Gene/Protein Disease Symptom Drug Enzyme Compound
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Query: UMLS:C0011570 (depression)
 172,036 document(s) hit in 31,850,051 MEDLINE articles (0.00 seconds)

We investigated the effect of flecainide on systolic time intervals in 6 healthy subjects. A randomized, double blind, cross-over study was designed using flecainide (2 mg/kg), propranolol (0.2 mg/kg) or saline. In comparison with placebo, flecainide increased heart rate, diastolic BP, QT-Index, QS2-Index, PEP, and reduced LVET-Index (p less than 0.05). It caused a significant increase in PR interval, QRS duration, and PEP/LVET (p less than 0.01). Propranolol, compared with placebo, decreased heart rate and systolic BP (p less than 0.05). It increased PR interval, PEP, and PEP/LVET ratio (p less than 0.05). In comparison with propranolol, flecainide increased heart rate and QRS duration (p less than 0.01, p less than 0.001 respectively). It increased diastolic BP, PR interval, QS2-Index, PEP, and PEP/LVET ratio, and decreased LVET-Index (p less than 0.05). These changes in STI induced by flecainide may be produced by depression of myocardial contractility. Intraventricular conduction delay may be an additional contributing factor.
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PMID:The effect of a new antiarrhythmic agent, flecainide acetate, on systolic time intervals. 661 15

The venous concentrations of epinephrine and norepinephrine and changes in ventilation, respiratory gases, circulation and ECG were determined in 20 young healthy male medical students during standardized stepwise ascent to 6000 m in a low pressure chamber, once without (control) and once with beta-receptor blockade (propranolol). The results show that the plasma concentration of norepinephrine increased significantly as a result of hypoxic hypoxia. The moderate increase in epinephrine was, besides the minor but significant hypoxic influence, mainly due to psychic tension. Since beta-receptor blockade does not prevent the respiratory and circulatory adjustment, beta-adrenergic stimulation is not thought to be necessary at altitude. Propranolol, on the contrary, lowers the hypoxia-induced increase in cardiac output and diminishes the ECG changes, in particular the S-T depression, significantly. By antagonizing the effects of epinephrine and by its central effects, propranolol improves subjective tolerance to altitude, and, on the other hand, by economizing the cardiac work load, the objective ability to withstand oxygen want.
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PMID:[Effect of catecholamines and propranolol on the acute acclimatization to high altitude in man]. 666 41

The central effects of propranolol, a lipophilic beta-adrenoceptor antagonist, were investigated in six healthy male volunteers using two flash fusion threshold (2FFT), simple reaction time (SRT), digital copying test (DCT), symbol digit modalities test (SDMT), Gibson spiral maze test (GSMT) and mood rating scales for tension, alertness, depression, detachment and anxiety. Compared to placebo, 2FFT was prolonged by propranolol 40, 80 and 160 mg at one or more times tested but not by propranolol 320 mg: the largest effect was seen at 3 h after 40 mg, and the effects of 40, 80 and 160 mg were significantly greater than 320 mg at 2 h. SRTs were significantly prolonged by all doses of propranolol at 2 and 3 h and by 40 and 80 mg doses at 5 h. DCT was lowered by 40 and 80 mg at 2 and 3 h by 80 mg at 5 h, and by 320 mg at 2 h, but the 160 mg dose had no effect. Propranolol impaired the expected retest gain of the SDMT with all doses except 320 mg and at 2 h after 40, 80 and 160 mg, performance was actually worsened. Mood rating scales showed increased detachment with 40 mg and decreased alertness with 80 and 320 mg. The results show that propranolol has central effects in man: the effects appeared to be greater with lower doses, 40 and 80 mg, than with higher doses, 160 and 320 mg.
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PMID:Central effects of single oral doses of propranolol in man. 669 87

The antiarrhythmic activity of the calcium entry blockers, verapamil, nifedipine and prenylamine, was assessed against arrhythmias occurring during 20 min of acute occlusion, or upon rapid reperfusion of the left anterior descending coronary artery (LAD) in anesthetized pigs. Propranolol, which may indirectly reduce calcium entry by blocking the facilitory action of catecholamines on slow channel conductance, was also evaluated for antiarrhythmic activity in this acute arrhythmia model. Only verapamil (0.2 mg/kg i.v.) reduced both the number of arrhythmias occurring during LAD occlusion and the incidence of ventricular fibrillation (VF) occurring after occlusion and reperfusion. Although both nifedipine (0.04-0.2 mg/kg i.v.) and propranolol (1-2 mg/kg i.v.) produced a slight but significant (P less than 0.05) dose-dependent decrease in the incidence of VF during the occlusion period only, this protection was accompanied by a significant increase in ectopic activity. The increase in ectopic activity produced by propranolol (1.0 mg/kg i.v.) persisted even in combination with verapamil (0.2 mg/kg i.v.) which given alone decreased the ectopic frequency. Prenylamine up to 5 mg/kg was without significant antiarrhythmic or antifibrillatory activity. However, unlike verapamil and nifedipine, this drug produced only slight changes in heart rate or blood pressure which suggested the presence of only minimal calcium entry blocking action on myocardial and vascular tissue at the doses we employed. Because the relative antifibrillatory efficacies of verapamil and nifedipine paralleled the relative efficacies reported for depression of atrioventricular conduction, this may implicate the slow inward current channel in the etiology of VF occurring during acute myocardial ischemia.(ABSTRACT TRUNCATED AT 250 WORDS)
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PMID:Acute coronary artery occlusion-reperfusion arrhythmias in pigs: antiarrhythmic and antifibrillatory evaluation of verapamil, nifedipine, prenylamine and propranolol. 669 12

We examined the effects of four antiarrhythmic drugs (quinidine, disopyramide, procainamide and propranolol) on sinus cycle length (SCL), sinoatrial conduction time (SACT) measured by a constant atrial pacing technique, and atrial developed tension (DT), using isolated blood-perfused dog atrial preparations. When an infusion rate of 10-40 micrograms/min of quinidine, disopyramide or procainamide was continuously given into the sinus node artery and propranolol at a rate of 1-4 micrograms/min, all the agents prolonged SCL and SACT, and reduced DT dose-dependently, but not in the same fashion. Propranolol caused almost a parallel action in prolongation of SCL and SACT, and reduction of DT in increasing doses. Quinidine, disopyramide and procainamide caused negative inotropic and chronotropic effects with only a small prolongation of SACT in a relatively small dose. At larger doses, quinidine and disopyramide produced a relatively more marked prolongation of SACT than procainamide. In the doses used, quinidine, disopyramide and procainamide caused relatively small depression of DT in contrast to propranolol. The order of potencies for inducing a prolongation of SACT was propranolol greater than quinidine = disopyramide greater than procainamide.
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PMID:Effects of 4 antiarrhythmic drugs on sinoatrial conduction time in isolated and blood-perfused dog atria. 672 25

The acute haemodynamic effects of beta-blockade with propranolol and combined alpha-blockade and beta-blockade with labetalol were compared in a randomised study in 12 patients with coronary artery disease proved by angiography. Propranolol induced significantly greater depression of left ventricular function both at rest and during exercise than labetalol. This difference was probably attributable to the vasodilator activity of labetalol and the associated reduction in afterload offsetting the haemodynamic disadvantages of blockade of cardiac beta-adrenoceptors alone. The haemodynamic advantages of combined alpha-blockade and beta-blockade over beta-blockade alone may thus have therapeutic implications for the use of these treatments in patients with coronary heart disease.
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PMID:Haemodynamic advantages of combined alpha-blockade and beta-blockade over beta-blockade alone in patients with coronary heart disease. 680 69

To evaluate the role of ventricular baroreceptors in humans, we studied the effects of propranolol on reflex vasoconstrictor responses to simulated orthostatic stress. We measured forearm vascular resistance in 10 normal males in the control state and during lower body negative pressure (LBNP) at -10 and -40 mm Hg before and after propranolol (0.1 mg/kg i.v.). Baseline forearm vascular resistance showed no significant change: 23.9 +/- 3.4 U (+/- SEM) before vs 28.0 +/- 0.5 U after propranolol. Reflex increases in forearm vascular resistance during LBNP at -10 and -40 mm Hg were 5.2 +/- 1.2 and 21.2 +/- 6.6 U before and 3.4 +/- 1.2 and 10.6 +/- 2.2 U, respectively, after propranolol. Thus, propranolol significantly (p less than 0.05) reduced responses to LBNP at -40 mm Hg. In contrast to the effects with LBNP, propranolol did not attenuate increases in forearm vascular resistance during the cold pressor test and handgrip, thus excluding a nonspecific depression of reflexes. We also studied the effects of propranolol on carotid baroreflex-mediated vasoconstrictor responses to neck pressure at 15 and 30 mm Hg. Propranolol had no significant effect on the vasoconstrictor responses to neck pressure. In conclusion, propranolol selectively attenuates vasoconstrictor responses to LBNP. We suggest that this results from a propranolol-induced decrease in the activity of cardiac ventricular baroreceptors. The results support the view that ventricular baroreceptors play an important role in reflex adjustments to orthostatic stress in humans.
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PMID:Effects of propranolol on reflex vascular responses to orthostatic stress in humans. Role of ventricular baroreceptors. 682 36

Studies were undertaken in intact rats to characterize the renin response to pentobarbital anesthesia and the mechanisms involved in this response. Aortic and peritoneal cavity cannulas were previously implanted to allow drug infusion, blood sampling and anesthesia to be performed without stress. A sustained 2-3-fold increase in plasma renin concentration (PRC) and a 10-15 mm Hg depression of mean arterial pressure were found in pentobarbital anesthesia. Circulating levels of epinephrine and norepinephrine were unchanged. Sympathetic stimulation by tyramine did not decrease and chronic renal denervation did not abolish the PRC rise by pentobarbital. Phenoxybenzamine given to conscious or anesthesized animals elevated PRC to similar levels. Propranolol was effective in suppressing PRC in anesthetized animals, regardless of the presence or absence of phenoxybenzamine. We concluded that the renin response to pentobarbital anesthesia is unrelated to changes in sympatho-adrenal activity. The response appears to be mediated by beta-adrenergic receptors. It is postulated that pentobarbital-induced relaxation of afferent arterioles or JG cells exposes previously concealed beta-receptor sites which increase the signal for the release of renin.
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PMID:Renin release by pentobarbital anesthesia in the rat: a role for vascular mechanisms. 704 Aug 89

Selective coronarography and pharmacological test with intravenous administration of ergometrin have been carried out in 100 patients. The test permits one to demonstrate the vasospastic form of angina pectoris, which is encountered in patients with different degrees of lesions of the coronary arteries and different tolerance to exercise. Lack of coincidence in localization of ischaemic zones in the myocardium in tests with exercise and intravenous injection of ergometrin according to myocardium scintigraphy with 201Tl points to the possibility of existence of two forms of angina pectoris in the same patient, differing not only in the pathogenetic mechanisms but also in the localization of the ischaemic changes supervening in the myocardium. According to the data of echocardiography during the anginal attack with rise of the ST segment there is a more pronounced dilatation of the left ventricle cavity and decrease of the myocardial contractility than in the anginal attack with depression of the ST segment. In patients with spontaneous angina pectoris and rise of the ST segment corinfar exerted marked antianginal effect. Inderal was ineffective. In patients with angina pectoris and depression of the ST segment there was no difference between the two drugs.
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PMID:[Role of the vasospastic factor in stenocardia in ischemic heart disease]. 706 83

Multistage treadmill stress testing was performed in 24 patients with idiopathic cardiomyopathy using Bruce protocol. 5 patients were considered to have hypertrophic obstructive cardiomyopathy (HOCM), 12 hypertrophic nonobstructive cardiomyopathy (HCM) and 7 congestive cardiomyopathy (CCM). Heart rate, systemic blood pressure, electrocardiographic changes and exercise tolerance were observed. The effect of propranolol on exercise tolerance was investigated in HOCM and HCM. 1) Exercise duration was less in patients with HCM and HOCM than in normal subjects (50 subjects) and greater than in 50 anginal patients. In CCM, exercise duration was the least. 2) Electrocardiographic changes observed in HCM and HOCM were increase of T waves and lessening of ST depression. In CCM, appearance of ventricular arrhythmia was noted in 4 of 7 patients. 3) Maximam exercise tolerance was reached at Bruce state III-IV in HOCM, stage III in HCM and stage II in CCM. 4) Propranolol administration resulted in improvement of exercise tolerance in 3 of 7 patients with HOCM and HCM.
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PMID:[Treadmill exercise testing in patients with idiopathic cardiomyopathy (author's transl)]. 719 Sep 56


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