MICROCALORIMETRIC STUDY OF MYOCARDIAL TISSUE METABOLISM IN HEART-FAILURE AFTER EXPERIMENTAL MYOCARDIAL-INFARCTION IN RATS

Using microcalorimetry and measuring oxygen consumption rate, we have studied metabolic activity in myocardial tissue from rats suffering fr om congestive heart failure (CHF) after ligation of the left coronary artery followed by myocardial infarction, comprising 30-40% of the end ocardial circumference, known to be large enough to induce heart failu re and neuroendocrine counter-regulation. The heat production in the p reserved part of the left ventricle, harbouring the myocardial infarct ion, was 0.94 +/- 0.05 mW g(-1) (n = 10) and not different from the co ntrols i.e g 0.94 +/- 0.05 mW g(-1), (n = 23). The oxygen consumption rate was 1.36 +/- 0.20 nmol O-2 s(-1) g(-1) in CHF myocardium and 1.55 +/- 0.24 nmol O-2 s(-1) g(-1) in the control rats, (n = 20), n.s. The calculated contribution from aerobic metabolism to total heat product ion was 71 +/- 9% in the CHF rats and 80 +/- 6% in the control group, n.s. In tissue samples taken from the region of the border of and into the macroscopically damaged area of the myocardial infarction (n = 5) , the value for heat production was 1.15 +/- 0.13 mW g(-1) and oxygen uptake 1.79 +/- 0.23 nmol O-2 s(-1) g(-1). These results show that the contribution from aerobic metabolism to total energy expenditure in p reserved left ventricular tissue is not higher than normal and suggest that the effects of left coronary occlusion are not limited to the ge neration of a myocardial infarction, but may also have a substantial i mpact on the ability of myocardial cells to increase metabolic activit y in macro- and microscopically preserved regions of the left ventricl e. In addition, the data demonstrate persistent metabolic activity wit hin the region of ischemically damaged myocardium not different from t hat found in undamaged myocardium.