Pedro Salinas , M.Dolores Perez , Rafael Fernandez-Sanpablo , Sagrario Fernandez-Gallardo , Mariano Sanchez-Crespo , Santos Barrigón
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引用次数: 4
摘要
研究了血小板活化因子(PAF)对兔离体动脉灌注室间隔缺血1 h -再灌注30 min后心肌损伤的影响。PAF对非缺血间隔的发展张力、±dT/dtmax、静息张力和活动状态次数无显著影响。PAF (100 nM)可显著降低缺血再灌注刺激后发育张力的恢复,从控制值20.9±3.5%降至10.5±1.8%,而静息张力无变化(15.7±2.8 g vs 15.6±1.3 g)。BN 52021 (20 μM)单独使用对缺血损伤的两项参数均无改变,但可拮抗PAF的加重作用。在从缺血控制实验中获得的流出液的任何样品中均未发现PAF活性的证据。基于目前的研究结果,我们认为PAF在加重缺血心肌损伤中起直接作用,并在此状态下抛弃心脏细胞作为PAF的来源。
Lack of platelet-activating factor release on acute myocardial ischemia in the isolated interventricular septum of rabbit heart
The effects of platelet-activating factor (PAF) on myocardial injury after 1 h global ischemia-30 min reperfusion were investigated in isolated arterially perfused interventricular septum of rabbit heart. PAF did not significantly affect developed tension, ±dT/dtmax, resting tension and the times of active state in non-ischemic septa. The recovery of developed tension was significantly reduced by PAF (100 nM), after an ischemia-reperfusion challenge, from the control value of 20.9 ± 3.5% to 10.5 ± 1.8%, without a change in the resting tension (15.7 ± 2.8 vs. 15.6 ± 1.3 g). BN 52021 (20 μM), alone did not modify either parameter of ischemic damage, but antagonized the aggravating effect of PAF. Evidence of PAF activity was not found in any of the samples of the effluent perfusate obtained from ischemic control experiments. On the basis of the present results, we suggest a direct role for PAF in aggravating the myocardial damage induced by ischemia, and discard heart cells as the source of PAF in this state.