Effect of Chronic Renal Failure on Heart

Publisher Website
Google Scholar
Abstract
This study examined the effects of chronic renal failure in rats with and without parathyroid glands on myocardial energy production, transfer and utilization as well as on cardiac index. Chronic renal failure was produced by 7/8 nephrectomy in rats weighing between 240 and 350 g with intact parathyroid glands (CRF-control) and in parathyroidectomized (CRF-PTX) rats maintained normocalcemic. The data were compared to results obtained in intact rats and in normocalcemic parathyroidectomized rats with normal renal function. There were significant (p < 0.01) decrements in myocardial content of ATP and creatine phosphate, mitochondrial oxygen consumption, and in the activity of both mitochondrial and myofibrillar creatine phosphokinase in CRF-control rats as compared to normal animals. The myocardial calcium content and the 45Ca uptake in CRF-control rats were significantly (p < 0.01) higher than in normal rats. In CRF-PTX animals, the myocardial content of ATP, mitochondrial oxygen consumption, 45Ca uptake and calcium content were normal, but PTX did not normalize the activity of mitochondrial and myofibrillar creatine phosphokinase. Parathyroidectomy in rats with normal renal function was associated with a significant reduction in the activity of creatine phosphokinase of myocardial mitochondria and myofibrils. There was a significant (p < 0.01) decrease in cardiac index in CRF-control rats as compared to normal animals, and cardiac index did not return to normal in CRF-PTX rats. The data indicate that (1) chronic renal failure in the presence of intact parathyroid glands is associated with impaired energy production, transfer and utilization by the myocardium and with a decrease in cardiac index; (2) the decrease in energy production (ATP content and mitochondrial oxygen consumption) is due to excess PTH and not to other consequences of chronic renal failure; (3) the impairment in energy transfer (mitochondrial creatine phosphokinase) and energy utilization (myofibrillar creatine phosphokinase) is most likely due to excess PTH, but complete lack of PTH did not correct these abnormalities, since absence of the hormone even in rats with normal renal function is associated with reduced activities of these enzymes; (4) the effects of PTH on the heart in a state of chronic renal failure is, at least partly, mediated by enhanced entry of calcium into the myocardium; (5) the optimal activity of creatine phosphokinase of the myocardial mitochondria and myofibrils requires physiological amounts of PTH and both excess of the hormone or its lack are deleterious to these enzymes and, hence, to energy transfer and utilization, and (6) total parathyroidectomy is not the procedure of choice for the prevention of uremic myocardiopathy.

This publication has 0 references indexed in Scilit: