[氯胺酮预处理对大鼠短暂局灶性脑缺血/再灌注后脑水肿及水通道蛋白4表达的影响]

[The effects of ketamine pretreated on cerebral edema and AQP4 expression after transient focal cerebral ischemia/reperfusion in rats].

作者信息

Cai Shu-Nü, Zhu Sheng-Mei

机构信息

Department of Anesthesiology, Zhejiang Cancer Hospital, Hangzhou 310022, China.

出版信息

Zhonghua Yi Xue Za Zhi. 2010 Jun 15;90(23):1648-51.

PMID:20979759

Abstract

OBJECTIVE

To investigate the effects of ketamine pretreatment on cerebral edema following brain ischemia reperfusion injury in rats and assess the involvement of Aquaporin 4 (AQP4) expression.

METHODS

Sixty-two healthy male Sprague-Dawley rats weighing 220 -250 g were randomly divided into 3 groups: sham operation group (group Sham, n = 18); saline group (group Vehicle, n = 22); ketamine pretreatment group (group Ketamine, n = 22) . The transient focal ischemia/reperfusion was induced by introducing a silicone-coated monofilament nylon suture from the right external carotid artery into the origin of the middle cerebral artery, removing it after 90 min. In group Ketamine, the rats were exposed to ketamine (5%, 1 mg x kg(-1) x min(-1)) for 30 min before suffered from cerebral ischemia. Similarly; in group Vehicle and group Sham, the animals received saline vehicle at the same time and infusion rate. After the neurologic exams were assessed at 24 h of reperfusion, the rats were sacrificed after anesthetized, and the brains were quickly removed. To estimate cerebral edema, the wet-dry ratio was measured. Western-blot was used to detect the expression of AQP4 in the border of the infarct region.

RESULTS

The neurologic function deficit was significantly serious in group Vehicle and group Ketamine compared to group Sham (P < 0.01). Ketamine pretreatment tended to improve neurologic outcome, but there was no statistical significance. The wet-dry weight ratio and AQP4 expression increased significantly in group Vehicle and group Ketamine III than those in group Sham (P < 0.01). Compared with saline vehicle, ketamine pretreatment did not decreased the wet-dry weight ratio significantly. AQP4 expression in group Ketamine was not significantly different from group Vehicle.

CONCLUSION

Ketamine pretreatment did not seem to improve the neurologic deficit outcome and attenuate edema, which was involved in no change of AQP4 expression.

摘要

目的

探讨氯胺酮预处理对大鼠脑缺血再灌注损伤后脑水肿的影响，并评估水通道蛋白4（AQP4）表达的参与情况。

方法

将62只体重220 - 250 g的健康雄性Sprague-Dawley大鼠随机分为3组：假手术组（假手术组，n = 18）；生理盐水组（溶媒组，n = 22）；氯胺酮预处理组（氯胺酮组，n = 22）。通过将硅胶涂层单丝尼龙缝线从右颈外动脉插入大脑中动脉起始处诱导短暂性局灶性缺血/再灌注，90分钟后取出。在氯胺酮组中，大鼠在脑缺血前接受氯胺酮（5%，1 mg·kg⁻¹·min⁻¹）30分钟。同样，在溶媒组和假手术组中，动物在相同时间以相同输注速率接受生理盐水。在再灌注24小时评估神经功能检查后，麻醉大鼠并处死，迅速取出大脑。为评估脑水肿，测量干湿比。采用蛋白质免疫印迹法检测梗死区域边界处AQP4的表达。

结果

与假手术组相比，溶媒组和氯胺酮组的神经功能缺损明显更严重（P < 0.01）。氯胺酮预处理倾向于改善神经功能结局，但无统计学意义。溶媒组和氯胺酮组的干湿重比和AQP4表达均显著高于假手术组（P < 0.01）。与生理盐水相比，氯胺酮预处理并未显著降低干湿重比。氯胺酮组的AQP4表达与溶媒组无显著差异。