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)

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

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

Changes in the exercise ECG caused by five different drugs are presented. Analysis of these changes indicate that these are related to the hemodynamic effects of the drugs, rather than to reduction of myocardial ischemia. Calcium antagonists (Verapamil) as well as drugs which reduce heart rate (Alinidine, Propranolol) do not change the relation between ST depression and heart rate in a given patient. Drugs which lower ventricular volume (Molsidomine, Nitroglycerine) reduce the amount of ST depression at the same heart rate during exercise.
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PMID:The effects of drugs on the exercise electrocardiogram. 731 92

The effects of the ionophore RO2-2985 (X537A) on KCl- and histamine-induced contractions in porcine coronary vascular smooth muscle were studied in vitro. Cumulative dose-response curves were constructed for KCl and histamine in the presence and absence of RO2-2985. The dose-response curve to KCl in the presence of RO2-2985 was shifted to the right with no change in the maximal response attained. Lineweaver-Burk and Hill plots indicated that responses to KCl involved a positive cooperative interaction between excitation and some step or steps in the contractile event and that RO2-2985 increased this cooperativity. The dose-response curve to histamine in the presence of the ionophore was significantly shifted to the right with a 40 to 50% depression in the maximal response. Propranolol inhibited norepinephrine-induced relaxation of KCl-contracted coronary strips but did not affect RO2-2985-induced relaxation. These results suggest that RO2-2985 competitively inhibits KCl-induced contractions but inhibition of histamine-induced contractions are of a mixed mechanism. Also, RO2-2985 does not appear to induce relaxation of coronary artery smooth muscle by liberating enodgenous catecholamines. Preliminary evidence supports involvement of prostaglandins in the mechanism of ionophore-induced coronary relaxation.
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PMID:Differential inhibitory effects of the ionophore RO2-2985 (X537A) on contractile responses to potassium and histamine in coronary artery smooth muscle. 735 71

A catheter-tip velocity transducer with two high-fidelity pressure manometers was used to evaluate the left ventricular (LV) hemodynamic effects of intravenous propranolol (10 mg). Nine patients without clinical evidence of heart failure were studied. Pulsatile ascending aortic blood flow velocity and pressure and LV pressure were measured continuously during drug administration. Beat-to-beat changes in stroke volume index, stroke work index, LV end-diastolic pressure, maximum blood flow velocity and acceleration, and maximum LV dP/dt were determined. Propranolol produced a decrease in maximum blood flow velocity (from 58 +/- 4.7 to 42 +/- 5.1 cm/sec, p less than 0.002), and acceleration (from 1181 +/- 130 to 847 +/- 117 cm/sec2, p less than 0.002, max dP/dt (from 1361 +/- 70 to 1146 +/- 63 mm Hg/sec, p less than 0.002), stroke volume index (from 47 +/- 3.0 to 38 +/- 3.2 ml/m2, p less than 0.002) and total stroke work index (from 702 +/- 33 to 603 +/- 44 mJ/m2 p less than 0.04), with little change in mean aortic pressure, peak systolic pressure and LV end-diastolic pressure. Depression in myocardial function was detectable within 1 minute after initiation of propranolol and persisted when negative chronotropic effects were eliminated by atrial pacing. The multisensor catheter technique allows rapid and safe detection of changes in cardiovascular function during propranolol administration in conscious man.
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PMID:Use of catheter-tip velocity--pressure transducer to evaluate left ventricular function in man: effects of intravenous propranolol. 736 37

Vasodilator responses to dopexamine, fenoldopam and dopamine, which are known to have agonist activity at D1-dopamine receptors, were examined in the rat isolated perfused kidney preparation. Perfusion pressure was raised by perfusing with the thromboxane TxA2 analogue, U46619, and vasodilator responses were observed as dose-related falls in perfusion pressure. Propranolol (10(-6) M) and prazosin (10(-6) M) were present throughout to eliminate beta 2 and alpha 1-adrenoceptor-mediated responses, respectively. The vasodilator responses were antagonized by SCH23390 (10(-9) M), indicating that they were mediated via D1-receptors. The displacements of the dose-response curves for fenoldopam, dopexamine and dopamine were, however, non-parallel with significant depression of the maxima to 30.2, 37.9 and 34.3%, respectively. In the presence of SCH23390 (10(-8) M) and prazosin (10(-6) M), dopexamine, isoprenaline and noradrenaline produced dose-related renal vasodilation. This was antagonized by propranolol indicating a role for beta-adrenoceptors. In the case of dopexamine, the maximum response was depressed in the presence of propranolol. The reason for the atypical blockade of vasodilator responses by SCH23390 was investigated. One possibility was the appearance of transient vasoconstrictor responses at higher doses of fenoldopam, dopexamine and dopamine, usually preceding the vasodilatation. The possibility was therefore considered that the vasoconstriction may have opposed the usual vasodilation at high doses and thus limited the size of the maximum vasodilation in the presence of SCH23390. The vasoconstriction by fenoldopam was not antagonized by S-sulpiride, the D2-receptor antagonist but was blocked by mianserin and therefore attributed to 5-HT2 receptor stimulation.(ABSTRACT TRUNCATED AT 250 WORDS)
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PMID:Atypical antagonism of D1-receptor-mediated vasodilator response in the perfused kidney by SCH23390. 747 26


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