In Vitro Evaluation of the Inhibitory Action of PGI₂ to Vasoconstrictions Induced by Various Prostaglandins, Serotonin and Hemoglobin Using the Canine Basilar Artery

Abstract

Current investigations have indicated that prolonged vasoconstriction in vasospasm following subarachnoid hemorrhage due to rupture of intracranial aneurysms is the result of a combined action of various vasoconstrictive agents such as serotonin, oxyhemoglobin, thrombin and prostaglandins. PGI₂ (prostacyclin), on the other hand, has been known to possess antagonistic actions to some of the above agents.
To elucidate the role of PGI₂ as a natural protecting factor against the occurrence of vasospasm, its inhibitory action against vasoconstrictions induced by serotonin, oxyhemoglobin, PGA₂, PGD₂, PGE₂ and PGF_2α was studied in vitro using the canine basilar artery. PGI₂ in concentration of 10^-6 M caused vasodilation ranging between 20 to 70% of the basal contraction developed by each agonist. Thus it was revealed that PGI₂ caused a significant dilation of the artery which had been constricted by any of the above agents. Since the progressive diminution in PGI₂ synthesis in experimental SAH has been previously demonstrated, the result of the present study indicates a possible benefit of the us₂ of PGI2 as well as the need for preservation of PGI₂ synthesis in any pharmacological treatment of vasospasm.