Respiratory movements alter the generation of prostacyclin and thromboxane A2 in isolated rat lungs: the influence of arachidonic acid-pathway inhibitors on the ratio between pulmonary prostacyclin and thromboxane A2

Prostaglandins. 1981 Mar;21(3):491-503. doi: 10.1016/0090-6980(81)90094-0.

Abstract

The influence of hyperventilation on the spontaneous generation of prostacyclin and thromboxane A2 by isolated rat lungs was studied. Both prostacyclin and thromboxane A2, as measured by RIA of their stable end-products, 6-oxo-PGF1 alpha and TXB2 respectively, were continuously released into the perfusate. However, the concentration of prostacyclin in the perfusate was higher than thromboxane A2. Under normal ventilation at a rate 40-50 breaths/min, the ratio between these two compounds was 5:1. Increasing the rate of respiration to 100 breaths/min preferentially stimulated the release of prostacyclin. During hyperventilation-stimulated release of prostacyclin and thromboxane A2. Hydroperoxy-fatty acids and tranylcypromine inhibited only the release of prostacyclin but did not affect the generation of thromboxane A2. Our findings confirm that the lung generates prostacyclin predominantly, and provide direct evidence that respiratory movements are involved in generation of pulmonary prostacyclin and thromboxane A2.

MeSH terms

  • 6-Ketoprostaglandin F1 alpha
  • Animals
  • Arachidonic Acids / metabolism*
  • Aspirin / pharmacology
  • Epoprostenol / metabolism*
  • Fatty Acids / pharmacology
  • Hyperventilation / metabolism*
  • Indomethacin / metabolism
  • Lung / drug effects
  • Lung / metabolism*
  • Male
  • Prostaglandins / metabolism*
  • Prostaglandins F / metabolism
  • Rats
  • Thromboxane A2 / metabolism*
  • Thromboxanes / metabolism*
  • Tranylcypromine / pharmacology

Substances

  • Arachidonic Acids
  • Fatty Acids
  • Prostaglandins
  • Prostaglandins F
  • Thromboxanes
  • Tranylcypromine
  • Thromboxane A2
  • 6-Ketoprostaglandin F1 alpha
  • Epoprostenol
  • Aspirin
  • Indomethacin