Abstract

Calcium antagonists may protect the myocardium against the consequences of ischemia. Phosphorus-31 nuclear magnetic resonance (31P NMR) was used to study the effect of nifedipine on intracellular acidosis and high energy phosphate depletion during global ischemia. Isolated rat hearts were paced (300 beats/min), perfused with a modified Tyrode solution for 30 min, made totally ischemic for 30 min (37 degrees C) and then reperfused for 30 min. When required, nifedipine (1 mg/l) was added to the perfusion fluid 10 min before ischemia. During ischemia intracellular pH fell from 7.11 +/- 0.03 (mean +/- S.E.M.) to 5.88 +/- 0.04 in the untreated hearts (n = 6), and from 7.11 +/- 0.03 to 5.95 +/- 0.02 in the treated hearts (n = 6). During the first 20 min of ischemia, intracellular pH was significantly higher in the treated than in the untreated hearts (P less than 0.001). Myocardial creatine phosphate (CP) content was depleted after 15 min of ischemia in the untreated hearts, and after 20 min of ischemia in the hearts treated with nifedipine. Myocardial adenosine triphosphate (ATP) content was depleted after 20 min of ischemia in the untreated hearts; ATP content in hearts that received nifedipine amounted to 23.5 +/- 6.2% of control after 30 min of ischemia. In contrast with the untreated hearts, the nifedipine-treated hearts showed a rapid recovery of CP content during reperfusion. The results indicate that nifedipine protects the myocardium against the metabolic consequences of ischemia and reperfusion.

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