The effect of the opiate receptor antagonist naloxone on myocardial contractility and relaxation after acute coronary occlusion in rabbits and the relationship between its effect and ?-adrenergie receptor were observed. The results showed that during the early stage of acute coronary occlusion myocardial contractility and relaxation were significantly increased and cardiac function was improved by naloxone; The action of naloxone can be abolised by ?-adrenergic receptor blocker propranolol. These results indicated that there was a close correlation between the action of naloxone on myocardial contractility and relaxation and the adrenergic nerve activity.

In the Langendorff's perfused isolated rat hearts, the myocardial postischemic reperfusion injury was induced by reperfusion for 30 min after stoppage of perfusion for 40 min. The effects of naloxone on the lactic acid dehydrogenase (LDH) content, the myocardial Ca contents, the myocardial malondialdiehyde (MDA) production and the myocardial superox-ide dismutase (SOD) activity were observedduring reperfusion. The results show that naloxone significantly decreased cardiac LDH release, attenuated myocardial Ca accumulation, reduced MDA production and prevented redution of SOD activity in comparison with the control in perfused isolated rat hearts with global ischemia (40 min) and reperfusion (30 min). It suggests that naloxone has protective effects on myocardial reperfusion injury.