摘要目的 探讨多器官功能障碍综合征(MODS)时胰岛β细胞超微结构和功能的变化,为临床治疗MODS高血糖提供理论依据.方法实验地点为福建省立医院动物房、福建省立陕院心血管研究所重点实验窜、福建省立医院病理科与福建医科大学电镜室.清洁级健康雄性SD大鼠16只,体质量180～220 g,随机分成2组,即:MODS组和埘照组,每组8只.MODS组大鼠腹腔内注射大肠杆菌菌液,同时钳断大鼠左下肢,造成感染复合创伤二次打击MODS大鼠模型.对照组给予等量生理盐水腹腔内注射.48 h后榆测有2个以上器官或系统功能障碍即为MODS组造模成功.成功造模后,两组大鼠心脏穿刺抽血,测定空腹血糖、血清胰岛素水平(抽血前禁食12 h).之后两组大鼠迅速腹腔内注射20%葡萄糖液(2 g葡萄糖/ks体质量),30 min后,再次心脏抽血测定糖负荷血糖及血清胰岛素水平.两组大鼠血糖的比较用成组t检验,血清胰岛素水平经自然对数转换正态化后进入成组t检验.抽血后取标本电镜下观察两组大鼠胰岛β细胞超微结构,免疫组化分析胰岛β细胞Bax蛋白表达.结果 和正常埘照组比较,MODS组大鼠空腹血糖、糖负荷30 min后血糖及Bax蛋白表达明显高于正常对照组(P<0.01).糖负倚30 min后,对照组大鼠血清胰岛素明显升高,而MODS组升高不明显,两组比较差异具有统计学意义(P<0.01).电镜下MODS大鼠胰岛β细胞出现空泡变性,少数细胞坏死,及出现线粒体肿胀,粗面内质网扩张等一系列趟微结构病理改变.结论 MODS大鼠胰岛β细胞超微结构出现明显病理改,变,其Bax蛋白表达明显增高.MODS大鼠血糖升高可能与胰岛β细胞出现的这些改变从而导致其胰岛素分泌不足有关.

abstractsObjective To explore the effect of multiple organ dysfunction syndrome (MODS) on the ultra-structure and function of pancreatic beta cells and to provide a theoretical basis for clinical treatment of high blood glucose in patients with MODS. Method This study was performed in the Animal Department of Fujian Provincial Hospital, the Key Laboratory of Fujian Provincial Cardiovascular Institute, the Pathology Department of Fujian Provincial Hospital and in the Electron Microscopic Department of Fujian Medical University. Sixteen pathogen-free male Sprague-Dawley rots weighing 180 ～ 220 g, were selected and randomly divided into MODS group and control group (8 rats per group). MODS was induced by intraperitoneal injection with bacterium c oli and cutting the left legs. Rats in the control group received an intraperitoneal injection of an equivalent volume of sodium chloride. The MODS model was considered successful when two or more organs showed dysfunction 48 h after the injection. The blood glucose and plasma insulin levels were measured in the fasting state and in response to a glucose load. All data were analyzed using t tests. The plasma insulin concentration was analyzed after logarithmic transforma-tion. The ultrastructure of the pancreatic beta cells was observed under an electron microscope. The expression of Bax was determined immunohistochemically. Results The blood glucose during fasting, the blood glucose level 30 min after a glucose load and the expression of Bax were significantly in the MODS group compared with the con-trol group (P <0.01). In addition, the plasma insulin concentration level was insignificantly increased 30 min af-ter the glucose load in the MODS group (P < 0.01). Pathological uhrastructural changes were found, as follows: most pancreatic beta cells in the MODS group exhibited vacuole degeneration, some were necrotized, the mitochen-dria had swollen and the rough endoplasmic reticulum had expanded. Conclusions The uhltrastructure of the pan-creatic beta cells in the MODS rats shewed significant pathologic changes, with increased expression of Bax. These pathological changes may he responsible for the decreased insulin secretion, which caused the increased blood glu-cose levels.