内毒素休克大鼠心肌三磷酸肌醇I型受体表达变化的研究

Expression of inositol 1,4,5-triphosphate receptor type I in the myocardial tissue of rats with endotoxic shock

目的探讨内毒素休克大鼠心肌三磷酸肌醇I型受体（inositoll，4，5-triphosphate receptor type I，IP、RI）表达水平的变化及其意义。方法健康雄性Wistar大鼠33只，随机分为4组：实验组3组，包括小剂量内毒素组（5mg／kg）、大剂量内毒素组（10mg／kg）和大剂量内毒素处死组（10mg／k譬，于平均动脉压上升至正常并稳定后处死），每组9只；对照组6只，仅注射生理盐水（4ml／kg）。各实验组大鼠股静脉分别注射内毒素建立内毒素休克动物模型，留取心肌组织，用免疫组织化学、免疫印记和胶体金免疫电镜技术检测大鼠心肌组织IPlR18平表达的变化。结果3个实验组大鼠心肌IP3RI表达均增强，均较对照组有显著差异（P〈0．01），其中以处死组增强最明显。IP3RI表达的强弱与大鼠平均动脉压水平高低相关。并且胶体金免疫电镜方法发现I^RI除表达增强外还可见异位表达，于心肌细胞膜附近可见大量表达。结论（1）IP3RI在内毒素休克大鼠心肌组织表达增强，且存在异位表达；（2）IP3RI表达的强弱与大鼠平均动脉压水平高低相关；（3）IR3RI可能影响心肌收缩性，并参与平均动脉压的调节。

Objective To investigate the changes of inositol 1,4,5-triphosphate receptor type I （ IP3 R I ） expression in the myocardial tissue of rats with endotoxic shock and probe the possible mechanisms of myocardial depression. Methods Thirty-three male Wistar rats were divided into four groups：control group （n = 6 ） were injected normal saline（ 4 ml/kg ）, and the other 3 groups （n = 9 ） were injected endotoxin via femoral vein with a different dose of 10 mg/kg, 5 mg/kg, and the artificial sacrificed group （ 10 mg/kg, the rats were sacrificed when the mean arterial pressure was first rapidly decreased, then gradually increased to the normal level）. IP3R I expression in the myocardial tissue of rats was detected by immunohistochemistry, Western blot and colloidal gold immunoelectron microscopy technique. Results IP3RIexpressions were increased significantly in each group of rats with endotoxic shock than in the control group （ P 〈 0. 01 ）, and most obviously enhanced in the the artificial sacrificed group. The expression of IP3RIwas related to the level of mean arterial pressure. Ectopic expression of IP3RIwas observed around the cell membrane of the cardiac myocytes. Conclusion （ 1 ） The expression of IP3 Rlenhances in the myocardial tissue of rats with endotoxic shock, and exists ectopic expression. （2） The expression of IP3 RIwas related to the level of mean arterial pressure. （3） IP3RI may be related to the cardiac contractility and involved in the regulation of mean arterial pressure.