Ji L L, Fu R G, Waldrop T G, Liu K J, Swartz H M
Department of Kinesiology, University of Illinois, Urbana 61801.
Can J Physiol Pharmacol. 1993 Oct-Nov;71(10-11):811-7. doi: 10.1139/y93-121.
Ischemia-reperfusion-induced myocardial oxidative changes were investigated in open-chest hearts of anesthetized rats. Surgical occlusion of the left anterior descending coronary artery for 30 min followed by 15 min reperfusion resulted in a significant decrease of reduced glutathione, an increase in glutathione disulfide, and an enhanced lipid peroxidation in rapidly frozen left ventricular tissues. Direct electron paramagnetic resonance spectroscopy revealed an increase in free radical concentration in ischemic cardiac tissues reperfused for 45 s, but the increase diminished at 15 min. these alterations were associated with decreased activities of myocardial glutathione peroxidase, glutathione reductase, and catalase. Ischemia resulted in a significant reduction of high-energy phosphate compounds and an accumulation of nucleotide degradation products, particularly adenosine, in the myocardium. Deterioration of cardiovascular function in reperfused animals was also evident. It is concluded that regional ischemia followed by reperfusion in situ can produce biochemical and physiological alterations consistent with free radical injury in rat hearts, and that an increased purine nucleotide degradation and a decreased antioxidant defense may be responsible for the observed changes.
在麻醉大鼠的开胸心脏中研究了缺血再灌注诱导的心肌氧化变化。手术阻断左冠状动脉前降支30分钟,随后再灌注15分钟,导致快速冷冻的左心室组织中还原型谷胱甘肽显著减少,二硫化谷胱甘肽增加,脂质过氧化增强。直接电子顺磁共振波谱显示,再灌注45秒的缺血心脏组织中自由基浓度增加,但在15分钟时增加减少。这些改变与心肌谷胱甘肽过氧化物酶、谷胱甘肽还原酶和过氧化氢酶的活性降低有关。缺血导致心肌中高能磷酸化合物显著减少,核苷酸降解产物尤其是腺苷积累。再灌注动物的心血管功能恶化也很明显。得出的结论是,原位局部缺血后再灌注可在大鼠心脏中产生与自由基损伤一致的生化和生理改变,并且嘌呤核苷酸降解增加和抗氧化防御降低可能是观察到的变化的原因。