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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 communication on free radical metabolism and inflammatory cytokines in traumatic hemorrhagic shock. Methods The New Zealand rabbit model of traumatic hemorrhagic shock was prepared by the middle part of the femur caused by its comminuted fracture combined with the femoral artery bleeding. Twenty - four New Zealand white rabbits were randomly divided into three groups (n = 8): traumatic shock group (group Ⅰ), traumatic shock group (group Ⅱ) and traumatic block group (group Ⅲ). Simulate the rescue process, the animal models were divided into traumatic, shock, recovery and observation period. Monitoring systolic blood pressure, diastolic blood pressure, mean arterial pressure, heart rate, respiration and other physiological indicators, and record the value of each point. At each time point, the blood of rabbits was collected and centrifuged. The supernatants were taken for detection of tumor necrosis factor-α (TNF-α), interleukin-1 (IL-1), interleukin- 10 (IL-10) and other inflammatory factors (ELISA method); at the same time detection of malondialdehyde (MDA), superoxide dismutase (SOD) and other free radical metabolism indicators. Results Blood transfusion and resuscitation after traumatic hemorrhagic shock significantly reduced the release of proinflammatory cytokines TNF-α, IL-1 and IL-6 (P <0.05) and significantly increased the release of anti-inflammatory cytokines IL-10 The early postponement of gap junctional communication could reduce the production and release of some proinflammatory cytokines such as TNF-α and IL-6 in wound shock stage, but had no significant change from baseline Significantly affected (P> 0.05). At the same time, blood transfusion also significantly reduced the production and release of MDA (P <0.05) and increased the production and release of antioxidant enzyme SOD (P <0.05), which were reduced by traumatic shock. The early resistance of gap junctional communication After breaking, it can reduce the generation and release of MDA in traumatic shock period without significant changes compared with the baseline value. There was no significant difference in SOD activity between the two groups (P> 0.05). Conclusion Blocking the gap junctions in the early stage of traumatic hemorrhagic shock can reduce the production and release of some proinflammatory cytokines and the free radical peroxidation, but have no significant effect on anti-inflammatory cytokines and antioxidant enzymes.