Salvage of ischemic myocardium by prostacyclin during experimental myocardial infarction.
Salvage of ischemic myocardium by prostacyclin during experimental myocardial infarction.
复制标题
实验性心肌梗死期间前列环素对缺血心肌的挽救作用。
DOI：
10.1016/s0735-1097(83)80164-8
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发表时间：
1983
影响因子：
24
通讯作者：
Becker,LC
中科院分区：
文献类型：
--
作者：
Melin,JA;Becker,LC
前列环素 (PGI2) 对梗死面积和局部心肌血流的影响是在 28 只麻醉犬中进行了 5 小时的冠状动脉闭塞研究。通过在处死前将染料注射到左心房来定义心肌灌注不足的区域。在三苯基四偶氮-Hum氯化物中温育后，通过左心室切片的面积测定法测定梗塞大小。冠状动脉前降支闭塞后 10 分钟开始，动物接受 Tris 缓冲液中的 PGI2（20 至 40 ng/kg 每分钟，n = 14）或单独的 Tris 缓冲液（对照，n = 14）。在输注 PGI2 期间，平均动脉压下降了 8%，但心率没有变化。与对照组相比，PGI2治疗犬的梗塞面积显着减小（p<0.005），左心室百分比（8.1% vs 17.7%）和低灌注区百分比（39.8% vs 77.3%）。在 5 小时输注期间，两组的局部心肌血流量均未发生显着变化。因此，在本研究的条件下，前列环素似乎通过直接的血流独立机制来保护缺血心肌。
The effects of prostacyclin (PGI2) on infarct size and regional myocardial blood flow were studied in 28 anesthetized dogs subjected to 5 hours of coronary occlusion. A region of myocardial hypoperfusion was defined by injection of dye into the left atrium just before sacrifice. Infarct size was determined by planimetry of left ventricular slices after incubation in triphenyl tetrazo-Hum chloride. The animals received either PGI2in Tris buffer solution (20 to 40 ng/kg per min, n = 14) or Tris buffer alone (control, n = 14) beginning 10 minutes after anterior descending coronary artery occlusion. During PGI2infusion, mean arterial pressure decreased by 8%, but heart rate was unchanged. Infarct size was significantly less (p<0.005) in PGI2-treated dogs compared with the control group, both as percent of left ventricle (8.1 versus 17.7%) and as percent of the hypoperfused zone (39.8 versus 77.3%). No significant changes in regional myocardial blood flow occurred over the 5 hour infusion period in either group. Thus, under the conditions of this study, prostacyclin appeared to protect ischemic myocardium by a direct flow-independent mechanism.