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在麻醉家兔心肌缺血 再灌注 (ischemia reperfusion ,IR)模型上 ,观察IR和缺血预处理 (ischemicprecon ditioning ,IP)对血流动力学、心外膜电图、心肌梗塞范围、心肌细胞凋亡和凋亡相关调控基因蛋白 (Fas、Bcl 2、Bax等 )的影响。所得结果如下 :(1)在IR过程中 ,动脉血压、心率和心肌耗氧量进行性降低 ;心外膜电图ST段在缺血期明显抬高 (P <0 0 0 1) ,再灌注时逐渐恢复至基础对照值。 (2 )单纯IR组的梗塞心肌占缺血心肌的 5 7 7±2 0 % ,IP组的梗塞心肌为 2 7 7± 1 5 % (P <0 0 1)。 (3)凝胶电泳显示 ,单纯IR组的缺血组织DNA呈云梯状 ,IP组则无明显云梯状 ;原位末端标记表明 ,IP组缺血未坏死心肌的凋亡细胞较IR组稀少 ;流式细胞术测得IR和IP组中缺血心肌的细胞凋亡率分别为 11 2± 0 4%和 6 35± 0 2 % (P <0 0 1)。 (4)与非缺血心肌相比 ,IR和IP组缺血心肌的Fas和Bax蛋白表达均明显增高 (P <0 0 5 ) ,且IR组的Fas蛋白表达较IP组的明显 (P <0 0 5 )。IR组缺血心肌Bcl 2 /Bax较非缺血心肌组织明显减小 (P <0 0 1)。以上结果表明 ,IP减少IR引发的心肌细胞凋亡 ,并减少IR心肌组织中Fas蛋白的表达。
The effects of IR and ischemic preconditioning (IP) on hemodynamics, epicardial electrocardiogram, myocardial infarct size, myocardial cell apoptosis were observed in a rat model of myocardial ischemia-reperfusion (IR) Apoptosis and apoptosis related genes (Fas, Bcl 2, Bax, etc.). The results obtained were as follows: (1) Arterial blood pressure, heart rate and myocardial oxygen consumption were decreased during IR; the ST segment in epicardial electromyogram was significantly elevated during ischemia (P <0.01) When gradually restored to the basic control value. (2) The infarcted myocardium in the IR group was 57.7 ± 20.0% of the ischemic myocardium, and the infarcted myocardium in the IP group was 27.7 ± 15.0% (P <0.01). (3) The results of gel electrophoresis showed that the DNA of ischemic tissue was ladder-like in IR group and no ladder was observed in IP group. The in situ terminal labeling showed that apoptotic cells in IP group were less than those in IR group; The apoptotic rates of ischemic myocardium in IR and IP groups measured by flow cytometry were 11 2 ± 0 4% and 6 35 ± 0 2%, respectively (P 0 01). (4) Compared with non-ischemic myocardium, the expression of Fas and Bax in IR and IP groups were significantly increased (P <0.05), and the expression of Fas protein in IR group was significantly higher than that in IP group (P < 0 0 5). Compared with non-ischemic myocardium, Bcl 2 / Bax in ischemic myocardium in IR group decreased significantly (P <0.01). The above results indicate that IP reduces IR-induced cardiomyocyte apoptosis and decreases Fas protein expression in IR myocardium.