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In the present study the effects of either H1 antagonist chloropyramine or H2 antagonist famotidine were investigated in isolated Langendorff’s rat hearts. Ischemia lasted 60 minutes. Perfusion with either 10 μmol/l chloropyramine or 10 μmol/l famotidine was initiated 10 minutes before ischemia and lasted till the end of the experiments. Registered were left ventricular pressure, heart rate, Q, coronary flow and ECG. The temperature in the left ventricle was kept at 38.5 ± 0.5 °C. The extent of myocardial damage was assessed by the release rate of the enzyme lactate dehydrogenase. In control experiments chloropyramine had negative chronotropic effect and increased Q. Its addition decreased the coronary flow during reperfusion, caused bradycardia and did not influence the lactate dehydrogenase release. In control experiments famotidine had positive inotropic and positive chronotropic effects and decreased Q. In control experiments famotidine increased the coronary flow. During reperfusion famotidine induced tachycardia and fibrillation. Famotidine did not influence the lactate dehydrogenase release during reperfusion. Results of our experiments indicate that in the rat heart additionaly to H1 receptors also H2 re- ceptors might exist and that both of them could be involved in the myocardial damage induced by ischaemia and reperfusion.