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Effects of subarachnoid hemorrhage on platelet-derived vasoconstriction of rabbit basilar artery
Journal article   Peer reviewed

Effects of subarachnoid hemorrhage on platelet-derived vasoconstriction of rabbit basilar artery

Yuichiro Tanaka, Neal F Kassell and James C Torner
Surgical neurology, Vol.32(6), pp.439-443
1989
DOI: 10.1016/0090-3019(89)90007-4
PMID: 2636797

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Abstract

The effects of subarachnoid hemorrhage on platelet-derived vasoconstriction of the isolated rabbit basilar artery were examined using an isometric tension recording method. The subarachnoid hemorrhage was induced by injecting arterial blood in the cisterna magna. The following points were confirmed: (1) the maximal contraction produced by the platelets (10 7/mL) treated with indomethacin or dazoxiben (thromboxane synthetase inhibitor) were suppressed (65% or 70% of the control); (2) the contraction of the arteries treated with ONO-3708 (thromboxane A 2 antagonist) or ketanserin was inhibited (73% or 8.4%), as was contraction after subarachnoid hemorrhage (67% or 14%); (3) platelet-induced contraction was potentiated after subarachnoid hemorrhage; and (4) serotonin-induced contraction was potentiated after subarachnoid hemorrhage. However, synthetic thromboxane A 2-induced contraction was not potentiated. The present experiments suggest that both serotonin and thromboxane A 2 contribute to vasoconstrictions induced by the platelets, before and after subarachnoid hemorrhage. The platelet-derived contraction response is potentiated after subarachnoid hemorrhage and serotonin is responsible for the increased reactivity.
Rabbit Basilar artery Platelet Thromboxane A 2 Serotonin Subarachnoid hemorrhage

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