Arachidonic acid metabolites in acute myocardial infarction

Angiology. 1996 Jul;47(7):649-61. doi: 10.1177/000331979604700703.

Abstract

Abnormalities of arachidonic acid metabolism are implicated in spasm and thrombosis in coronary arteries. Therefore, arachidonic acid metabolites were examined in patients with acute myocardial infarction (AMI). Plasma levels of thromboxane B2 (TXB2), 6-keto-prostaglandin F1 alpha (6KPGF1 alpha), leukotriene B4 (LTB4), and slow reacting substance of anaphylaxis (SRS-A) composed of leukotriene C4 (LTC4), leukotriene D4 (LTD4) and leukotriene E4 (LTE4), were measured in 19 AMI patients. Plasma levels of TXB2, LTB4, and SRS-A in systemic artery blood were significantly elevated during the acute stage (within twenty-four hours after the onset of chest pain) of AMI (TXB2, 0.36 ng/mL; LTB4, 0.75 ng/mL; and SRS-A [LTC4+LTD4+LTE4], 0.96 ng/mL compared with those of normal controls (TXB2, 0.18 ng/mL; LTB4, 0.44 ng/mL; and SRS-A (LTC4+LTD4+LTE4], 0.31 ng/mL). These values decreased to near-normal control levels by one month after the AMI attack. The findings in this study suggest that abnormalities of arachidonic acid metabolism accompany, and may play a role in the pathogenesis of, AMI.

MeSH terms

  • 6-Ketoprostaglandin F1 alpha / blood
  • Adult
  • Aged
  • Arachidonic Acid / blood*
  • Female
  • Humans
  • Leukotriene B4 / blood
  • Male
  • Middle Aged
  • Myocardial Infarction / blood*
  • SRS-A / blood
  • Thromboxane B2 / blood

Substances

  • SRS-A
  • Leukotriene B4
  • Arachidonic Acid
  • Thromboxane B2
  • 6-Ketoprostaglandin F1 alpha