Journal of Okayama Medical Association
Published by Okayama Medical Association

Full-text articles are available 3 years after publication.

脳血管攣縮の発生機序と治療に関する実験的研究 第2編 実験的遅発性脳血管攣縮に対する PGI2 analogue, Thromboxane A2 合成酵素阻害剤, Ca 拮抗剤の効果

元木 基嗣 岡山大学医学部脳神経外科教室
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The effects of a PGI2 analogue (OP-41483), a thromboxane A2 synthetase inhibitor (OKY-046) and a Ca blocker (nifedipine) on the diameter of constricted basilar arteries and on the regional cerebral blood flow (r-CBF) in the brain stem were investigated in the cat delayed spasm model. The experiment was performed three days (72 hours) after artificial subarachnoid hemorrhage. The basilar artery was exposed transclivally, and more advanced vasospasm was produced by topical application of a lysed erythrocyte solution for 5 to 6 hours which domonstrated no more vascular dilatation even by topical application of papaverine hydrochloride (0.01mg/ml). In the delayed spasm model, the intravenous administration of neither OP-41483 (8μg/kg), OKY-046 (60mg/kg) nor nifedipine (0.003mg/kg) affected the vascular diameter. OP-41483 increased r-CBF in the brain stem in 3, and nifedipine increased it in 4 out of the 5 studied delayed spasm models, whereas OKY-046 never increased r-CBF (n=5). There was no significant difference in the amount of fatty acids including arachidonic acid between normal and constricted arteries. This study suggested that thromboxane A2 is not the major factor of cerebral vasospasm and OKY-046 might not be effective on vascular diameter or r-CBF at the late spasm stage. However, the PGI2 analogue (OP-41483) and Ca blocker (nifedipine) may be effective in increasing r-CBF even at the late spasm stage.
cerebral vasospasm
thromboxane A2