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羟乙基淀粉大分子及超氧化物歧化酶对心肌再灌注损伤的影响

Hydroxyethyl starch macromolecule and superoxide dismutase effects on myocardial reperfusion injury.

作者信息

Oz M C, Zikria B A, McLeod P F, Popilkis S J

机构信息

Department of Surgery, College of Physicians and Surgeons, Columbia University, New York, New York.

出版信息

Am J Surg. 1991 Jul;162(1):59-62. doi: 10.1016/0002-9610(91)90203-p.

DOI:10.1016/0002-9610(91)90203-p
PMID:1712154
Abstract

Myocardial reperfusion injury may be due to biophysical changes (e.g., endothelial cell junctional separations), as well as biochemical mechanisms (e.g., oxygen free radical activity). Superoxide dismutase (SOD), a free radical scavenger, may be effective in reducing chemical injury. Fractions of hydroxyethyl starch (HES-Pz), a large macromolecule, have been shown to decrease microvascular permeability associated with reperfusion-induced biophysical alterations. A comparison of SOD to HES-Pz was performed using a canine model of 1-hour left anterior descending coronary artery (LAD) clamping followed by 24 hours of reperfusion. Amounts of the test solution equal to 10% of the dog's blood volume were administered intraatrially to the animals just before release of the LAD clamp. Six dogs received Ringer's lactate, 7 were given 600,000 IU of SOD, 13 received 6% HES-Pz, and 9 were given SOD and HES-Pz. The ratio of infarct to area at risk was 20 +/- 3% in the control dogs receiving Ringer's lactate, 16 +/- 4% in animals receiving SOD alone (p = NS), 6 +/- 3% in dogs receiving HES-Pz alone (p less than 0.05), and 8 +/- 3% in dogs given a combination of SOD and HES-Pz (p less than 0.05). HES-Pz alone and with SOD significantly reduced reperfusion injury, although addition of SOD to HES-Pz did not have an additive effect. Appropriate-sized macromolecules may act by reducing ischemia-induced microvascular permeability.

摘要

心肌再灌注损伤可能归因于生物物理变化(如内皮细胞连接分离)以及生化机制(如氧自由基活性)。超氧化物歧化酶(SOD)作为一种自由基清除剂,可能在减轻化学损伤方面有效。羟乙基淀粉(HES-Pz)的组分是一种大分子物质,已被证明可降低与再灌注诱导的生物物理改变相关的微血管通透性。使用犬左前降支冠状动脉(LAD)夹闭1小时后再灌注24小时的模型,对SOD和HES-Pz进行了比较。在松开LAD夹之前,将等于犬血容量10%的测试溶液经心房给予动物。6只犬接受乳酸林格液,7只给予600,000国际单位的SOD,13只接受6%的HES-Pz,9只给予SOD和HES-Pz。接受乳酸林格液的对照犬梗死面积与危险面积之比为20±3%,单独接受SOD的动物为16±4%(p=无显著性差异),单独接受HES-Pz的犬为6±3%(p<0.05),接受SOD和HES-Pz联合治疗的犬为8±3%(p<0.05)。单独使用HES-Pz以及与SOD联合使用均显著降低了再灌注损伤,尽管在HES-Pz中添加SOD并没有相加效应。大小合适的大分子可能通过降低缺血诱导的微血管通透性发挥作用。

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