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European Heart Journal 1983 4(11):819-822;
Copyright © 1983 by the European Society of Cardiology.
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© 1983, by the European Society of Cardiology

Diltiazem and nitrendipine suppress hypoxic contracture in quiescent ventricular myocardium

PHILIP D. HENRY and ANDREW M. WAHL

Department of Medicine, Section of Cardiology, Baylor College of Medicine Houston, Texas, USA

Received 7 January 1983; revised 4 May 1983; .

Correspondence to. Philip D. Henry, M.D., Section of Cardiology, Suite F-905, The Methodist Hospital, Baylor College of Medicine, 6535 Fannin, Houston, Texas 77030 U.S.A.

Abstract

Calcium blocking agents may protect the ischaemic heart by reducing ventricular afterload and cardiac contractility, or by augmenting myocardial perfusion. To determine whether protection is mediated in part by mechanisms unrelated to myocardial work and perfusion, we examined effects of diltiazem and nitren-dipine on unperfused myocardium subjected to hypoxia. Rabbit right ventricular papillary muscles were mounted in a myograph containing Krebs buffer equilibrated at 37°C with 95% O2–5% CO2. During brief electrical pacing at a frequency of 12 min–1 a preload of 1363±60 mg produced a maximal isometric force development of 4892±273mg(SE; n = 113). After 60 min without pacing, the quiescent muscles were pre-equilibrated randomly for 20 min without drug for control (C=38), or with 10–6 diltiazem (n = 38) or 10–6 mol–1 nitrendipine (n = 38). Changes in resting force during equilibration did not exceed ±12 mg. Subsequent sudden de-oxygenation with 95% N2–5% CO2 evoked in controls an increase in force beginning after 16±1 min. The onset of hypoxic contracture was significantly (P<0.1) delayed in treated muscles and started after 31 ± 3 min with diltiazem and after 23±2 min with nifedipine. Peak contracture was significantly (P<0.1) inhibited by diltiazem and nitrendipine compared to controls, respective values averaging 264±22 mg, 480±44 mg and 895±70 mg. Thus, calcium blockers delayed and suppressed hypoxic contracture in quiescent myocardium, demonstrating that the drugs acted directly on cardiac muscle in the absence of rhythmic electrical and mechanical activity.

Key Words: Hypoxic contracture • calcium-antagonists • diltiazem • nitrendipine • cardioplegia


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