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深度低温循环停搏所致脑损伤的机制及辅酶Q10的保护作用

Mechanisms of brain injury with deep hypothermic circulatory arrest and protective effects of coenzyme Q10.

作者信息

Ren Z, Ding W, Su Z, Gu X, Huang H, Liu J, Yan Q, Zhang W, Yu X

机构信息

Department of Pediatric Cardiothoracic Surgery, Xinhua Hospital, Shanghai Second Medical University, People's Republic of China.

出版信息

J Thorac Cardiovasc Surg. 1994 Jul;108(1):126-33.

PMID:8028355
Abstract

Sixteen dogs, divided randomly into a control group and coenzyme Q10 group (10mg/kg, intraperitoneally before the operation), underwent deep hypothermic circulatory arrest with cardiopulmonary bypass, as is done clinically. At four time points cerebral cortex and cerebrospinal fluid specimens were collected to study free radical formation, energy metabolism, and ultrastructure. During cardiopulmonary bypass cerebral electron spin resonance spectra and malondialdehyde contents were progressively higher than before bypass, especially at the 60 minutes of circulatory arrest and 30 minutes of reperfusion (p1 < 0.01, p2 < 0.05). In the coenzyme Q10 group at the latter two time points, they had increased less than in the control group at same time points (p1 < 0.02, p2 < 0.005). Adenosine triphosphate content in the cortex during bypass decreased gradually from the prebypass level (p1 < 0.02, p2 = p3 < 0.001), while lactate in cerebrospinal fluid increased (p1 < 0.05, p2 = p3 < 0.001). In the coenzyme Q10 group, adenosine triphosphate at the latter two time points was greater than that in the control group (p1 = p2 < 0.05), while the lactate changes were not significantly different from control at each time point (all p > 0.05). Ultrastructure of the cortex was normal before bypass and almost normal during bypass, but it was obviously abnormal at 60 minutes of circulatory arrest and more seriously abnormal at 30 minutes of reperfusion. In the coenzyme Q10 group the abnormality was obviously reduced. The results suggest that oxygen-derived free radicals and abnormal energy metabolism might play critical roles in brain ischemia/reperfusion injury. Coenzyme Q10 could protect the brain by improving cerebral metabolism.

摘要

16只狗被随机分为对照组和辅酶Q10组(10mg/kg,术前腹腔注射),如同临床操作那样,在体外循环下进行深低温停循环。在四个时间点采集大脑皮质和脑脊液标本,以研究自由基形成、能量代谢及超微结构。在体外循环期间,大脑电子自旋共振光谱和丙二醛含量逐渐高于体外循环前,尤其是在停循环60分钟和再灌注30分钟时(p1<0.01,p2<0.05)。在辅酶Q10组的后两个时间点,它们的增加幅度小于对照组在相同时间点的增加幅度(p1<0.02,p2<0.005)。体外循环期间皮质中的三磷酸腺苷含量从体外循环前水平逐渐下降(p1<0.02,p2 = p3<0.001),而脑脊液中的乳酸增加(p1<0.05,p2 = p3<0.001)。在辅酶Q10组,后两个时间点的三磷酸腺苷含量高于对照组(p1 = p2<0.05),而乳酸变化在每个时间点与对照组相比无显著差异(所有p>0.05)。旁路手术前皮质超微结构正常,旁路手术期间几乎正常,但在停循环60分钟时明显异常,在再灌注30分钟时异常更严重。在辅酶Q10组,异常明显减轻。结果表明,氧衍生自由基和异常能量代谢可能在脑缺血/再灌注损伤中起关键作用。辅酶Q10可通过改善脑代谢来保护大脑。

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