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

Abstract

The role of prostanoids in respiratory failure during circulatory shock of intestinal origin was investigated in anesthetized, non-ventilated dogs by measuring PGF 2α thromboxane B 2 (TXB 2) and 6-keto prostaglandin F 1α (PGF 1α) 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 artrial blood pressure (MABP), arterial and mixed venous pO 2, hyperventilation and a more than 2 fold increase in levels of prostanoid studied within 5 min. At the same time, arterial and mixed venous pCO 2 and pH remained unchanged. Thereafter, 6-keto PGF 1α concentration decreased so that at 60 min post release it was not significantly different from that of control values. PGF 2α and TXB 2 levels rose continously during shock. Respiratory failure which occured after declamping was characterized by low pO 2 and oxygen saturation and hyperventilation throughout the experiment. Pulmonary metabolism of PGF 2α 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 PGF 2α and thromboxane A 2 released by intestinal tissues might play an important role in the development of respiratory failure in shock caused by intestinal ischemia.