Release of prostaglandin--like substances into cerebral venous blood in conditions injurious to brain in the dog.

Hypo- and hypercapnia produced in dogs had no effect on the level of endogenous prostaglandin-like substances (PLS) bioassayed continuously in sagittal sinus blood. Increased release of endogenous PLS, predominantly of prostaglandin E-like substance into cerebral venous blood occurred in conditions injurious to brain, such as hypoxia cerebral ischemia and embolism. It may be concluded that increased output of PLS into cerebral venous blood is not related to functional changes in cerebral blood flow, but results from cerebral and/or cerebrovascular damage. Enchanced generation of endogenous prostaglandins and their release into cerebral venous blood preceed the development of structural alterations evoked by hypoxia and ischemia in brain.