Comparative Effects Of Verapamil Research Articles

Comparative Effects of Verapamil, Nicardipine, and Nitroglycerin on Myocardial Ischemia/Reperfusion Injury

The aim of this experiment was to establish whether verapamil, nicardipine, and nitroglycerin have (1) infarct size-limiting effects and (2) antiarrhythmic effects in in vivo rabbit hearts during ischemia/reperfusion. Rabbits received regional ischemia by 30 min of left anterior descending coronary artery occlusion followed by 3 hours of reperfusion under ketamine and xylazine anesthesia. The animals were randomly assigned to the following 4 treatment groups: a control group, a verapamil group, a nicardipine group, and a nitroglycerin group. A continuous infusion of verapamil, nicardipine, or nitroglycerin was initiated 5 min prior to ischemia. Infarct size/area at risk decreased in verapamil, and nitroglycerin. The incidence of ischemia-induced arrhythmia decreased in nicardipine, verapamil and nitroglycerin. The incidence of reperfusion-induced arrhythmias decreased in verapamil and nitroglycerin. From the present experimental results, verapamil and nitroglycerin rather than nicardipine did afford significant protection to the heart subjected to ischemia and reperfusion in a rabbit model.

H011 Comparative effects of verapamil and amlodipine on modulation of autonomic nervous system in healthy volunteers

H011 Comparative effects of verapamil and amlodipine on modulation of autonomic nervous system in healthy volunteers

Comparative effects of verapamil and nitroprusside on left ventricular function in patients with hypertension

The effects of verapamil were compared with those of nitroprusside at matched mean arterial pressures and heart rates in 10 symptomatic hypertensive patients during cardiac catheterization. Simultaneous radionuclide angiography and micromanometer pressure measurements were obtained to assess left ventricular pressure-volume relations. Compared with control conditions, verapamil increased left ventricular end-diastolic volume index from 57 ± 16 to 70 ± 28 ml/m2 (p = 0.05) without a significant increase in left ventricular end-diastolic pressure (from 10 ± 4 to 13 ± 6 mm Hg). Despite a downward and rightward shift in the end-systolic pressure-volume relation indicating negative inotropic effects, ejection fraction did not decrease significantly (from 52 ± 9% to 46 ± 9%); cardiac index and stroke volume index remained unchanged. The change in stroke volume index with verapamil was directly related to the magnitude of change in end-diastolic volume index (r = 0.82, p < 0.005), suggesting that the increase in enddiastolic volume did not arise purely from negative inotropic effects. Systemic vascular resistance index decreased from 42 ± 8 to 34 ± 7 mm Hg-min-m2/liter (p < 0.05).In contrast, nitroprusside decreased left ventricular end-diastolic volume index from 57 ± 16 to 41 ± 10 ml/m2 (p < 0.05), cardiac index from 3.2 ± 0.7 to 2.8 ± 0.6 liters/min per m2 (p < 0.05) and stroke volume index from 28 ± 6 to 24 ± 5 ml/m2 (p < 0.01), with no change in systemic vascular resistance index (40 ± 10 mm Hg·min·m2). The end-systolic pressure-volume relation shifted downward and leftward in all patients, stemming from altered left ventricular loading.Thus, in equihypotensive doses, verapamil and nitroprusside have markedly different effects on left ventricular function. The peripheral vasodilation and apparent improvement in left ventricular filling during verapamil balanced the negative inotropic effects, resulting in maintenance of stroke volume and cardiac index. The primary hypotensive effect of verapamil was a decrease in systemic vascular resistance, whereas that of nitroprusside was a decrease in cardiac index stemming from reduced left ventricular preload.

Comparative effects of verapamil and D-600 on the contractile responses produced by neurotransmitters and depolarizing agents in the rat isolated seminal vesicle

1. 1. The comparative effects of verapamil and D-600, on isometric contractions produced by noradrenaline, acetylcholine, phenylephrine, clonidine, carbachol and high potassium, were studied in rat isolated seminal vesicle. 2. 2. The aim was to see if verapamil and D-600 differed, in their selectivity, of blocking calcium, channels, and hence inhibition of isometric contractions produced in this preparation. 3. 3. Verapamil (1 μM) and D-600 (9.5 μM), selectively, reduced the isometric contractions, greater reductions occurred in the KCl-induced contractions (control EC 50 19 ± 1.5 mM, in verapamil 58 ± 1.3 mM, and in D-600 37 ± 2.0 mM, means ± SE, n = 8, P < 0.001, <0.01, respectively). 4. 4. It was concluded that KCl-induced contractions were voltage-dependent, whereas noradrenaline operated via both voltage and receptor-mediated mechanisms. 5. 5. The clinical relevance of these results was discussed, and it may help our current understanding of the pharmacological management of sexual dysfunction.

The comparative effects of verapamil and a new dihydropyridine calcium channel blocker on digoxin pharmacokinetics

Conflicting conclusions have been reported about interaction of calcium channel blockers with digoxin. The effects of verapamil (240 mg/day) and a new dihydropyridine calcium channel blocker, isradipine (15 mg/day), on the pharmacokinetics of 1 mg intravenous digoxin were compared. All 24 volunteer subjects were healthy, male, nonobese, and aged 18 to 38 years. Groups of 12 subjects received each oral agent over 15 days, with collections of blood and urine for 72 hours after intravenous digoxin. Significant (P less than 0.05) reduction in nonrenal (7.01 +/- 1.97 to 4.00 +/- 1.86 L/hr) and total clearance (14.1 +/- 2.6 to 11.5 +/- 2.5 L/hr) were induced by verapamil, without change in renal clearance. A near-significant (P less than 0.1) increase in peripheral volume of distribution contributed to prolonged elimination half-life (23.1 +/- 4.4 to 34.3 +/- 9.7 hours). By contrast, isradipine caused only a 9% reduction in volume of distribution. Verapamil causes digoxin accumulation by reducing nonrenal elimination. No evidence of clinically relevant interaction of isradipine with digoxin was seen.

Comparative Effects of Verapamil, Nifedipine, and Diltiazem on Contractile Function in the Isolated Immature and Adult Rabbit Heart

Comparative Effects of Verapamil, Nifedipine, and Diltiazem on Contractile Function in the Isolated Immature and Adult Rabbit Heart

Comparative effects of verapamil and sodium nitroprusside on contraction and 45Ca uptake in the smooth muscle of rabbit aorta, rat aorta and guinea‐pig taenia coli

The effects of verapamil and sodium nitroprusside on muscle tension and 45Ca uptake activated in different ways were compared in rabbit aorta, rat aorta and guinea-pig taenia coli. In rabbit aorta, K-induced contraction was specifically inhibited by verapamil and noradrenaline-induced contraction by sodium nitroprusside. In rat aorta, both K-induced and noradrenaline-induced contractions were inhibited by verapamil or by sodium nitroprusside also. In taenia, both K- and histamine-induced sustained contractions were inhibited by verapamil but not by sodium nitroprusside. The effect of verapamil was competitively antagonized by external Ca, while that of sodium nitroprusside was not. High K, noradrenaline and histamine increased the rate of 45Ca uptake in aortae and taenia. In rabbit aorta the increment in response to high K was specifically inhibited by verapamil and the increment induced by noradrenaline was specifically inhibited by sodium nitroprusside. In rat aorta, increments induced by both high K and noradrenaline were inhibited by verapamil and by sodium nitroprusside. In taenia, the increments induced by high K and by histamine were inhibited by verapamil but not by sodium nitroprusside. These results suggest different characteristics of Ca entry systems in these smooth muscles. In rabbit aorta, there seem to be two Ca channels, one of which is activated by high K and inhibited by verapamil, while the other is activated by noradrenaline and inhibited by sodium nitroprusside. In rat aorta, both K- and noradrenaline-activated Ca pathways are sensitive to both verapamil and sodium nitroprusside whereas, in taenia, both K- and histamine-activated Ca pathways are sensitive only to verapamil.

Antiarrhythmic and hemodynamic effects of calcium channel blocking agents during coronary arterial reperfusion: Comparative effects of verapamil and nifedipine

To determine the comparative actions of the calcium channel blocking agents verapamil and nifedipine on coronary flow and ventricular arrhythmias during myocardial reperfusion, 24 open chest dogs underwent proximal occlusion of the left anterior descending coronary artery. Regional myocardial blood flow (ml/mln per 100 g) was quantltated by microspheres (strontium [ 85Sr]and cerium [ 141Ce]) 20 minutes after coronary occlusion and 10 minutes after reperfusion. Dogs were randomly assigned to one of three groups 20 minutes after coronary occlusion: (1) control group ( n = 8); (2) dogs given intravenous verapamil ( n = 8), 0.2 mg/kg body weight in 5 minutes followed by an infusion of 0.01 mg/kg per min; or (3) dogs given nifedipine ( n = 8), 100 μg/kg in 5 minutes followed by an infusion of 3 μg/kg per min. Ten minutes after reperfusion, transmural regional myocardial blood flow in the ischemic zone was unchanged by verapamil and nifedipine (p = not significant [NS]versus control value). The endocardial/epicardial ratio in the hyperemlc zone tended to be lowered by the calcium blocking agents compared with that observed in control animals. Coronary resistance during reperfusion was similar ( p = NS) in animals treated with verapamil and nifedipine. Ventricular tachycardia or fibrillation occurred in six dogs In the control group (tachycardia in three and fibrillation in three). Among dogs given verapamil, none had ventricular tachycardia and one of eight had ventricular fibrillation ( p <0.05 versus control value). Four of the eight dogs given nifedipine, had ventricular tachycardia (two dogs) or fibrillation (two dogs) ( p = NS versus control and verapamil values). Thus, verapamil and nifedipine had similar effects on central and coronary hemodynamics during myocardial reperfusion. However, verapamil, in contrast to nifedipine, decreased reperfusion ventricular arrhythmias. These data suggest that despite similar calcium channel blocking actions, verapamil and nifedipine possess different antiarrhythmic effects.

Comparative effects of verapamil and nifedipine on reactive hyperemia, and ventricular arrhythmias during coronary artery reperfusion

Comparative effects of verapamil and nifedipine on reactive hyperemia, and ventricular arrhythmias during coronary artery reperfusion