家兔严重挤压伤后心肌组织继发损伤的实验研究

Analysis of secondary damage to myocardial tissues after severe crush injury in rats

目的观察家兔严重挤压伤后心肌组织心钠素(ANP)、内皮素-1(ET-1)及心肌组织超微结构的病理改变,以探讨严重挤压伤后心肌继发受损情况及其相关机制。方法制作挤压伤家兔动物模型,42只家兔随机分为正常对照组(n=6)和挤压伤组(n=36),挤压伤组按挤压后解压时间点分为6个亚组,即解压即刻,解压6、12、24、48、72h亚组,每个亚组6只家兔。采用全自动生化分析仪检测血清尿素氮(BUN)、肌酐(Cr)、钾离子(K+)、肌酸激酶(CK)浓度;采用化学发光法检测血清肌红蛋白(MYO)、肌钙蛋白I(cTnI)、肌酸激酶同工酶(CK-MB)浓度。取家兔心肌标本,采用放射免疫法检测心肌心钠素(ANP)和内皮素(ET-1)的含量;取心肌标本行HE染色或制作电镜切片,在光镜及电镜下观察伤后不同时间点心肌结构的改变。结果与挤压前比较,挤压伤后12～24h,CK、CK-MB、cTnI显著升高(P<0.05),心肌组织ANP、ET-1含量下降(P<0.05)。光镜及电镜下观察,心肌细胞出现病理改变,且随时间延长,病理改变逐渐加重,以12～24h最为明显,其后逐渐减轻并消失。结论严重挤压伤可致心肌组织发生继发性损伤和心功能障碍,心肌标志物、ANP、ET-1与病理形态的变化趋势基本一致。

Objective To examine atrial natriuretic peptide（ANP） and endothelin-1（ET-1） and ultrastructural pathologic changes in myocardial tissues in rabbits after severe crush injury and to investigate the secondary damage to myocardial tissues after severe injury and its mechanism.Methods A crush injury model was established in rabbits.Forty-two rabbits were randomly assigned into one control group（n=6） and one crush injury group（n=36）.The crush injury group was further divided to six subgroups based on the time after crush release,i.e.,immediately after release and at 6,12,24,48,and 72h after release;each subgroup has six rabbits.The level of blood urea nitrogen,Cr,K＋,and CK in serum is detected with an automatic biochemical analyzer.Myoglobin（MYO）,cardiac troponin I（c-TnI）,and CK-MB in the serum were measured using the chemiluminescence method.The myocardial tissues were collected from the same part of rabbit in each group and the content of ANP and ET-1 was determined by radio-immunoassay and the morphologic changes（at different times after the injury） in hematoxylin and eosin-stained myocardial tissue samples were observed under light microscopy and electron microscopy.Results The levels of CK,CK-MB and c-TnI in serum 12-24h after crush are apparently higher than that before crush（P〈0.05）,whereas the content of ANP and ET-1 in the myocardial tissue drops（P〈0.05）.Observation under light microscopy and electron microscopy revealed progressive pathologic changes in the myocytes,with the most severe myocardial damage observed within 12-24h after crush injury.The damage subsequently decreased and eventually disappears.Conclusions Severe crush injury may induce secondary damage to myocardial tissues and cardiac function.The changing trend in the cardiac markers ANP and ET-1 is consistent with the pathologic changes in myocytes during crush injury.