Rat myocardium and phenomenon "no reflow" were studied histologically, morphometrically and electron microscopically under the conditions of normothermic pre- and postischemic perfusion of the isolated heart with solutions of various osmolality containing K+ 30 mmol/l. The Langendorff model was used. Cardiomyocyte swelling is regarded as a possible factor in the development of phenomenon "no reflow". Pre-ischemic perfusion with a hyperpotassium solution prevents the myocardium ischemic contracture; postischemic reperfusion enhances the myocardium vacuole degeneration and contractural damage of the right ventricle cardiomyocytes. An increase of the cardioplegic solution osmolality results in the mosaic damage of the left ventricle, a decrease of contracture surface of the right ventricle. Its myocardium resistance to the ischemic/reperfusion damage under the condition of the normothermic heart reperfusion, including that with the hyperpotassium solutions, is found greater as compared to the left ventricle.
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