Changes of humoral indicators and cardiomyocyte apoptosis in rats with heart failure

Abstract

The presence of circulating pro-inflammatory cytokines correlates directly with the severity of heart failure (HF) and independently predicts a poor prognosis. We hypothesized that blood-borne cytokines and angiotensin II may contribute to neurohumoral excitation in HF. The present study was undertaken to observe the changes of humoral indicators and cardiomyocyte apoptosis in rats with HF. Rats underwent coronary ligation (CL) to induce MI, or sham CL (SHAM). Four weeks later, left ventricular end-diastolic pressure increased (n=10, P<0.05) in HF rats compared with SHAM. HF rats had higher (P<0.05) plasma levels of angiotention II (197.28±10.37 vs 119.22±9.35 pg/ml, HF vs SHAM, n=10), tumor necrosis factor-α (TNF-α) (106.42±8.34 vs 59.41±7.48 pg/ml, HF vs SHAM, n=10), interleukin (IL)-1β (128.57±9.74 vs 63.94±8.35 pg/ml, HF vs SHAM, n=10), IL-6 (116.72±9.38 vs 48.76±7.66 pg/ml, HF vs SHAM, n=10) and norepinephine (250.32±10.64 vs 172.68±8.16 pg/ml, HF vs SHAM, n=10) than SHAM rats. HF rats had higher (P<0.05) myocardial apoptosis rate (0.095±0.014 vs 0.031±0.002, HF vs SHAM, n=10) than SHAM rats. Myocardial infarction was confirmed morphologically at the end of experiments. The myocardial infarction-induced increases in pro-inflammatory cytokines in plasma, angiotensin II in plasma and cardiomyocyte apoptosis in myocardium may contribute to neurohumoral excitation in heart failure.