Experimental myocardial infarction in rats acclimated to simulated high altitude.

In rats exposed to a simulated high altitude of 3500 m or 6000 m for 6--7 weeks, myocardial necrosis was produced by ligation of the left coronary artery close to its origin, by ligation of the descending branch of the left coronary artery (true infarcts), or by administration of a large dose of isoprenaline. The same was done in control sea-level animals. The extent of the necrosis 24 hours after its induction was estimated from the activity of creatine phosphokinase in the tissue of the left ventricle and, in rats continuously exposed to 6000 m, also by measuring the surface of necrosis marked histochemically with phosphorylase activity in histological slides. In rats continuously exposed to 3500 m the extent of the isoprenaline-induced necrosis was smaller than in the controls, but there was no difference in true infarction. In rats intermittently exposed to 6000 m, no difference in the extent of any type of experimental necrosis was found when compared with sea-level rats. In rats continuously exposed to 6000 m, the extent of all types of experimental necrosis was smaller than in control animals. In histological sections of hearts with true infarctions it was possible to distinguish between the intact tissue, a zone of total necrosis and a zone of partial necrosis. Whether the main trunk or the descending branch of the left coronary artery was ligated, the extent of the zone of total necrosis in rats continuously exposed to 6000 m was smaller, the zone of partial necrosis was larger only in rats with a ligature of the trunk, and the extent of intact myocardium was not different when compared with control sea-level animals with the same type of myocardial infarction.