丙泊酚对失血性休克致兔心肌损伤Cx43表达的影响

目的 探讨丙泊酚对失血性休克兔心肌损伤缝隙连接蛋白43(Cx43)表达的影响.方法 将雄性新西兰白兔24只采用随机数字表法分为假手术(S)组、失血性休克(HS)组及丙泊酚处理(P)组.采用Wigger's改良法制作失血性休克动物模型;P组于放血前10 min注射丙泊酚5 mg/kg,并以20 mg/(kg·h)的速度持续输注至休克后120 min;S组及HS组输注等容量生理盐水.于放血前即刻(T0)、休克30 min(T1)、60 min(T2)、90 min(T3)和120 min(T4)采集动脉血.采用ELISA法测定兔血清肌钙蛋白I(cTnI)浓度;采用自动血气分析仪检测动脉血乳酸水平;采用HE染色观察心肌病理损伤;采用Western blot法检测兔心肌Cx43表达.结果 T1~T4时HS组与P组血清cTnI浓度和动脉血乳酸水平高于S组,且P组低于HS组(P<0.05);T1~T4时HS组和P组血清cTnI浓度和动脉血乳酸水平高于T0时,且逐渐升高(P<0.05).S组心肌细胞形态正常,肌纤维排列整齐,细胞核均匀一致;HS组心肌细胞肿胀,纤维排列不规则或断裂,间质内有大量炎性细胞浸润,胞核崩解;P组心肌细胞轻度变性,少量心肌纤维断裂,细胞间隙略增宽.HS组和P组心肌Cx43含量低于S组,但P组高于HS组(P<0.05).结论 丙泊酚可减轻失血性休克心肌损伤,其机制可能与上调Cx43表达有关.

Effect of Propofol on Cx 43 Expression in Rabbits with Myocardial Injury Induced by Hemorrhagic Shock

Objective To investigate the effect of Propofol preconditioning on connexin 43 (Cx43) protein ex-pression in rabbits with myocardial injury induced by hemorrhagic shock. Methods Twenty-four male New Zealand rab-bits were randomly divided into sham operation group ( group S, n=8 ) , hemorrhagic shock group ( group HS, n=8 ) and Propofol group ( group P, n=8 ) . The wigger 's modified method was used for establishing hemorrhagic shock mod-els. Group P was injected with 5 mg/kg Propofol 10 minutes before bloodletting, and the injection was remained at the speed of 20 mg·kg-1·h-1 lasting to the 120th minutes after shock. Group S and HS were injected with the same volume of normal saline. Blood samples were collected at the time of bloodletting ( T0 ) , 30 min ( T1 ) , 60 min ( T2 ) , 90 min ( T3 ) and 120 min ( T4 ) after shock. CTnI concentration in serum was determined by enzyme linked immunosorbent assay ( ELISA);lactate level was detected by arterial blood gas analyzer;heart tissues were stained by HE in order to observe the pathological changes by optical microscope, and Cx43 expressions in heart tissue were detected by Western blot moth-od. Results On T1 , T2 , T3 and T4 , values of serum cTnI concenreations and lactate levels in group HS and P were sig-nificantly higher than those in group S, and the values in group P were significantly lower than those in group HS ( P<0. 05);values of serum cTnI concenreation and lactate levels in group HS and P were higher than those on T0 , and the tendency was increased gradually (P<0. 05). The myocardial cells and fibers showed a normal morphology in group S;the myocardial cells were swelling and fibers were broken, inflammatory cells infiltrated in intercellular space and cell nu-cleus disintegrated in group HS; the myocardial cells were injured lightly and only a small amount of myocardial fibers broken with broadening intercellular space in group P. Compared with those in group S, the expression of Cx43 decreased in group HS and P,but it higher in group P than that in group HS (P<0. 05). Conclusion Propofol can attenuate the myocardial damage induced by hemorrhagic shock, and its mechanism may be related to upregulating Cx43 expression.