Sudden pressure elevation can trigger acute muscle cell death of the heart and aorta

The object of this study was to clarify whether or not the acute muscle cell death of the aortic media observed in normal rabbits treated with Russell’s viper venom (RVV) and angiotensin II (Ang) is a result of either acute hypertension or the apoptotic effect of angiotensin II. The incidence and mean % area necrosis of the aorta and left ventricle in the rabbits receiving RVV and Ang (group 1) were compared with those in rabbits receiving Ang and saline (group 2), RVV and saline (group 3), RVV, Ang type 1 receptor blocker (CV 11974) and Ang (group 4), RVV, Ang and nicardipine, dihydropyridine derivative (group 5) and RVV, Ang type 2 receptor blocker (PD 123319) and Ang (group 6). The incidence as well as the mean % area of acute muscle necrosis of the aortic media and left ventricle in groups 3, 4 and 5 were found to be significantly lower than those in either group 1or group 6. The mean % area of acute spotty myocardial necrosis in group 2 (Ang, saline) was also significantly higher than that in groups 3, 4 and 5. There was no evidence of cells with positive in situ nick end labeling (TUNEL reaction). As a result, the acute muscle necrosis of the aortic media and left ventricle was considered to be due to the sudden elevation in the blood pressure, but not due to apoptosis mediated through Ang type 2 receptor. We thus conclude that a sudden increase in blood pressure may be one of the triggering mechanisms for an acute onset of cardiovascular disorders.