摘要
目的研究远程缺血预处理(RIPC)对大鼠蛛网膜下腔出血(SAH)后脑水肿及水通道蛋白4(AQP4)的影响。方法 72只SD大鼠随机分为三组:A组为假手术组,B组为SAH模型组,C组为RIPC+SAH组。通过驱血带阻断下肢血流10min,放开10min,两侧下肢交替进行,每侧进行3次,施行RIPC。枕大池二次自体注血法制备SAH模型。分别在造模后8h、1、3、7d每组各取6只断头取脑,用干湿比重法检测脑组织含水量,免疫组化检测脑组织AQP4含量。结果与A组比较,造模后8h、1、3、7d时B、C组脑组织含水量和AQP4含量明显增加(P<0.05)。与B组比较,C组脑组织含水量明显减少(P<0.05),AQP4含量明显降低(P<0.05)。结论 AQP4在大鼠SAH后脑水肿的病理生理中起着重要的作用,RIPC通过下调AQP4的表达减轻脑水肿的程度。
Objective To observe the influence of the remote ischemic preconditioning (RIPC) on the brain edema and Aquaporin 4 (AQP4) protein after cerebral hemorrhage in rats. Methods Seventy-two SD rats were randomly divided into three groups: sham operationl group (group A), SAH group (group B), SAH + RIPC group (group C). RIPC was induced by compressing the two lower limbs alternately with a tourniquet for three cycles of ten-minute ischaemia followed by ten-minute reperfusion. Autologous blood was injected into the cisterna magna twice to set SAH model. Rats were sacrificed respectively at 8 h,1 d,3 d and 7 d after modeling. Brain water content was calculated using the ratio of brain wet and dry, the expression of AQP4 was observed with immunohistochemistry. Results Compared with group A, brain wet content and AQP4 expression of groups B and C increased significantly at 8 h, 1,3, 7 d after modeling(P^0.05). Compared with group B, brain water content of group C decreased significantly (P(0.05), and AQP4 expression reduced significantly (P(0. 05). Conclusion AQP4 plays an important role in pathophysiological mechanisms of brain edema after SAH, remote ischemic preconditioning (RIPC) can down-regulate the expression of AQP4, so as to reduce the degree of cerebral edema.
出处
《临床麻醉学杂志》
CAS
CSCD
北大核心
2013年第11期1108-1110,共3页
Journal of Clinical Anesthesiology
基金
2013年江西省卫生厅科技项目(20121939)