Myocardial metabolism and performance in hypoxia: effect of epinephrine

Abstract

Effects of epinephrine (10(-5) M) on mechanical performance, glycolysis, glycogenolysis, lipolysis, and metabolism of adenine nucleotides were studied in isolated hypoxic rabbit hearts. The exposure of hearts to hypoxia decreased their mechanical performance and heart rate, but increased their utilization of glucose by 50% and the release of lactate by 139%. Myocardial stores of glycogen and ATP declined by 53 and 84%, respectively, but their breakdown products such as lactate, pyruvate, AMP, and inosine accumulated in these hearts. Myocardial content of free fatty acids decreased, and the amount of glycerol increased in hypoxic hearts. Epinephrine stimulated mechanical performance and heart rate of hypoxic hearts, but decreased myocardial glycogen and ATP even more by 62 and 33%, respectively. Though glucose utilization remained unchanged, the release of lactate increased by 66% from hypoxic hearts treated with epinephrine. However, epinephrine failed to stimulate myocardial lipolysis in hypoxic hearts. These metabolic changes due to epinephrine would lead to accelerated depletion of energetic reserves in hypoxic heart and its earlier deterioration.

Relation of myocardial oxygen consumption and function to high energy phosphate utilization during graded hypoxia and reoxygenation in sheep in vivo.

“…Maintenance or even slight increases in cardiac function during hypoxia are findings consistent with those published by previous investigators when employing ventilated sheep as a model (17,25). However, dissociation of functional parameters from myocardial intracellular phosphate levels as occurred during this study is fairly specific to the particular study conditions (2,(26)(27)(28). Intracellular phosphate as well as pH have been implicated as regulators of contractile function during hypoxia or ischemia (24,27,29).…”

“…In contrast, decreases in Pi occur independently of pH, but are not associated with myocardial contractile depression in the present model studied in vivo. Previously, dissociation of cardiac function and intracellular phosphate concentration has been noted only in myocardium receiving substantial adrenergic stimulation during hypoxia or ischemia (28,31). This has occurred during catecholamine stimulation in hypoxic buffer-perfused hearts (28), and regionally ischemic myocardium in vivo (31).…”

Alterations in Intercostal Muscle Morphology and Biochemistry in Patients with Obstructive Lung Disease1,2

“…Although this study demonstrated a relation between pulmonary function and labile muscle fuels, it would be fortuitous if the biochemical changes described reflected the state of the contractile machinery (or degree of fatigue) of the intercostal muscles. There is convincing evidence that increasing work (4,16,(34)(35)(36), and decreasing oxygen (37) predictably decrease muscle ATP, PC, and glycogen, with a corresponding increase in lactate. This combination was present in 13 of 52 biopsy specimens, most commonly in the EXT specimens.…”