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一种铁螯合剂对低温引起的血管淤滞所致细胞损伤的影响。

The effects of an iron chelator on cellular injury induced by vascular stasis caused by hypothermia.

作者信息

Iyengar J, George A, Russell J C, Das D K

机构信息

Department of Surgery, University of Connecticut School of Medicine, Farmington 06032-9984.

出版信息

J Vasc Surg. 1990 Nov;12(5):545-51.

PMID:2172571
Abstract

Rewarming of a cooled rabbit leg was associated with the generation of oxygen-derived free radicals, shown to be instrumental for tissue injury occurring during rewarming. The present study used a compound that, by its ability to bind with free iron, can remove hydroxyl radical (OH.) from tissue. Deferoxamine reduced tissue injury during cooling and rewarming, as evidenced by its ability to decrease tissue release of lactic acid dehydrogenase and creatine kinase. Deferoxamine also reduced the formation of OH. and lipid peroxidation during the rewarming phase. This compound did not have any effect on the arterial blood flow pattern, which uniformly decreased during cooling and was restored during rewarming. The results of this study indicate the efficacy of deferoxamine in reducing cellular injury associated with cold and rewarming and further suggest a role for oxygen-derived free radicals in the pathophysiology of cold-rewarming injury.

摘要

冷却后的兔腿复温与氧自由基的产生有关,氧自由基被证明在复温过程中导致组织损伤起重要作用。本研究使用了一种化合物,该化合物因其与游离铁结合的能力,能够从组织中清除羟自由基(OH·)。去铁胺减少了冷却和复温过程中的组织损伤,这可通过其降低乳酸脱氢酶和肌酸激酶的组织释放能力得以证明。去铁胺还减少了复温阶段OH·的形成和脂质过氧化。该化合物对动脉血流模式没有任何影响,动脉血流在冷却过程中一致减少,并在复温过程中恢复。本研究结果表明去铁胺在减少与寒冷和复温相关的细胞损伤方面具有有效性,并进一步提示氧自由基在冷-复温损伤的病理生理学中发挥作用。

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