内源性内皮素在动脉缺血和再灌注后心肌和冠状动脉内皮损伤大鼠:研究与应用波生坦、混合ETA-ETB拮抗剂。
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理查德•V Kaeffer N, Hogie M,特隆C,布兰科T, Thuillez C
内源性内皮素在动脉缺血和再灌注后心肌和冠状动脉内皮损伤大鼠:研究与应用波生坦、混合ETA-ETB拮抗剂。
Br J杂志。1994年11月,113 (3):869 - 76。
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7858879 (在PubMed]
- 文摘
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1。先前的研究表明,endothelin-1 (ET-1)可能发挥作用在心肌缺血和再灌注。这项研究是为了测试新的nonpeptide的影响内皮素ETA和ETB受体拮抗剂,应用波生坦,在心肌梗死大小、室性心律失常,冠状动脉缺血和再灌注后内皮功能障碍。2。麻醉雄性Wistar鼠受到20分钟缺血(左冠状动脉阻塞)其次是1 h(冠状动脉内皮功能障碍评估)或2 h(梗塞大小评估)再灌注,紧随其后的是15分钟或5分钟缺血再灌注(再灌注心律失常的评价)。血管研究进行冠状动脉段1.5 - 2毫米(内部直径250 - 300微米)切除远端闭塞的网站和安装在丝肌动描记器等长张力记录。区域风险和梗塞大小取决于墨汁注入和三苯基四唑染色法,利用计算机分析后放大部分的彩色视频采集。3所示。应用波生坦,服用剂量实际上废除了加压反应大ET-1(3毫克公斤,静脉输液前局部贫血)并不影响心率、动脉压力或速度压力产品局部贫血之前,在缺血和再灌注期间。应用波生坦并不影响reperfusion-induced心室纤维性颤动的发生率(控制:86%,n = 14; bosentan: 93%, n = 15), and did not modify infarct size (% of area at risk: controls: 63 +/- 4, n = 10; bosentan: 60 +/- 6, n = 8). Ischaemia followed by reperfusion markedly reduced the endothelium-dependent relaxations to acetylcholine(maximal response: sham: 59 +/- 4%, n = 9; ischaemia-reperfusion: 26+/- 6%, n = 8; P<0.01), characteristic of reperfusion-induced endothelial dysfunction, and this dysfunction was not prevented by bosentan (maximal response to acetylcholine: 25 +/-5%, n = 9; P<0.01 vs sham; P = NS vs ischaemia/reperfusion).4. These experiments suggest that endogenous endothelin does not contribute to myocyte or coronary endothelial injury in this rat model of ischaemia and reperfusion.