Copyright © 1990 by the European Society of Cardiology.
© 1990 The European Society of Cardiology
Nisoldipine improves blood flow to skeletal muscles in conscious pigs with chronic heart failure
Department of Cardiology, Thoraxcenter, Erasmus University Rotterdam Rotterdam, The Netherlands
*Department of Pharmacology, Erasmus University Rotterdam Rotterdam, The Netherlands
Received 13 June 1989; revised 6 October 1989; .
Correspondence: P.D. Verdouw, PhD, Laboratory for Experimental Cardiology, Thoraxcenter, Erasmus University Rotterdam, P.O. Box 1738, 3000 DR Rotterdam, The Betherlands.
Abstract
We studied the acute effects of the calcium antagonist nisoldipine in 10 conscious pigs with chronic heart failure. Left ventricular dysfunction was induced by permanent ligation of the left circumflex coronary artery. Two to three weeks after myocardial infarction the effects of four consecutive 10 min intravenous infusions of nisoldipine (0.05;0.1; 0.25 and 0.5 fig kg1 min1) or its solvent on systemic haemodynamics were evaluated. In addition, we used the radioactive microsphere technique to study the distribution of cardiac output after each dose of nisoldipine. Nisoldipine significantly (P<0.05) increased heart rate (from 144 ±9 to 161 ±8 beats min1), cardiac output (from 21 ±0.1 to 2.9 ± 0.21 min1), stroke volume (from 14 ±1 to 18 ±1 ml) and left ventricular dP/dtmax (from 2600 ± 100 to 3500 ± 250 mmHg s1), but had no effect on arterial blood pressure. Left ventricular end-diastolic pressure (from 19±2 to 16±1 mmHg) and systemic vascular resistance (from 52 ±3 to 37 ±3 mmHg min l1) decreased after nisoldipine. The nisoldipine-induced increase in cardiac output did not affect blood flow to the kidneys, brain, liver or skin, but perfusion of the stomach (84%), adrenals (84%) and normal myocardium (from 200 ±25 to 321 ±38 ml min1 100 g1) as well as infarcted myocardium (from 41 ±8 to 61 ±19 ml min1 100 g1) increased significantly. The largest fraction of the increase in cardiac output was, however, used for the improvement of skeletal muscle blood flow (from 13 ±5 to 62±13 ml min1 100 g1). It is concluded that nisoldipine increases cardiac output in conscious pigs with heart failure, primarily by decreasing peripheral vascular resistance. The increment in cardiac output is distributed preferentially to the skeletal muscles.
Key Words: Heart failure myocardial infarction systemic haemodynamics regional blood flows coronary collateral flow nisoldipine pigs