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. PGI
2 (prostacyclin), on the other hand, has been known to possess antagonistic actions to some of the above agents.
To elucidate the role of PGI
2 as a natural protecting factor against the occurrence of vasospasm, its inhibitory action against vasoconstrictions induced by serotonin, oxyhemoglobin, PGA
2, PGD
2, PGE
2 and PGF
2α was studied
in vitro using the canine basilar artery. PGI
2 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 PGI
2 caused a significant dilation of the artery which had been constricted by any of the above agents. Since the progressive diminution in PGI
2 synthesis in experimental SAH has been previously demonstrated, the result of the present study indicates a possible benefit of the us
2 of PGI2 as well as the need for preservation of PGI
2 synthesis in any pharmacological treatment of vasospasm.
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