Hypoventilation and elevation of end-expiratory pressure release a substance which relaxes isolated arteries and disaggregates platelets in the presence of cyclooxygenase inhibitors.

A prostacyclin-like substance was detected by bioassay in the blood of dogs and cats during hypoventilation and increased end-expiratory pressure. This biologically active material, most likely originating from lungs, relaxed isolated vascular strips and disaggregated platelets. Its release was not prevented by indomethacin or aspirin.

Effect of prostaglandin E2 and of indomethacin upon cerebral and pulmonary consequences of exposure to hyperbaric oxygen in rats.

There are few data in the literature suggesting that endogenous prostaglandins (PGs) might be involved in the pathomechanism of seizures. Since the mechanism of seizures inducted by exposure to oxygen high pressure (OHP) is not fully elucidated, this study was designed to investigate the effect of exogenous PG s and of indomethacin (a Pg synthesis inhibitor) upon the development and consequences of seizures in rats exposed to OHP (5 ata). In the animals pretreated with PGE2 (1 ng/kg s.

Inhibitory effect of hydrocortisone on the release of prostaglandins from dog's brain in hypoxia and cerebral embolism.

Cerebral hypoxia and embolism evoke the release of prostaglandin (PG)-like substances, predominantly of E type, into cerebral venous blood. This has been shown by bioassay used for monitoring the level of PG-like substances in sagittal sinus blood (ssb) in dogs. Hypoxia was induced by inhalation of 8% O2 in N2, embolism by an injection of air into internal carotid artery.