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作 者:陈学云[1] 张希洲[2] 戴建新[3] 孙树汉[3] 陈德昌[4] 杨兴易[4]
机构地区:[1]第二军医大学附属长征医院普外科,上海200003 [2]湖北宜昌市第一人民医院急救中心 [3]第二军医大学基础医学部医学遗传学教研室 [4]第二军医大学长征医院急救科
出 处:《中华实验外科杂志》2008年第6期740-742,共3页Chinese Journal of Experimental Surgery
摘 要:目的观察大鼠脓毒症和脓毒性休克时内皮素-1(ET-1)和内皮素A受体(ETAR)基因在肺、肾和小肠黏膜中的表达变化以及各脏器功能受损情况。方法24只雄性大鼠随机分为正常组、对照组、脓毒症组和脓毒性体克组;通过脓毒症和脓毒性休克大鼠模型,采用逆转录.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肾、肺和小肠黏膜组织ET-1和ETAR基因表达情况,同时检测其血清丙氨酸转氨酶(ALT)、白蛋白(A)、尿素氮(BUN)、肌酐(Cr)和动脉血气变化。结果脓毒症组肾肺肠组织ET-1 mRNA表达相对量分别为87%、74%、82%,ETAR mRNA为82%、65%、78%;脓毒性休克组肾肺肠组织ET-1 mRNA表达相对量分别为98%、85%、93%,ETAR mRNA为95%、80%、91%;较正常组和对照组均明显增加(P〈0.01)。脓毒性休克组大鼠血清ALT为288.50±194.10、BUN 58,00±5.20,Crl33.67±18.70,较正常组、对照组和脓毒症组均显著上升,差异有统计学意义(P〈0.01);脓毒症组血清ALT为97.17±6.30、BUN 30,17±2,30、Cr75.83±6.70,较正常组明显升高(P〈0.01)。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 (endothefin receptor subtype A, ETAR) raRNA expression in some organs (kidney ,lung and small intestinal mucous membrane) in the sepsis and styptic shock rats. Methods The sepsis and septic shock rat models were established. Twenty-four male rats were randomly divided into sepsis group, septic shock group,con- trol group and normal group. RT-PCR was used to detect mRNA expression of the ET-1, ETAR and glu- cose-6-phosphodehydrogenase (G-6-PD) in kidney ,lung and small intestinal mucous membrane tissue. Serum BUN, Cr, ALT and A were determined, The arterial oxygen tension (PaO2 ) and arterial carbon dioxide partial pressure ( PaCO2 ) were measured in every group, Results : ET-1 mRNA and ETAR mRNA expression in the sepsis group and septic shock group was significandy higher than in normal group ( P 〈 0.01 ) (In the sepsis group,ET-1 mRNA was 87% ,74% ,82% and ETAR mRNA was 82% ,65% ,78% ; In septic shock group,ET-I mRNA was 98% ,85% ,93% and ETAR mRNA was 95% ,80% ,91% in kidney,lung and intestine,respectively), There was significant difference between the normal/control group and sepsis/shock group ( P 〈 0, 01 ) in BUN, Cr, ALT ( ALT 288.50 ± 194.10, BUN 58.00 ± 5.20, Cr 133.67 ±18.70 in the sepsis shock groupi ALT 97.17 ±6.30,BUN 30.17 ±2.30,Cr 75.83 ±6.70 in the sepsis group). The PaO2 and PaCO2 of mice in sepsis/shock group were decreased in the early stage, but in the later stage,the PaCO2 was increased and the PaO2 decreased. Conclusion A higher expression of ET-1 mRNA and ETAR mRNA may be one of the startup factors on multiple organ dysfunction syndrome (MODS) and may play an important role in pathogenesis of sepsis and septic shock.
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