Abstract
Correlation of cardiomyocyte apoptosis with duration of hypertension, severity of hypertension and caspase-3 expression in hypertensive rats was analyzed. Sixty male Sprague-Dawley (SD) rats were selected and randomly divided into the observation group (n=30) and control group (n=30), and the rat models of hypertension were established by virtue of transverse aortic constriction (TAC). The rats in the two groups were further divided into the 7-day subgroup (n=10), 14-day subgroup (n=10) and 28-day subgroup (n=10), respectively according to their survival time after TAC. The blood pressure values of the rats in each group were measured through intubation of carotid artery to calculate the mean arterial pressure (MAP). The conditions of cardiomyocyte apoptosis were detected using terminal dexynucleotidyl transferase-mediated dUTP nick end labeling (TUNEL) assay. Enzyme-linked immunosorbent assay (ELISA) was applied to measure the expression of caspase-3 in the myocardial tissues, and correlation analysis was performed. The MAPs in 7-, 14- and 28-day subgroups of the observation group were significantly higher than those in the corresponding subgroups of the control group (P<0.05). The 7-, 14- and 28-day subgroups of the observation group had remarkably elevated myocardial caspase-3 expression levels compared with the subgroups of the control group (P<0.05). The apoptosis rates of myocardial cells in the three subgroups of the observation group were obviously higher than those in the corresponding subgroups of the control group (P<0.05). Pearson's correlation analysis indicated that the cardiomyocyte apoptosis rate of hypertensive rats was positively correlated with the duration of hypertension, severity of hypertension and caspase-3 expression (P<0.05). Hypertension can induce apoptosis of myocardial cells, and the apoptosis becomes more serious with the constantly elevated level and prolonged duration of hypertension. In addition, the activity of caspase-3 has a close correlation with cardiomyocyte apoptosis.