Nayler W J, Buckley D J, Leong J
Department of Medicine, University of Melbourne, Austin Hospital, Heidelberg, Victoria, Australia.
Cardioscience. 1990 Mar;1(1):61-4.
Hearts which are made ischemic for relatively short periods of time, and then re-perfused, exhibit a temporary decline in tension-generating activity but are not irreversibly injured". Experiments were undertaken to find out whether such "stunned" hearts develop a perfusion defect, and whether chemically heterogeneous Ca(2+)-antagonists provide protection, when used prophylatically. "Stunning" was produced by repetitive 10 minute episodes of ischemia, followed by 15 minutes of reperfusion. The experimental model was the Langendorff-perfused rat heart, and the perfusion buffer was Krebs-Henseleit solution at 37 degrees C. To detect perfusion defects, fuchsin dye was added to the buffer. No evidence of a perfusion defect was obtained. Nevertheless, 10(-8)M nifedipine. 10(-8)M verapamil, 10(-8)M felodipine, and 10(-7)M diltiazem all conferred protection, as gauged by recovery of function after three successive 10 minute episodes of ischemia.
心脏在经历相对较短时间的缺血后再灌注，会出现张力产生活动的暂时下降，但不会受到不可逆损伤。进行了实验以确定这种“顿抑”心脏是否会出现灌注缺陷，以及化学性质各异的钙拮抗剂在预防性使用时是否能提供保护。“顿抑”是通过重复10分钟的缺血发作，随后再灌注15分钟产生的。实验模型是Langendorff灌注的大鼠心脏，灌注缓冲液是37摄氏度的Krebs-Henseleit溶液。为了检测灌注缺陷，在缓冲液中加入了品红染料。未获得灌注缺陷的证据。然而，10(-8)M硝苯地平、10(-8)M维拉帕米、10(-8)M非洛地平和10(-7)M地尔硫䓬均能提供保护，这是通过连续三次10分钟缺血发作后功能的恢复来衡量的。
