摘要
目的探讨缝隙连接通讯对创伤失血性休克自由基代谢和炎症因子的影响。方法采取钳夹一侧股骨中段致其粉碎性骨折合并股动脉放血的方式制备新西兰兔创伤失血性休克模型。将制成模型的24只新西兰大白兔随机分为三组(n=8):创伤休克组(Ⅰ组),创伤休克复苏组(Ⅱ组)和创伤阻断组(Ⅲ组)。模拟救援过程,将各动物模型分为创伤期、休克期、复苏期和观察期。监测收缩压、舒张压、平均动脉压、心率、呼吸等生理指标,并记录各时点的数值。在各个时点抽取兔血,离心,取上清检测肿瘤坏死因子-α(TNF-α)、白细胞介素-1(IL-1)、白细胞介素-6(IL-6)、白细胞介素-10(IL-10)等炎症因子(ELISA法);同时检测丙二醛(MDA)、超氧化物歧化酶(SOD)等自由基代谢指标。结果创伤失血性休克后血液回输复苏可显著减少促炎因子TNF-α、IL-1、IL-6的释放(P<0.05),显著增加抗炎因子IL-10的释放(P<0.05);缝隙连接通讯早期阻断后,可减少创伤休克期TNF-α、IL-6等部分促炎因子的产生释放而较基础值无显著变化,对IL-10等抗炎因子与Ⅱ组比较无显著影响(P>0.05)。同时,血液回输也可显著减少自由基过氧化反应指标MDA的产生释放(P<0.05),增加因创伤休克而降低的抗氧化酶SOD的产生释放(P<0.05);缝隙连接通讯早期阻断后,可减少创伤休克期MDA的产生释放而较基础值无显著变化,对抗氧化酶SOD与Ⅱ组比较无显著影响(P>0.05)。结论在创伤失血性休克早期阻断缝隙连接通讯,可减少部分促炎因子的产生释放和自由基的过氧化反应,而对抗炎因子和抗氧化酶无显著作用。
Objective To investigate the effect of gap junctional intercellular communication on free radical and inflammatory factor for traumatic hemorrhagic shock.Methods After the model of New Zealand white rabbits with traumatic hemorrhagic shock,24 rabbits were randomly divided into 3 groups(n=8,each):traumatic hemorrhagic group(groupⅠ),traumatic shock and resuscitation group(groupⅡ)and blocking traumatic shock group(groupⅢ).The process of each animal model had four periods:traumatic period(30 min),shocked period(60 min),resuscitation period(45 min)and observation period(135 min).The SBP,DBP,MAP,HR,RR were recorded at the beginning and the end of every period(T1,T2,T3,T4,T5).Rabbit blood was extracted and centrifuged,and TNF-α,IL-1,IL-6,IL-10,MDA,SOD ware detected by enzyme linked immunosorbent assay(ELISA).Results Blood transfusion recovery after traumatic hemorrhagic shock can significantly reduce the pro-inflammatory cytokines TNF-α,IL-1,IL-6(P<0.05),can significantly increase anti-inflammatory factor IL-10(P<0.05);Gap junctional intercellular communication early blocked may reduce some pro-inflammatory cytokine(TNF-α,IL-6),and it had no significant changes compared with baseline.But anti-inflammatory factor IL-10 had no significantly effect,and it had no significant effect compared withⅡgroup(P>0.05).At the same time,blood transfusion can be significantly reduced MDA(P<0.05),significantly increased SOD(P<0.05);gap junctional intercellular communication early blocked can reduce MDA,and it had no significant changes compared with baseline.But in antioxidant enzymes SOD had no significantly effect,and compared withⅡgroup it had no significant effect(P>0.05).Conclusions Gap junction communication was early blocked in traumatic hemorrhagic shock will reduce the production of some pro-inflammatory cytokine and free radical peroxidation,but will not significantly affect anti-inflammatory factor and antioxidant enzymes.
出处
《中华临床医师杂志（电子版）》
CAS
2012年第19期5877-5880,共4页
Chinese Journal of Clinicians(Electronic Edition)
基金
上海市长宁区卫生局基金(20094Q18001)
关键词
缝隙接合部
休克
创伤性
自由基
炎症因子
Gap junctions
Shock,traumatic
Free radicals
Inflammatory factor
