beta-adrenoceptor blockade (2 mg/kg i.v. propranolol). Using SR angiography, we observed that the number of opaque third- and fourth-generation vessels (100-300 microm) for CH-rats was significantly fewer than the number for N-rats. The magnitude of HPV was not different between CH-rats and N-rats. Beta-adrenoceptor blockade accentuated the HPV in 200- to 300-microm vessels for CH-rats, but even more so in N-rats. However, in CH-rats, beta-adrenoceptor blockade also accentuated the HPV in 100- to 200-microm vessels. In summary, we utilized SR to assess gross blood flow changes and functional changes (i.e., HPV) of the pulmonary circulation in PAH. These results highlight the benefits of SR for assessing pulmonary circulatory pathology. Of particular importance, future use of SR will provide an effective method for assessing potential therapeutic treatments for PAH.
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Brain cytochrome P450 2D (CYP2D) metabolises exogenous neurotoxins, endogenous substances and neurotransmitters. Brain CYP2D can be regulated in an organ-specific manner, but the possible regulatory mechanisms are poorly understood. We investigated the involvement of miRNAs in the selective regulation of brain CYP2D by testosterone and the corresponding alteration of the pharmacological profiles of tramadol by testosterone.
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This paper describes the inhibitory effect produced by propranolol pre-treatment on lipid synthesis in flank organs from intact, gonadectomized, and isoproterenol-treated male hamsters. Furthermore, the effect induced by the same treatments on gland sebum composition is reported.
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Tobacco withdrawal is characterized by a negative mood state and relatively mild somatic symptoms. Increased noradrenergic transmission has been reported to play an important role in opioid withdrawal, but little is known about the role of noradrenergic transmission in nicotine withdrawal.
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COX inhibitors and β-adrenergic blockers were recently shown to reduce cancer progression in animal models through various mechanisms. These include the prevention of immune suppression during the critical perioperative period, and the preclusion of direct promoting effects of catecholamines and prostaglandins on malignant tissue growth. To assess the safety of such pharmacological treatments in the context of oncologic surgery, the current study evaluates wound healing efficacy in the skin, muscle, and colon tissues in rats undergoing colonic anastomosis.
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The patient was a 62-year-old woman with a personal history of chronic alcoholism and a medical history of duodenal ulcer, congestive heart failure, atrial fibrillation, dilated cardiomyopathy, and recurring urinary tract infections. She had osteoporosis, cirrhosis of the liver and portal hypertension. She had undergone surgery for multiple arm fractures after an accidental fall in the previous year and had received NSAIDs without concomitant gastric protection. On the fourth day of hospitalization she had an episode of haematemesis. The patient continued to take NSAIDs as required, as well as habitual medication of propranolol 40 mg/day, spironolactone 25 mg/day, furosemide 40 mg/day, pantoprazole 40 mg/day and strontium 2 g/day. Upper digestive endoscopy (UDE) revealed level I/II (Baveno) oesophageal varicose veins with no signs of haemorrhage and portal hypertensive gastropathy. The duodenal bulbous was deformed by an extensive ulcer with blood clots and one vessel was visible along the antero-superior portion (Forrest IIa classification). Numerous superficial ulcers with haemosiderin pigment at D2 were observed. Endoscopic haemostasis was achieved with epinephrine and bipolar probe. Food was suspended and the patient received continuous intravenous treatment with pantoprazole 8 mg/h. UDE repeated after 48 hours showed no signs of haemorrhaging from the ulcer. After 72 hours, the pantoprazole dose was changed to 40 mg every 12 hours and food was allowed. After 12 days with no recurrence of the haemorrhagic incident, the patient was prescribed oral pantoprazole 40 mg once daily and released from hospital.
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The mechanisms underlying metabolic inhibition of sympathetic responses within exercising skeletal muscle remain incompletely understood. The aim of the present study was to test whether alpha(2)-adrenoreceptor-mediated vasoconstriction was more sensitive to metabolic inhibition than alpha(1)-vasoconstriction during dynamic knee-extensor exercise. We studied healthy volunteers using two protocols: (1) wide dose ranges of the alpha-adrenoreceptor agonists phenylephrine (PE, alpha(1) selective) and BHT-933 (BHT, alpha(2) selective) were administered intra-arterially at rest and during 27 W knee-extensor exercise (n= 13); (2) flow-adjusted doses of PE (0.3 microg kg(-1) l(-1)) and BHT (15 microg kg(-1) l(-1)) were administered at rest and during ramped exercise (7 W to 37 W; n= 10). Ultrasound Doppler and thermodilution techniques provided direct measurements of femoral blood flow (FBF). PE (0.8 microg kg(-1)) and BHT (40 microg kg(-1)) produced comparable maximal reductions in FBF at rest (-58 +/- 6 versus-64 +/- 4%). Despite increasing the doses, PE (1.6 microg kg(-1) min(-1)) and BHT (80 microg kg(-1) min(-1)) caused significantly smaller changes in FBF during 27 W exercise (-13 +/- 4 versus-3 +/- 5%). During ramped exercise, significant vasoconstriction at lower intensities (7 and 17 W) was seen following PE (-16 +/- 5 and -16 +/- 4%), but not BHT (-2 +/- 4 and -4 +/- 5%). At the highest intensity (37 W), FBF was not significantly changed by either drug. Collectively, these data demonstrate metabolic inhibition of alpha-adrenergic vasoconstriction in large postural muscles of healthy humans. Both alpha(1)- and alpha(2)-adrenoreceptor agonists produce comparable vasoconstriction in the resting leg, and dynamic thigh exercise attenuates alpha(1)- and alpha(2)-mediated vasoconstriction similarly. However, alpha(2)-mediated vasoconstriction appears more sensitive to metabolic inhibition, because alpha(2) is completely inhibited even at low workloads, whereas alpha(1) becomes progressively inhibited with increasing workloads.
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We examined 44 hyperthyroid patients and 19 euthyroid healthy controls. Patients were divided into three groups according to the treatment: Propylthiouracil (PTU) group, PTU + propranolol (PRP) group, PTU + PRP + vitamin E (vitE) group.
A lot of patients suffer from abdominal pain, nausea and vomiting. They are often seen in many departments and specialities. A few of these may suffer from abdominal migraine and can be treated well with antimigraine medication. This is a case report of a 25-year-old woman predisposed to migraine and with migraine headache who suffered from attacks of abdominal pain, anorexia, nausea and vomiting. She was thoroughly examined without any signs of abdominal pathology and was then referred to a neurological specialist who successfully treated her with propranolol.
It has been reported that stress-related activation of the noradrenergic system strengthens the formation of aversive memories and that beta-adrenergic receptors seem to be involved in this emotional memory processing. In this study, the effects of beta-adrenergic compounds on the extinction of contextual conditioned fear responses were evaluated. Rats were trained with footshock in a conditioning box. In the 3 days following the training, the animals were re-exposed to the apparatus and received either a single or repeated intraperitoneal injections of the beta-adrenergic antagonist propranolol, the beta-adrenergic agonist isoproterenol, or saline 30 min before (acquisition of extinction) or immediately after (consolidation of extinction) the extinction sessions. A drug-free session was performed on the last day. While repeated isoproterenol treatment facilitated the consolidation of contextual fear extinction, repeated propranolol administration impaired the acquisition and the consolidation of this process. Further, the role of ventromedial prefrontal cortex (vmPFC) in the extinction of contextual conditioned fear was tested with an immunohistochemistry assay. Our results show a reduction in Fos-protein expression between the first and the last extinction session. In a follow-up experiment, intra-vmPFC microinjection of isoproterenol before the first extinction session facilitated the extinction of contextual fear. This facilitation was antagonized by pre-treatment with atenolol, suggesting that this change is mediated by beta-1-adrenergic activity. Our results reinforce the role of the vmPFC in fear extinction mechanisms, suggesting that vmPFC-beta-1-adrenergic receptor activation underlies part of the facilitation of the fear extinction processes.
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At initial hemodynamic assessment, SMV contraction augmented mean diastolic blood pressure by 24.6% (from 61 +/- 7 to 76 +/- 9 mm Hg). Presystolic pressure was reduced by 15% (from 60 +/- 8 to 51 +/- 7 mm Hg) after an assisted beat. Four animals died early, 1 from a presumed arrhythmia, and 3 during propranolol-induced hypotension. The other 6 animals survived for 273, 596, 672, 779, 969, 1,081, and 1,510 days. Diastolic augmentation was 27.4% at 1 year (93 +/- 9 vs 73 +/- 6 mm Hg; n = 5), 34.7% at 2 years (85 +/- 6 vs 63 +/- 7 mm Hg; n = 3), 21.2% (89 +/- 10 vs 73 +/- 8 mm Hg; n = 2) at 3 years, and 34.5% (78 vs 58 mm Hg; n = 1) after 4 years in circulation. After 4 years, the isolated SMV was able to maintain a pressure of over 80 mm Hg while ejecting fluid at 20 mL/s. No animal showed evidence of SMV rupture or thromboembolism.
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Frequent migraine sufferers who failed to respond to 5 weeks of optimized acute migraine drug therapy were randomized to a 2 (Behavioral Migraine Management+, Behavioral Migraine Management-) × 2 (β-blocker, placebo) treatment design.
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Acute experiments with dogs showed that irritation of the sympathetic trunk in the thoracic cavity is more likely to amplify than inhibit duodenal contractions. This stimulating effect is better seen with alpha- and beta-adrenoreceptors blocked by phentolamine hydrochloride and inderal and cannot be eliminated with dizergol used to block S1,2 receptors of the cellular membranes in smooth muscles. On the evidence and literary data it was deduced that the sympathetic trunk contains some serotoninergic nervous fibers potent to stimulate contractions of the duodenum.
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The mean observation times were 4.1 years in the TIPS group and 3.6 years in the EVL group. Although the probability of rebleeding was higher in the EVL group (29.9%) than in the TIPS group (19.4%), the difference was not statistically significant. Three of five patients of the EVL group successfully underwent TIPS placement after treatment failure. The probability of TIPS dysfunction requiring shunt revision was 89 %. Hepatic encephalopathy was observed more often in the TIPS group (40.5%) than in the EVL group (20.5%; P < 0.05). The probability of survival was similar in both groups (TIPS group 75.9%, EVL group 82.2%; n.s.).
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A novel pharmacogel was developed for the enhanced transdermal delivery of propranolol hydrochloride (PH). The synthesized prodrugs, propranolol palmitate hydrochloride (PPH) and propranolol stearate hydrochloride (PSH) self-assembled to form gel simply upon mixing alcoholic solution of prodrug with an aqueous solution in a specified ratio. By varying the ratio of prodrug, alcohol and water, three-component phase diagram was constructed which revealed isotropic-gel-vesicular dispersion regions, respectively concomitant to increasing the ratio of water. The gel phase is termed 'Pharmacogel' and exhibits birefringence under plane-polarized light corroborating the presence of lamellar liquid crystals. The pharmacogel by virtue of high chemical potential gradient and improved physicochemical properties showed the enhanced in-vitro skin permeation flux of 51.5+/-3.7 and 42.5+/-3.1 microg/cm(2)/h from PPH and PSH gel, respectively, as compared to 1.9+/-0.1 microg/cm(2)/h for control; and decrease in lag time (1.8 and 2.8 h for PPH and PSH gel, respectively) compared to control (7.6 h) was observed. The admixing of egg lecithin (EL) in increasing ratio concomitantly decreased the flux values to 31.7+/-2.1 microg/cm(2)/h (at a mole ratio of 50:50 PPH:EL) and increased the lag time. In the gel containing 50% EL, the addition of span 40 and cholesterol slightly reduced the permeation while sodium deoxycholate and Tween-80 improved it. The plasma drug levels following transdermal application of control were low (C(max)=23 ng/ml) while in PPH gel, it increased with time reaching C(max) of 94 ng/ml at 8 h post-application of PPH gel (C(max) of 75 ng/ml at 12 h post application of PL5 gel) and maintained for longer times. The AUC(0-32 h) for PPH gel was much higher (1968 ng h/ml) than control (AUC(0-18 h) was 239 ng h/ml), while EL mixed gel also showed better absorption (AUC(0-32 h) was 1707 ng h/ml). The gel formulations also caused less irritation than control, while mixed gel showed least irritation. This novel self-assembled pharmacogel providing high transdermal permeation with many variables to regulate the delivery is therefore having a great potential in percutaneous delivery.
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Calcium pumping into the endoplasmic reticulum (ER) lumen is thought to be coupled to a countertransport of protons through sarcoplasmic/endoplasmic reticulum calcium ATPase (SERCA) and the members of the ClC family of chloride channels. However, pH in the ER lumen remains neutral, which suggests a mechanism responsible for proton re-entry. We studied whether cation-proton exchangers could act as routes for such a re-entry. ER Ca(2+) uptake was measured in permeabilized immortalized hypothalamic neurons, primary rat cortical neurons and mouse cardiac fibers. Replacement of K(+) in the uptake solution with Na(+) or tetraethylammonium led to a strong inhibition of Ca(2+) uptake in neurons and cardiomyocytes. Furthermore, inhibitors of the potassium-proton exchanger (quinine or propranolol) but not of the sodium-proton exchanger reduced ER Ca(2+) uptake by 56-82%. Externally added nigericin, a potassium-proton exchanger, attenuated the inhibitory effect of propranolol. Inhibitors of small conductance calcium-sensitive K(+) (SK(Ca)) channels (UCL 1684, dequalinium) blocked the uptake of Ca(2+) by the ER in all preparations by 48-94%, whereas inhibitors of other K(+) channels (IK(Ca), BK(Ca) and K(ATP)) had no effect. Fluorescence microscopy and western blot analysis revealed the presence of both SK(Ca) channels and the potassium-proton exchanger leucine zipper-EF-hand-containing transmembrane protein 1 (LETM1) in ER in situ and in the purified ER fraction. The data obtained demonstrate that SK(Ca) channels and LETM1 reside in the ER membrane and that their activity is essential for ER Ca(2+) uptake.
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Venous compliance was derived from the relationship between changes in mean circulatory filling pressure (MCFP) and changes in blood volume (BV). Measurements were performed before and after i.v. propranolol (7.5 mg/Kg) or placebo in rats with portal hypertension due to PPVL and sham operated controls.
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Mitochondria represent a possible drug target with unexplored therapeutic and toxicological potential. The possibility was suggested that antidepressants, mood stabilizers and other drugs may show some therapeutic and/or toxic effects through their action on mitochondrial functions. There are no sufficient data about the effect of these drugs on mitochondrial respiration in the brain. We investigated the in vitro effects of amitriptyline, fluoxetine, tianeptine, ketamine, lithium, valproate, olanzapine, chlorpromazine and propranolol on mitochondrial respiration in crude mitochondrial fractions of pig brains. Respiration was energized using substrates of complex I or complex II and dose dependent drug-induced changes in mitochondrial respiratory rate were measured by high-resolution respirometry. Antidepressants, but not mood stabilizers, ketamine and propranolol were found to inhibit mitochondrial respiratory rate. The effective dose of antidepressants reaching half the maximal respiratory rate was in the range of 0.07-0.46 mmol/L. Partial inhibition was found for all inhibitors. Differences between individual drugs with similar physicochemical properties indicate selectivity of drug-induced changes in mitochondrial respiratory rate. Our findings suggest that mood stabilizers do not interfere with brain mitochondrial respiration, whereas direct mitochondrial targeting is involved in mechanisms of action of pharmacologically different antidepressants.
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The average age at presentation was 3.1 months (3 weeks to 9 months). The patients received oral propranolol, with dosage varying among study centers. The patients were treated for an average of 7.1 months. Treatment of 5 infantile hemangioma patients with oral propranolol produced a significant reduction in the size of the hemangioma in 4 (80%) of the patients and a minimal improvement in one patient. No patient had significant adverse events during the treatment period.
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Effects of the tricyclic antidepressant clomipramine on plasma glucose levels in mice were studied. Clomipramine at doses ranging 5 - 20 mg/kg elicited significant hyperglycemia in mice. Hyperglycemia elicited by clomipramine was not reduced by pretreatment with the 5-hydroxytryptamine (5-HT) depleter p-chlorophenylalanine. The 5-HT(1/2/5/7)-receptor antagonist methysergide and the 5-HT(2A/2B/2C)-receptor antagonist LY 53857 enhanced clomipramine-induced hyperglycemia, while the 5-HT(1A/1B)-receptor antagonist (-)-propranolol and the 5-HT(3/4)-receptor antagonist tropisetron did not affect it. The 5-HT(2B/2C)-receptor antagonist SB 206553 facilitated hyperglycemia induced by clomipramine, although the 5-HT(2A)-receptor antagonist ketanserin was without effect. Clomipramine-induced hyperglycemia was reduced by prior adrenalectomy. These results suggest that clomipramine induces hyperglycemia in mice by blocking the 5-HT(2B )and/or 5-HT(2C) receptors, which results in facilitation of adrenaline release.
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Iron deficiency (ID) results in ventricular hypertrophy, believed to involve sympathetic stimulation. We hypothesized that with ID 1) intravenous norepinephrine would alter heart rate (HR) and contractility, 2) abdominal aorta would be larger and more distensible, and 3) the beta-blocker propanolol would reduce hypertrophy.
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Activated blood platelets play a key role in the genesis of many pathological states. Several studies have documented that beta-blockers can influence platelet aggregation. Carvedilol, a third generation non-selective agent with vasodilatory properties, is successfully used in pathological states accompanied with platelet hyperreactivity, however information on its antiplatelet activity is lacking.
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To examine treatment indications, efficacy and side effects of oral beta-blockers for the treatment of problematic hemangiomas.
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Two Romanian (Caucasian) young patients presented with hypokalemic paralysis. TSH, FT4, TT3 was measured by immunochemiluminescence. Case report 1. Patient O.R, aged 19, presented marked asthenia and lower limbs paralysis, following high carbohydrate meal. He declared 10 kg weight loss on hypocaloric diet and mild sweating. Biochemical data revealed moderate hypokalemia (K+=2.6 mmol/L) and thyrotoxicosis (TSH<0.03 mIU/L, FT4=30 pmol/L, TT3=315 ng/dL). Case report 2. Patient T.A., aged 18, presented 2 episodes of weakness and flaccid paralysis, with hypokalemia, precipitated by effort, without any sign of thyrotoxicosis. Biochemical data revealed severe hypokalemia (K+=1.8 mmol/L) and thyrotoxicosis (TSH<0.03 mIU/L, FT4=24 pmol/L, TT3=190 ng/dL). Treatment with intravenous potassium, thereafter methimazole and propranolol were administered in both cases, with the maintenance of normal kalemia and thyrotoxicosis' control.
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A heart rate <100 beats/min may be present in 5% of fetuses with arrhythmia. In this study, we sought to define the feasibility of in utero diagnosis of the underlying mechanisms and the postnatal outcome.
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1. Fenoldopam mesylate, a benzazepine derivative, is a D1 receptor agonist that lowers blood pressure through vasodilation of renal, mesenteric, coronary and cerebral vascular beds. 2. Experiments were performed in rats, and mean carotid blood pressure and heart rate were registered. Two series of experiments were performed: (1) fenoldopam as control group and (2) fenoldopam after pretreatment with one of the following drugs: the D1 antagonist SCH 23390, the D2 antagonist sulpiride, the selective beta1-adrenergic antagonist atenolol, the selective beta2-adrenergic antagonist ICI 118.551, the nonselective beta-adrenergic antagonist propranolol and the neurotoxin that destroys catecholaminergic nerve terminals 6-hydroxydopamine (6-OH-DA). 3. Fenoldopam produced a dose-dependent hypotensive effect that was not modified by pretreatment of the rat with atenolol or propranolol; however, ICI 118.551 produced a significant reduction of the hypotensive response induced by fenoldopam. 4. Pretreatment of the animals with SCH 23390 produced a significant dose-related reversal of the rat blood pressure reduction induced by low doses of fenoldopam. Sulpiride produced a result similar to that induced by pretreatment with SCH 23390. 5. The pretreatment of the animals with 6-OH-DA surprisingly attenuated the response induced by fenoldopam and produced only a significant reversal of the reduction of mean blood pressure induced with the lower dose of fenoldopam. 6. The findings obtained in the present work do not provide further evidence of direct participation of beta2-adrenergic receptors on the mechanism of action of fenoldopam. Its action seems to be mainly due to activation of D1 cardiovascular receptors.
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To characterize membrane-receptor peculiarities in adrenergic and histaminergic systems under model peroxide effect in bronchial asthma (BA).
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Major depression is a neuropsychiatric disorder that can involve profound dysregulation of mood. While depression is associated with additional abnormalities besides reduced mood, such as cognitive dysfunction, it is not well established that sensory perception is also altered in this disorder (aside from in psychotic depression). Recent studies have shown that visual processing, in as early a stage as the retina, is impaired in depression. This paper examines the hypothesis that major depression can involve alterations in sensory perception.