Constrictor action of oxyhemoglobin in monkey and dog basilar arteries in vivo and in vitro.

Angiographic studies on anesthetized dogs and Japanese monkeys showed that oxyhemoglobin (HbO2) injected into the cisterna magna produced a constriction of the basilar artery; the maximal constriction was attained 2-4 h later. Intracisternal injections of autologous blood, prostaglandin (PG) E2 and PGF2 alpha also constricted the artery to a similar extent, although the peak response was obtained much later (approximately 1 wk) with blood and was earlier (approximately 20 min) with PGs. The vasoconstrictor action of HbO2 was almost abolished by treatment for 5 h with aspirin in dogs and monkeys, whereas treatment of dogs with OKY 046, a thromboxane A2 synthesis inhibitor, did not significantly alter the action. In isolated monkey basilar arteries, HbO2 elicited a concentration-related contraction, which was suppressed by treatment with aspirin and by endothelium denudation. The basilar arteries responded to PGE2 and PGF2 alpha with contractions comparable to those caused by elevated external K+. Levels of PGE2, PGF2 alpha, and 6-keto-PGF1 alpha in the nutrient solution bathing dog and monkey cerebral arteries were increased by HbO2; the increment was depressed by endothelium denudation and by treatment with indomethacin. These findings suggest that cerebral artery constriction caused by HbO2 in vivo and in vitro is associated mainly with the release of vasoconstrictor PGs, such as PGE2 and PGF2 alpha. Endothelium appears to play an important role in the release of PGs. Cerebral vasospasm elicited by intracisternal injections of HbO2 may be a useful model for the analysis of mechanisms underlying the provocation of delayed vasospasm after subarachnoid hemorrhage.