摘要: <正>In the isolated rabbit heart of recirculating nonpulsatile perfusion circuit, furyl-dihydropyridines I 20μmol/L greatly reduced the leakage of myocardial enzymes and the concentration of malondialdehyden （MDA） in plasma, decreased the myocardial calcium and sodium content, maintained normal coronary vascular resistance and prevented reperfusion arrhythmias of regional postischemic reperfusion hearts. Its mechanism of protecting the ischemic-reperfused myocardium might be associated with the diminution of calcium influx of myocardial cells and celluar lipid peroxidation induced by oxygen free radicals.