Guski H, Meyer R, Fernández-Britto J E
Institute of Pathology, School of Medicine (Charité), Humboldt University of Berlin, FRG.
Exp Pathol. 1991;41(2):79-97. doi: 10.1016/s0232-1513(11)80005-8.
Experimental studies were conducted into 170 adult male Wistar rats for the purpose of analysis of cellular adaptation processes of the myocardium to acute ischemia. One group of the animals were exposed to physical endurance training, i.e. 180 h of swimming exercises, up to 3 h daily. Positive verification of cardiac hypertrophy was considered a measure of accomplished cellular adaptation. Training-induced increase of relative and absolute heart weight was 25 and 30%, respectively. Acute myocardial ischemia had been produced by ligature of the left coronary artery. There were no significant differences between trained and untrained animals for incidence and size of infarction and postoperative lethality, while cardiac decompensation was less often recorded from trained animals. To study cellular adaptation as well as differences between trained and untrained animals, tissue samples were taken from the non-ischemic part of the left ventricle and checked by means of histology, electron microscopy, morphometry, quantitative histochemistry, and histo-autoradiography 1, 2, 4, 7, and 14 days after occlusion of the coronary artery. The studies have shown endurance training to result in unambiguous modification of structural as well as functional response of the nonischemic heart. Included in such structural modification at cellular level are significant changes in mitochondrial membranes, sarcoplasmic reticulum, and T-system. Structural modification was reflected in changes to the oxidative enzymes and DNA metabolism. Different patterns of cellular reaction could be positively verified up to 14 days after myocardial infarction.