Effects of gap junctional intercellular communication on free radical and inflammatory factor for traumatic hemorrhagic shock

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(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 withⅡgroup(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 withⅡgroup it had no significant effect(P0.05).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.