Effects of cardiosphere-derived cell transplantation on cardiac mitochondrial oxygen consumption after myocardial infarction in rats.

Abstract

It is postulated that impaired mitochondrial energy-producing ability may lead to the development of chronic heart failure following an acute myocardial infarction. In this study, the effects of transplantation of cardiosphere-derived cells (CDCs) into the viable cardiac tissue after a myocardial infarction on the cardiac mitochondrial oxygen consumption rate (OCR) were examined. CDCs isolated from adult rat cardiac tissue fragments were cultured. Myocardial infarction was induced by ligation of the left ventricular coronary artery in rats. Immediately after coronary artery ligation (CAL), approximately 1 million CDCs were injected into the viable myocardium around the infarct area. Eight weeks after CAL, animals without transplantation showed signs of heart failure such as impaired cardiac pump function. Furthermore, the mitochondrial OCR of the viable cardiac tissue in rats with heart failure was reduced. In contrast, the cardiac pump function and mitochondrial OCR were preserved without a reduction in the infarct size in the animals with transplantation of CDCs. These results suggest that the transplantation of CDCs into the infarcted rat heart contributes to a preservation of mitochondrial function, leading to an improvement of cardiac contractile function without regeneration of cardiac tissues.