Myocardial metabolism and performance in hypoxia: effect of epinephrine

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.

Download Full-text

Oxygen radical mechanisms of brain injury following ischemia and reperfusion

Journal of Applied Physiology ◽

10.1152/jappl.1991.71.4.1185 ◽

1991 ◽

Vol 71 (4) ◽

pp. 1185-1195 ◽

Cited By ~ 469

Author(s):

R. J. Traystman ◽

J. R. Kirsch ◽

R. C. Koehler

Keyword(s):

Fatty Acids ◽

Brain Injury ◽

Free Fatty Acids ◽

Blood Brain Barrier ◽

Adenine Nucleotides ◽

Oxygen Radical ◽

Brain Barrier ◽

Ischemia And Reperfusion ◽

Radical Scavengers ◽

Blood Brain

This review addresses current understanding of oxygen radical mechanisms as they relate to the brain during ischemia and reperfusion. The mechanism for radical production remains speculative in large part because of the difficulty of measuring radical species in vivo. Breakdown of lipid membranes during ischemia leads to accumulation of free fatty acids. Decreased energy stores during ischemia result in the accumulation of adenine nucleotides. During reperfusion, metabolism of free fatty acids via the cyclooxygenase pathway and metabolism of adenine nucleotides via the xanthine oxidase pathway are the most likely sources of oxygen radicals. Although leukocytes have been found to accumulate in some models of ischemia and reperfusion, their mechanistic role remains in question. Therapeutic strategies aimed at decreasing brain injury have included administration of radical scavengers at the time of reperfusion. Efficacy of traditional oxygen radical scavengers such as superoxide dismutase and catalase may be limited by their inability to cross the blood-brain barrier. Lipid-soluble antioxidants appear more efficacious because of their ability to cross the blood-brain barrier and because of their presence in membrane structures where peroxidative reactions can be halted.

Download Full-text