全脑缺血后即刻和延迟轻度低温对内源性抗氧化酶和能量代谢物的影响。

Effects of immediate and delayed mild hypothermia on endogenous antioxidant enzymes and energy metabolites following global cerebral ischemia.

机构信息

Department of Neurology, Zhongnan Hospital of Wuhan University, Center for Cerebral Vascular Diseases, Medical College of Wuhan University, Wuhan, Hubei 430071, China.

出版信息

Chin Med J (Engl). 2011 Sep;124(17):2764-6.

PMID:22040438

Abstract

BACKGROUND

The optimal time window for the administration of hypothermia following cerebral ischemia has been studied for decades, with disparity outcomes. In this study, the efficacy of mild brain hypothermia beginning at different time intervals on brain endogenous antioxidant enzyme and energy metabolites was investigated in a model of global cerebral ischemia.

METHODS

Forty-eight male Sprague-Dawley rats were divided into a sham-operated group, a normothermia (37°C - 38°C) ischemic group and a mild hypothermic (31°C - 32°C) ischemia groups. Rats in the last group were subdivided into four groups: 240 minutes of hypothermia, 30 minutes of normothermia plus 210 minutes of hypothermia, 60 minutes of normothermia plus 180 minutes of hypothermia and 90 minutes of normothermia plus 150 minutes of hypothermia (n = 8). Global cerebral ischemia was established using the Pulsinelli four-vessel occlusion model for 20 minutes and mild hypothermia was applied after 20 minutes of ischemia. Brain tissue was collected following 20 minutes of cerebral ischemia and 240 minutes of reperfusion, and used to measure the levels of superoxide dismutase (SOD), glutathione peroxidase (GSH-Px), reduced glutathione (GSH) and adenosine triphosphate (ATP).

RESULTS

Mild hypothermia that was started within 0 to 60 minutes delayed the consumption of SOD, GSH-Px, GSH, and ATP (P < 0.05 or P < 0.01) in ischemic tissue, as compared to a normothermic ischemia group. In contrast, mild hypothermia beginning at 90 minutes had little effect on the levels of SOD, GSH-Px, GSH, and ATP (P > 0.05).

CONCLUSIONS

Postischemic mild brain hypothermia can significantly delay the consumption of endogenous antioxidant enzymes and energy metabolites, which are critical to the process of cerebral protection by mild hypothermia. These results show that mild hypothermia limits ischemic injury if started within 60 minutes, but loses its protective effects when delayed until 90 minutes following cerebral ischemia.

摘要

背景

几十年来，人们一直在研究脑缺血后低温治疗的最佳时间窗，但结果存在差异。在本研究中，我们在全脑缺血模型中研究了轻度脑低温在不同时间间隔开始对脑内源性抗氧化酶和能量代谢物的疗效。

方法

48 只雄性 Sprague-Dawley 大鼠分为假手术组、常温（37°C-38°C）缺血组和轻度低温（31°C-32°C）缺血组。后一组大鼠再分为四组：240 分钟低温组、30 分钟常温加 210 分钟低温组、60 分钟常温加 180 分钟低温组和 90 分钟常温加 150 分钟低温组（n=8）。用 Pulsinelli 四血管闭塞模型建立全脑缺血 20 分钟，然后在缺血 20 分钟后应用轻度低温。在脑缺血 20 分钟和再灌注 240 分钟后采集脑组织，测量超氧化物歧化酶（SOD）、谷胱甘肽过氧化物酶（GSH-Px）、还原型谷胱甘肽（GSH）和三磷酸腺苷（ATP）的水平。