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N-ω-硝基-L-精氨酸甲酯和地塞米松可减轻小鼠骨骼肌的缺血再灌注损伤。

Ischaemia-reperfusion injury in mouse skeletal muscle is reduced by N omega-nitro-L-arginine methyl ester and dexamethasone.

作者信息

Knight K R, Zhang B, Morrison W A, Stewart A G

机构信息

Bernard O'Brien Institute of Microsurgery, St. Vincent's Hospital, Fitzroy, Melbourne, Australia.

出版信息

Eur J Pharmacol. 1997 Aug 13;332(3):273-8. doi: 10.1016/s0014-2999(97)01101-1.

DOI:10.1016/s0014-2999(97)01101-1
PMID:9300260
Abstract

We have developed a model of ischaemia-reperfusion injury in C57BL/6 mice involving ischaemia for 0.5 to 2.5 h with an elastic tourniquet on one hind limb and reperfusion for 24 h, analogous to a well-established model of ischaemia-reperfusion injury in the rat. Viability was assessed in tissue homogenates of the gastrocnemius muscles from the affected and contralateral control limb by a triphenyl tetrazolium chloride dye reaction, measuring the activity of the oxidative mitochondrial enzymes. After 1.5 h ischaemia and 24 h reperfusion, viability in the ischaemic-reperfused limb was 13%, with the control muscle regarded as 100% viable. Significant improvements in viability to 86% (P < 0.05) and 56% (P < 0.05) were achieved, with administration 30 min prior to tourniquet release, of the nitric oxide (NO) synthase inhibitor nitro-L-arginine methyl ester (L-NAME, 30 mg/kg) and the anti-inflammatory glucocorticoid dexamethasone (2.5 mg/kg) respectively, with similar findings in the rat tourniquet model.

摘要

我们建立了一种C57BL/6小鼠缺血再灌注损伤模型,使用弹性止血带对一侧后肢进行0.5至2.5小时的缺血处理,然后再灌注24小时,这类似于已建立的大鼠缺血再灌注损伤模型。通过氯化三苯基四氮唑染料反应评估受影响肢体和对侧对照肢体腓肠肌组织匀浆的活力,测量氧化线粒体酶的活性。缺血1.5小时再灌注24小时后,缺血再灌注肢体的活力为13%,对照肌肉视为100%存活。在止血带松开前30分钟分别给予一氧化氮(NO)合酶抑制剂硝基-L-精氨酸甲酯(L-NAME,30mg/kg)和抗炎糖皮质激素地塞米松(2.5mg/kg),可使活力显著提高至86%(P<0.05)和56%(P<0.05),在大鼠止血带模型中也有类似发现。

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