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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 observe the pathological changes of myocardial tissue atrial tissue ANP, ET-1 and myocardial ultrastructure after severe crush injury in rabbits to investigate the secondary myocardial damage after severe crush injury And its related mechanisms. Methods 42 rabbits were randomly divided into normal control group (n = 6) and crush injury group (n = 36). The crush injury group was divided into 6 A subgroup, that is, decompression immediately, decompression 6,12,24,48,72 h subgroups, each subgroup of 6 rabbits. Serum urea nitrogen (BUN), creatinine (Cr), potassium (K +) and creatine kinase (CK) concentrations were measured by automatic biochemical analyzer. The levels of myoglobin (MYO), troponin I (cTnI), creatine kinase isoenzyme (CK-MB) concentrations. The contents of ANP and ET-1 in myocardium were detected by radioimmunoassay. HE staining or electron microscopy was used to observe the myocardial samples. The morphological changes were observed under light and electron microscopes Time myocardial structural changes. Results Compared with those before compression, the levels of CK, CK-MB and cTnI were significantly increased (P <0.05) and the contents of ANP and ET-1 in myocardium were decreased at 12 ~ 24h after crush injury (P <0.05). Light and electron microscopy, pathological changes of myocardial cells, and with time, gradually increased pathological changes, the most obvious in 12 ~ 24h, and then gradually reduce and disappear. Conclusion Severe crush injury can cause secondary myocardial injury and cardiac dysfunction. The changes of myocardial markers, ANP, ET-1 and pathological morphology are basically the same.