失血性休克大鼠复苏前后胃Cajal 间质细胞及Cx43的变化

目的：探讨失血性休克复苏前后大鼠胃Cajal间质细胞及间隙连接蛋白Connexin 43（Cx43）的变化。方法：SD大鼠随机均分为对照组与实验组。对照组大鼠行假手术；实验组大鼠通过放血制作失血性休克模型，维持休克状态1 h后行液体复苏。分别于休克1 h和复苏治疗后3，6，12，24 h取大鼠胃组织于电镜下观察Cajal细胞超微结构；免疫荧光染色及Western blot检测Cx43的表达。结果：电镜显示实验组休克1 h时Cajal细胞水肿、核皱缩、基膜破坏；复苏治疗后3，6 h无明显变化，12 h时结构开始逐渐恢复，至24 h Cajal细胞恢至接近对照组状态。免疫荧光染色发现实验组Cx43荧光强度于休克1 h明显减弱，但从复苏治疗后逐渐升高，至24 h基本接近对照组。Western blot法显示Cx43蛋白表达量变化与免疫荧光染色结果相一致。结论：失血性休克能导致Cajal细胞损伤与Cx43表达减少，两者改变所造成细胞间信息传递缺陷可能是失血性休克时胃肠道动力障碍的重要原因之一。

Alterations of interstitial cells of Cajal and connexin 43 in stomach of hemorrhagic shock rats before and after resuscitation

Objective: To investigate the alterations of interstitial cells of Cajal (ICC) and gap junction protein connexin 43 (Cx43) in the stomach of hemorrhagic shock rats before and after resuscitation. Methods: SD rats were equally randomized into control group and experimental group. Rats in control group underwent sham operation, while rats in experimental group were subjected to hemorrhagic shock by means of exsanguination, and the shock state was maintained for 1 h before fluid resuscitation. At 1 h after shock induction and 3, 6, 12 and 24 h after resuscitation treatment respectively, the gastric tissues were excised from the rats, and their ICC ultrastructure was observed by transmission electron microscope and Cx43 expression was detected by both immunofluorescence staining and Western blot analysis. Results: Under electron microscope, the gastric ICC presented severe edema, nuclear shrinkage and basal membrane rupture at 1 h after shock, which showed little or no recovery at 3 and 6 h after resuscitation treatment, but began to recover gradually at 12 h and returned to the appearance of control group at 24 h after resuscitation treatment. Immunofluorescence staining showed that the Cx43 fluorescence intensity in experimental group was markedly reduced at 1 h after shock, but gradually increased after resuscitation and approximately reached the control level at 24 h after resuscitation. The results of Western blot analysis for the expression level profiles of Cx43 protein were consistent with those of immunofluorescence staining. Conclusion: Hemorrhagic shock can cause both ICC injury and Cx43 expression reduction, and the intercellular communication defect resulting from both changes may be one of the important reasons for gastrointestinal dynamic disturbance during hemorrhagic shock.