Fukai T, Egashira K, Numaguchi K, Hata H, Takahashi T, Kasuya H, Sakata M, Shimokawa H, Takeshita A
Research Institute of Angiocardiology, Kyushu University School of Medicine, Fukuoka, Japan.
Cardiovasc Res. 1995 Aug;30(2):193-9.
The role of endothelin-1 (ET-1) in the pathogenesis of coronary artery spasm is not well understood. We aimed to determine if ET-1 is involved in serotonin-induced coronary spasm in the swine model.
In 10 miniature pigs, a segment of the left anterior descending coronary artery was denuded and irradiated with X-ray. Three months after endothelial denudation, coronary vasomotion was assessed in vivo by quantitative arteriography.
Intracoronary serotonin at 10 micrograms/kg provoked coronary spasm (augmented narrowing of the luminal diameter) at the denuded site (diameter reduction 93 +/- 4%) but not at the non-denuded control site (19 +/- 4%, P < 0.01) associated with ST segment elevation in the region perfused by the denuded artery. Intracoronary administration of ET-1 at 25 ng/kg caused mild vasoconstriction of the denuded (26 +/- 4) and non-denuded site (16 +/- 3%, n.s.), but provoked ST segment elevation in the regions perfused by both the denuded and non-denuded arteries. The treatment with an endothelin antagonist (BQ123 0.1 mg/kg) significantly attenuated coronary vasoconstriction and ST segment elevation evoked with ET-1, but did not alter serotonin-induced vasoconstriction either at the denuded or control site.
The results of this study suggest that endogenous ET-1 may not be involved in the pathogenesis of serotonin-induced coronary spasm in our swine model.
内皮素 -1（ET -1）在冠状动脉痉挛发病机制中的作用尚未完全明确。我们旨在确定ET -1是否参与猪模型中5-羟色胺诱导的冠状动脉痉挛。
选取10只小型猪，对其左前降支冠状动脉的一段进行内皮剥脱并给予X射线照射。内皮剥脱3个月后，通过定量血管造影术在体内评估冠状动脉的血管运动情况。
冠状动脉内注射10微克/千克的5-羟色胺可在剥脱部位诱发冠状动脉痉挛（管腔直径显著变窄）（直径减少93±4%），而在未剥脱的对照部位则不会（19±4%，P<0.01），且与剥脱动脉供血区域的ST段抬高相关。冠状动脉内注射25纳克/千克的ET -1可导致剥脱部位（26±4）和未剥脱部位（16±3%，无统计学意义）出现轻度血管收缩，但在剥脱和未剥脱动脉供血区域均诱发ST段抬高。用内皮素拮抗剂（BQ123 0.1毫克/千克）治疗可显著减轻ET -1诱发的冠状动脉血管收缩和ST段抬高，但在剥脱或对照部位均未改变5-羟色胺诱导的血管收缩。
本研究结果表明，在我们的猪模型中，内源性ET -1可能不参与5-羟色胺诱导的冠状动脉痉挛的发病机制。
