急性可卡因诱导兔基底动脉内皮素-1依赖性收缩。

Seong Hun Yoon, Mario Zuccarello, Robert M Rapoport
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引用次数: 11

摘要

据推测,急性可卡因使用引起的缺血性中风涉及脑血管系统的收缩。然而,这种收缩的机制尚不清楚。本研究检验了是否通过内皮素-1介导了可卡因的收缩。古柯碱灌注诱导兔基底动脉原位维持收缩。内皮素A和B受体拮抗剂PD145065可使其松弛。这些结果支持了急性可卡因暴露引起的脑血管收缩是通过内皮素-1释放的假设。内皮素受体拮抗剂可能在涉及可卡因收缩的脑血管病理生理方面具有治疗益处。
本文章由计算机程序翻译,如有差异,请以英文原文为准。
Acute cocaine induces endothelin-1-dependent constriction of rabbit basilar artery.

It has been postulated that ischemic stroke due to acute cocaine usage involves constriction of the cerebral vasculature. However, the mechanism underlying the constriction remains unclear. This study tested whether cocaine constriction was mediated via endothelin-1. Cocaine suffusion induced maintained constriction in the rabbit basilar artery in situ. The constriction was relaxed by PD145065, an endothelin A and B receptor antagonist. These results support the hypothesis that constriction of the cerebral vasculature due to acute cocaine exposure is via endothelin-1 release. Endothelin receptor antagonists may be of therapeutic benefit in cerebrovascular pathophysiologies involving cocaine constriction.

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