Role of prostanoids in respiratory failure during circulatory shock of intestinal origin in dogs.

The role of prostanoids in respiratory failure during circulatory shock of intestinal origin was investigated in anesthetized, non-ventilated dogs by measuring PGF2 alpha thromboxane B2 (TXB2) and 6-keto prostaglandin F1 alpha (PGF1 alpha) in arterial and mixed venous (right ventricle) blood samples during superior mesenteric artery occlusion-induced (SMAO) shock. Release of the SMAO caused a dramatic decrease in mean arterial blood pressure (MABP), arterial and mixed venous pO2, hyperventilation and a more than 2 fold increase in levels of prostanoid studied within 5 min. At the same time, arterial and mixed venous pCO2 and pH remained unchanged. Thereafter, 6-keto PGF1 alpha concentration decreased so that at 60 min post release it was not significantly different from that of control values. PGF2 alpha and TXB2 levels rose continuously during shock. Respiratory failure which occurred after declamping was characterized by low pO2 and oxygen saturation and hyperventilation throughout the experiment. Pulmonary metabolism of PGF2 alpha was significantly reduced in shock. Indomethacin significantly attenuated the magnitude of postocclusion hypotension and respiratory failure, furthermore reduced prostanoid production. The present results suggest that PGF2 alpha and thromboxane A2 released by intestinal tissues might play an important role in the development of respiratory failure in shock caused by intestinal ischemia.