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对开心手术病人心肌缺血／再灌注过程中冠状静脉窦血中的红细胞流变性变化和红细胞膜分子结构的改变进行了研究。结果表明，再灌注即刻心脏产生大量自由基，并持续到再灌注第２０分钟时才大幅度回落；于再灌注后的２０分钟的自由基产生时相期间，除红细胞膜蛋白分子和脂质分子的τｐ、τｌ均明显延长外，还伴有血浆ＭＤＡ水平的明显增加和ＳＯＤ活性的显著降低，及红细胞内ＧＳＨ－Ｐｘ活性升高；与此同时其红细胞膜蛋白分子的α螺旋先减少后渐回复和β折叠渐增加并伴有羧基（ＣＯＯＨ）和氨基（ＮＨ３）的减少，而其红细胞膜脂质分子的磷氧双键（Ｐ＝Ｏ）、羰基（Ｃ＝Ｏ）和多不饱和键（Ｃ＝Ｃ）则增加；说明（１）再灌注期间氧自由基分别引起了红细胞膜蛋白分子碳端和氮端的改变及膜磷脂分子亲水区和疏水区化学结构的变化，（２）蛋白分子碳、氮端的变化造成了膜蛋白分子构象的改变，（３）蛋白分子和磷脂分子化学结构及构象的改变是红细胞膜这些分子流动性明显恶化的根本原因。
The change of erythrocyte rheology and the change of molecular structure of erythrocyte membrane in coronary sinus blood flow during myocardial ischemia / reperfusion in patients undergoing heart surgery were studied. The results showed that a large amount of free radicals were produced in the heart immediately after reperfusion, and continued to decrease significantly until the 20th minute of reperfusion. During the free-radical generation phase of 20 minutes after reperfusion, except for membrane proteins and lipid molecules Of τp, τl were significantly prolonged, but also accompanied by a significant increase in plasma MDA levels and significantly decreased SOD activity and erythrocyte GSH-Px activity increased; at the same time the red blood cell membrane protein alpha helix first decreased gradually Reversion and β-sheet increase with concomitant reduction of carboxyl (COOH) and amino (NH3), while phosphoryl double bonds (P = O), carbonyl groups (C = O) and polyunsaturated bonds of erythrocyte membrane lipid molecules (C = C) increased; (1) Oxygen radicals during reperfusion caused changes in the carbon and nitrogen end of erythrocyte membrane proteins and changes in the chemical structure of hydrophilic and hydrophobic regions of membrane phospholipids respectively. (2) Protein Changes in the molecular carbon and nitrogen ends cause changes in the molecular conformation of the membrane protein, (3) changes in the chemical structure and conformation of the molecular and phospholipid molecules These molecules are the root cause of the red cell membrane fluidity significantly deteriorated.