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Background and Aim: Cardiovascular diseases are the leading cause of morbidity and mortality worldwide. Increased histamine level in the cardiac tissue has deleterious effects after ischemia-reperfusion occurrence. Regarding the existence of histamine type 2 receptors in the heart and their decisive role in inflammation, in the present study the cardioprotective effects of ranitidine in the factors effective gainst LV functions and the extent of the infarcted area were studied. Materials and Methods: Thirty-two male Balb/C mice were divided into 4 equal groups. The control group received saline the others were administered 400 mg/kg ranitidine, ip. Group RE just on the test day R14 and R28 groups for 14 and 28 consecutive days, respectively. Then, the hearts of the subjects were isolated and subjected to Langendorff-perfusion with induced global ischemia for 30 minutes followed by reperfusion of 60 minutes. Left ventricular systolic (LVSP), and end diastolic pressures (LVEDP), heart rate (HR) and coronary flow (CF) were measured, and left ventricular developed pressure (LVDP= LVSP-LVEDP) and contractility (+dp/dt) calculated. Myocardial infarct size was determined by triphenyltetrazolium chloride staining. Results: Ranitidine can significantly increase LVSP and decrease infarct size especially in R28 compared to the control group (P<0.01). Conclusion: It was found that ranitidine of 400 mg/kg dose, esp. during chronic phase can be cardioprotective against ischemia-reperfusion damage through improvement of cardiac performance.

Keywords: Ranitidine, Ischemia, Reperfusion, Injury, Histamine

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