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