摘要
目的 :探讨实验动物脓毒症和脓毒性休克时内皮素 - 1(endothelin- 1,ET- 1)和内皮素 A受体 (ETAR)基因在肺、肾和小肠粘膜中的表达情况以及各脏器功能受损情况。方法 :2 4只雄性大鼠随机分为正常组、对照组、脓毒症组和脓毒性休克组 ;通过持续静脉泵注大肠杆菌内毒素 (L PS)复制大鼠脓毒症和脓毒性休克模型 ;运用反转录 -聚合酶链反应 (RT- PCR)以葡萄糖- 6 -磷酸脱氢酶 (G- 6 - PD)基因为内参照基因 ,分别检测脓毒症和脓毒性休克组肺、肾脏和小肠粘膜组织 ET- 1和 ETAR基因表达情况 ,同时检测其血清丙氨酸转氨酶 (AL T)、白蛋白 (A )、尿素氮 (BU N)、肌酐 (Cr)和动脉血气的变化。结果 :脓毒症和脓毒性休克组大鼠脏器组织 ET- 1和 ETAR基因表达产物较正常组和对照组均明显增加 (P <0 .0 1) ;脓毒性休克组大鼠血清AL T、BUN和 Cr较正常组、对照组和脓毒症组均显著上升 (P<0 .0 1) ,脓毒症组上述指标也较正常组明显上升 (P<0 .0 1) ;脓毒症组和脓毒性休克组早期动脉血气分析为低氧和呼吸性碱中毒 ,脓毒性休克组后期出现明显的低氧血症和 CO2 潴留。 结论 :ET- 1和 ETAR参与了脓毒症和脓毒性休克的病理生理过程 ,且很可能是参与脓毒症和脓毒性休克并发多脏器功能障碍综合征 (MODS)启动的因子之一。
Objective: To investigate changes of the endothelin-1(ET-1) and its receptor (endothelin receptor subtype A, ET AR ) mRNA expression in some organs(kidney, lung and small intestinal mucous membrane) in the sepsis and septic shock rats. Methods: Twenty-four male rats randomized into sepsis group, septic shock group, control and normal group was infused with endotoxin(LPS) via indwelling right atria catheters except normal and control group. RT-PCR was used to detect kidney, lung and small intestinal mucous membrane tissue mRNA expression of the ET-1 , ET AR and glucose-6-phospho dehydrogenase(G-6-PD) in every group.Serum BUN, Cr, ALT and A were determined. The arterial oxygen tension (PaO 2) and arterial carbon dioxide partial pressure(PaCO 2)were measured in every group. Results: ET-1 mRNA and ET AR mRNA expression in the sepsis group and septic shock group were significantly higher than in normal group. There were significant differences between the normal/control group and sepsis/shock group in BUN,Cr,ALT,PaO 2 and PaCO 2. Conclusion: A higher expression of ET-1 mRNA and ET AR mRNA may be one of the startup factors on multiple organ dysfunction syndrome (MODS) and may play an important role on pathogenesis in sepsis and septic shock.
出处
《第二军医大学学报》
CAS
CSCD
北大核心
2001年第9期839-842,共4页
Academic Journal of Second Military Medical University
关键词
脓毒症
脓毒性休克
内皮素-1
内皮素A受体
septicemia
shock,septic
endothelins
receptors,endothelin
gene expression
