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Mechanisms of accumulation of arachidonic acid in cultured myocardial cells during ATP depletion

Publication ,  Journal Article
Gunn, MD; Sen, A; Chang, A
Published in: American Journal of Physiology - Heart and Circulatory Physiology
December 1, 1985

Previous studies have suggested that the accumulation of free arachidonic acid may be of major importance in the pathophysiology of myocardial ischemia. The purpose of the present study was to determine if the release of arachidonic acid from myocardial cells was more dependent on the extent of ATP depletion than on the inhibition of fatty acid oxidation. In addition, these studies were designed to determine if arachidonic acid release only occurred when ATP was depleted beyond a critical threshold level. To examine the relationship between arachidonic acid release and ATP depletion, cultured myocardial cells from neonatal rat hearts were labeled with [ 3 H]arachidonate and [ 14 C]palmitate. In response to ATP depletion with various metabolic inhibitors [ 3 H]arachidonic acid and [ 14 C]palmitic acid were released from phospholipids. Phosphatidylcholine, phosphatidylethanolamine, and phosphatidic acid were the major esterified sources of the arachidonate. The release of both fatty acids was related to the extent of ATP depletion and not whether a glycolytic or respiratory inhibitor was utilized. Various combinations and doses of metabolic inhibitors were used, and experimental conditions that produced a greater than 75% decrease in ATP content were associated with the accumulation of arachidonic acid. These results suggest that an ATP-dependent step may be linked to the accumulation of arachidonic acid during myocardial ATP depletion. It is suggested that myocardial cells may release arachidonic acid directly in response to ATP depletion.

Duke Scholars

Published In

American Journal of Physiology - Heart and Circulatory Physiology

ISSN

0363-6135

Publication Date

December 1, 1985

Volume

18

Issue

6

Related Subject Headings

  • Cardiovascular System & Hematology
  • 1116 Medical Physiology
  • 0606 Physiology
 

Citation

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MLA
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Gunn, M. D., Sen, A., & Chang, A. (1985). Mechanisms of accumulation of arachidonic acid in cultured myocardial cells during ATP depletion. American Journal of Physiology - Heart and Circulatory Physiology, 18(6).
Gunn, M. D., A. Sen, and A. Chang. “Mechanisms of accumulation of arachidonic acid in cultured myocardial cells during ATP depletion.” American Journal of Physiology - Heart and Circulatory Physiology 18, no. 6 (December 1, 1985).
Gunn MD, Sen A, Chang A. Mechanisms of accumulation of arachidonic acid in cultured myocardial cells during ATP depletion. American Journal of Physiology - Heart and Circulatory Physiology. 1985 Dec 1;18(6).
Gunn, M. D., et al. “Mechanisms of accumulation of arachidonic acid in cultured myocardial cells during ATP depletion.” American Journal of Physiology - Heart and Circulatory Physiology, vol. 18, no. 6, Dec. 1985.
Gunn MD, Sen A, Chang A. Mechanisms of accumulation of arachidonic acid in cultured myocardial cells during ATP depletion. American Journal of Physiology - Heart and Circulatory Physiology. 1985 Dec 1;18(6).

Published In

American Journal of Physiology - Heart and Circulatory Physiology

ISSN

0363-6135

Publication Date

December 1, 1985

Volume

18

Issue

6

Related Subject Headings

  • Cardiovascular System & Hematology
  • 1116 Medical Physiology
  • 0606 Physiology