[Alterations of the myocardium and adrenergic nerves of the isolated rat heart under conditions of total ischemia and normothermic cardioplegic reperfusion].

The increase of the ischemic period from 30 to 60 min did not enhance the degree of the contractural myocardial damage in connection with progression of "no reflow" phenomenon. Endogenous catecholamines do not play a decisive role in genesis of ischemic (reperfusion) heart damage. Cardioplegic reperfusion with a high K+ content results in a considerable loss of mediator from the adrenergic nerve fibres thus leading to the partial isolated heart desympathization.

[Myocardium of the isolated rat heart in postischemic cardioplegic normothermic reperfusion].

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".