缝隙连接通讯在创伤失血性休克兔液体复苏中的作用

The role of gap junctions on severe hemorrhagic shock rabbits in fluid resuscitation

目的探讨缝隙连接通讯在创伤失血性休克兔液体复苏中的作用。方法采取钳夹一侧股骨中段致其粉碎性骨折复合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16只新西兰大白兔随机分为两组(n=8):传统复苏组(Ⅰ组)和缝隙连接通讯阻断复苏组(Ⅱ组)。模拟救援过程,将各动物模型分为创伤失血期(1期)、院前救援期(2期)、院内复苏期(3期)。监测并记录各时点的SBP、DBP、MAP、HR、RR等生理指标和兔存活时间。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)、白介素-1(IL-1)、白介素-6(IL-6)、白介素-10(IL-10)等炎症因子,采用酶联免疫吸附法;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,缝隙连接通讯在创伤失血性休克兔复苏中具有重要作用。

Objective To investigate the role of gap junctions on severe hemorrhagic shock rabbits in fluid resuscitation. Methods The model of 16 New Zealand white rabbits with traumatic hemorrhagic shock caused by comminuted fracture with femoral artery bleeding were randomly divided into 2 groups（n=8）： conventional resuscitation group（groupⅠ）,blocking gap junctions resuscitation group（groupⅡ）.The process of each animal model had three periods： traumatic hemorrhagic period（30 min）,pre-hospital treatment period（60 min） and in-hospital resuscitation period（60 min）.The SBP,DBP,MAP,HR,RR and rabbit survival time were recorded at the beginning and the end of every period.Rabbit blood was extracted and centrifuged,and TNF-α,IL-1,IL-6,IL-10,MDA,SOD ware detected by enzyme linked immunosorbent assay. Results Blood transfusion recovery after traumatic hemorrhagic shock can significantly reduce the pro-inflammatory cytokines TNF-α,IL-1,IL-6（P0.05）,can significantly increase anti-inflammatory factor IL-10（P0.05）.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 with Ⅱ group（P0.05）.At the same time,blood transfusion can be significantly reduced MDA（P0.05）,significantly increased SOD（P0.05）.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 with Ⅱ group it had no significant effect（P0.05）. Conclusion 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 effect anti-inflammatory factor and antioxidant enzymes.Gap junctional intercellular communication plays impartment role in rabbits with traumatic hemorrhagic shock.