Llesuy S, Milei J, Picone V, González Flecha B, Beigelman R, Boveris A
Instituto de Química y Fisicoquímica Biológica, Facultad de Farmacia y Bioquímica, Universidad de Buenos Aires, Argentina.
Mol Cell Biochem. 1995 Apr 12;145(1):45-51. doi: 10.1007/BF00925712.
The aim of this study was to test the effect of vitamins A and E in reducing oxyradical effects and myocardial damage after ischemia-reperfusion in the rabbit heart. Oxyradical effects were indirectly assessed by hydroperoxide initiated chemiluminescence and myocardial damage was evaluated by qualitative and quantitative electron microscopy. Left anterior coronary artery was ligated in control and vitamin-treated rabbits for 30 min and then reperfused for 10 min. Rabbits were pretreated with 150 mg vitamin E and 60,000 IU vitamin A 24 h before surgery. After 10 min of reperfusion full-thickness needle samples were obtained from five different myocardial areas (three ventricular and two septal areas) and used for the determination of hydroperoxide-initiated chemiluminescence and ultrastructural damage. In the control group, hydroperoxide-initiated chemiluminescence was 18,400 +/- 500 cpm/mg protein for the non-ischemic and non-reperfused ventricular areas, and 40,500 +/- 1,800 cpm/mg protein for ischemic-reperfused ventricular areas. In the vitamin-treated group, hydroperoxide-initiated chemiluminescence was decreased by 8% in the non ischemic and non reperfused ventricular areas and by 51-75% in the ventricular ischemic and reperfused areas. The two septal areas in the control group gave chemiluminescences of 6,800 +/- 1,200 cpm/mg protein (non ischemic-non reperfused) and 17,000 +/- 2,000 cpm/mg protein (ischemia-reperfusion). In the vitamin-treated group, chemiluminescence decreased by 4 and 58%, respectively. The ischemia-reperfused areas showed extensive edema, margination of nuclear chromatin and swollen mitochondria with disrupted cristae including rupture of the inner and outer mitochondrial membranes.(ABSTRACT TRUNCATED AT 250 WORDS)
本研究的目的是测试维生素A和E对减轻兔心脏缺血再灌注后的氧自由基效应和心肌损伤的作用。通过氢过氧化物引发的化学发光间接评估氧自由基效应,并用定性和定量电子显微镜评估心肌损伤。对对照组和维生素处理组的兔子结扎左冠状动脉前降支30分钟,然后再灌注10分钟。兔子在手术前24小时接受150毫克维生素E和60,000国际单位维生素A预处理。再灌注10分钟后,从五个不同的心肌区域(三个心室区域和两个间隔区域)获取全层针吸样本,用于测定氢过氧化物引发的化学发光和超微结构损伤。在对照组中,非缺血和非再灌注心室区域的氢过氧化物引发的化学发光为18,400±500 cpm/毫克蛋白质,缺血再灌注心室区域为40,500±1,800 cpm/毫克蛋白质。在维生素处理组中,非缺血和非再灌注心室区域的氢过氧化物引发的化学发光降低了8%,心室缺血和再灌注区域降低了51 - 75%。对照组的两个间隔区域的化学发光分别为6,800±1,200 cpm/毫克蛋白质(非缺血 - 非再灌注)和17,000±2,000 cpm/毫克蛋白质(缺血 - 再灌注)。在维生素处理组中,化学发光分别降低了4%和58%。缺血再灌注区域显示广泛水肿、核染色质边缘化以及线粒体肿胀,嵴断裂,包括线粒体内外膜破裂。(摘要截断于250字)