维生素C对挤压伤缺血/再灌注引起的心肌功能损伤的影响

Vitamin C reduces ischemia/reperfusion-induced muscle damage in rat crush injury model

目的观察维生素C(vitamin C,VitC)对大鼠挤压综合征(crush syndrome,CS)模型缺血/再灌注引起心肌损伤的改善情况,以及对生存率的影响。方法 SD大鼠随机分为对照组、CS组、CS+VitC-10组、CS+VitC-20组、CS+VitC-40组,复制CS模型,大鼠双侧后肢挤压6h,然后再灌注生理盐水以及不同剂量VitC(10、20、40mg/kg)6h,收集血液用于生化分析,同时收集组织样品用于RT-PCR与Western Blot分析。结果挤压伤后CS组血钾(K+)、尿素氮(urea nitrogen,BUN)、肌酐(creatinine,Cr)、肌酸激酶(creatine kinase,CK)、肌钙蛋白I(cardiac troponin I,cTnI)、肌酸激酶心肌同功酶(creatine kinase MB,CK-MB)、血浆心钠素(atrial natriuretic factor,ANP)较对照组升高,但CS组血钙(Ca2+)、内皮素1(endothelin-1,ET-1)较对照组下降(P<0.05);与CS组相比,CS+VitC-10、20、40组K+、BUN、Cr、CK的含量显著降低,Ca2+、ET-1含量显著升高(P<0.05)。VitC-20组和VitC-40组的生存率高于CS组(P<0.05)。结论 VitC对CS模型缺血/再灌注引起的心肌损伤具有细胞保护作用,并有助于提高大鼠CS模型的生存率。

Objective To observe the effects of vitamin C（VitC）in ischemia/reperfusioninduced muscle damage and the survival rates in rat crush syndrome（CS）model.Methods SD rats were randomly divided into control group,CS group,CS＋VitC-10 group,CS＋VitC-20 group and CS＋VitC-40 group.To create a crush injury model,SD rats were subjected to bilateral hind limb compression with rubber tourniquets for 6h,followed by reperfusion for 6h.Saline for the CS group or VitC（10,20 and 40 mg/kg）for the VitC-treated groups were intravenously administered immediately before reperfusion.Blood samples were collected for biochemical analysis,and tissue samples for RT-PCR and Western Blot assay.Results Compared with those of control group,K＋,urea nitrogen（BUN）,creatinine（Cr）,creatine kinase（CK）,cardiac troponin I（cTnI）,creatine kinase MB（CK-MB）and atrial natriuretic factor（ANP）were significantly increased in CS group,but Ca2＋and endothelin-1（ET-1）in CS group were significantly reduced（P〈0.05）.Compared with those of CS group,K＋,BUN,Cr and CK were significantly decreased,while Ca2＋and ET-1in VitC-10,VitC-20 and VitC-40 group were significantly increased（P〈0.05）.The survival rate of VitC-20 and VitC-40 group were much higher than that of CS group（P〈0.05）.Conclusion VitC reduces ischemia/reperfusion-induced muscle necrosis through its cytoprotective action and contributes to improved survival rate in rat CS model.