• Xiao-Bing Jia, Lu-Si Li, Jian-Ning Ye, and Xu Zhang.
• Department of Neurology, Southwest Hospital, Third Military Medical University, Chongqin 400038, China.
• Zhongguo Wei Zhong Bing Ji Jiu Yi Xue. 2008 Jun 1; 20 (6): 361-4.

ObjectiveTo reproduce an ischemic brain injury coma model and explore the arousal effect of Orexin-A.MethodsAn ischemic brain injury coma model was reproduced in rats by partial four-vessel occlusion (4-VO with a needle of 0.60 mm in diameter in the lumen to create stenosis of the internal carotid arteries). One hundred and twenty minutes after the onset of coma, Orexin-A or its antagonist (SB-334867) was given intraventricularly, and the time of coma and changes in electroencephalogram (ECG) were observed, and the unit discharge of neurons in the prefrontal cortex was recorded.ResultsPartial occlusion of four internal carotid arteries, reducing the lumens to 0.60 mm, could prolong the time of coma to 6-8 hours with the rats still alive. The duration of coma showed a significant difference compared with that in rats who underwent 0.45 mm or 0.70 mm stenosis of the internal carotid arteries (F=344.43, P<0.01). Intraventricular Orexin-A in a dose of 4 nmol/10 microl could obviously decrease the duration of coma with a decrease in alpha wave and increase in unit discharge rate of neurons in coma rats (P<0.05 or P<0.01), but no significant change was observed when the dose was 2 nmol/10 microl.Conclusion(1)Creating stenosis of all four internal carotid arteries is suitable to reproduce ischemic brain injury with coma in rats. (2)Intracerebroventricular injection of Orexin-A (4 nmol) has a potent arousal effect on ischemic brain injury coma in rats.

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