Aims: Right ventricular (RV) function is considered an independent predictor of mortality and development of heart failure (HF) in patients with left ventricle dysfunction following myocardial infarction (MI). The functional and molecular mechanisms that may explain the RV dysfunction are still poorly understood. Our study was conducted to investigate RV contractility and the myocardium protein involved in the calcium handling following MI in rats.
Main methods: MI was surgically induced in male Wistar rats to create transmural infarctions involving 40-60% of the left ventricle surface. Infarcted rats were divided into two groups: those that presented classical signs of congestive heart failure (HF group) and those that did not (INF group), and compared to control animals (Sham). RV contractility was studied using isometric contraction in isolated strips and isovolumetric pressure in isolated heart.
Key findings: Inotropic responses in RV strips were preserved in the INF group but were reduced in the HF group (3.75 mM Ca(2+) treatment: Sham = 163 ± 18; INF = 148 ± 19; HF = 68 ± 11 g/g*; *p < 0.05; 5 × 10(-5) M isoproterenol: Sham = 151 ± 15, INF = 134 ± 17, HF = 52 ± 7 g/g*; *p < 0.05). An increase in SERCA-2a protein expression in the RV was observed in the INF group but not in the HF group, which could explain the preserved inotropic response in these animals.
Significance: Increased SERCA-2a protein expression may play a role in the preservation of RV function post-MI. Therefore, therapeutic strategies that attempt to increase SERCA protein expression levels may be useful for the treatment of HF.
Keywords: Heart failure; Myocardial contractility; Myocardial infarction; Right ventricle.