Role of 12-HPETE in the Pathogenesis of Cerebral Vasospasm

Abstract

Delayed cerebral vasospasm occurring between the 4th day and the 14th day after subarachnoid hemorrhage (SAH) affects the patient outcome seriously. Its occurrence correlates to the presence and the amount of subarachnoid clot. It is different from ordinary constriction of vessel, since the cerebral vasospasm is delayed onset and long lasting contraction of the vessel which also involves histological changes. Although almost all substances which existed in blood clot had been investigated as candidates caused delayed vasospasm, no substance by itself had been accepted as a cause. Watanabe et al.¹ and Shimizu et al.² reported that 12-hydroxyeicosatetraenoic acid (12-HETE) was detected in subarachnoid clot using the canine SAH model, and 5–1 ipoxygenase pathway of arterial wall with vasospasm was much activated compared with the control vessel. Moreover, 12-hydroperoxyeicosatetraenoic acid (12-HPETE) injected into canine major cistern was produced delayed onset and long lasting vasospasm comparable to the canine SAH model. The injected 12-HPETE into the canine major cistern was decreased rapidly and disappeared from cerebrospinal fluid (CSF) at 6 hours after its injection³. It was interesting and curious that the vasospasm occurred after 12-HPETE disappeared from CSF. The present study was aimed to clarify the trace of injected 12-HPETE into canine major cistern.