Department of Forensic Pathology, Zhongshan School of Medicine, Sun Yat-Sen University, Guangzhou, PR China.
Heart Lung Circ. 2013 Apr;22(4):284-90. doi: 10.1016/j.hlc.2012.11.008. Epub 2012 Dec 14.
Muscle crush injury commonly occurs after earthquakes, collapse of buildings and sjambok beatings, and it often induces crush syndrome if not treated promptly. The general manifestation of crush syndrome is the presence of myoglobinuria with acute renal failure. However, whether cardiomyocyte injury is induced after muscle crush injury has not been investigated. The aim of this study was to observe the effects of muscle crush injury on cardiomyocyte injury and its relationship to the changes of ANP and ET-1 levels after muscle crush injury in rats.
Muscle crush injury was produced in Male Sprague-Dawley rats. Forty-eight rats were divided into six groups. The changes of electrocardiogram (ECG) were recorded. The serum levels of K(+), Ca(2+), urea, creatinine (CR), creatine kinase (CK), creatine kinase-myocardial band (CK-MB) and cardiac troponin I (cTnI) were detected by automated biochemical analysis and automated chemiluminescence assay, respectively. The myocardial and plasma levels of ANP and ET-1 were investigated by radioimmunoassay. Myocardial apoptosis and caspase-3 protein expression were quantitatively analysed by TUNEL-staining and Western blotting, respectively.
After six hours of decompression, the serum levels of K(+) and urea increased and ST-segment elevated and heart rates decreased pronouncedly over 48h, CR increased and Ca(2+) decreased considerably over 24h. The serum levels of CK-MB and cTnI increased significantly from 6h to 24h and CK increased markedly from 0h to 24h after decompression and then decreased slowly. However, after 48h of decompression, the serum levels of cTnI were still higher than those of the control group. Plasma levels of ANP and ET-1 increased and myocardial ANP and ET-1 decreased progressively over 48h, and changed significantly from 6h to 48h after decompression. The number of TUNEL-positive myocytes and caspase-3 protein expression were higher from 6h to 48h after decompression. Moreover, the levels of K(+), urea, CR, CK, CK-MB, cTnI and caspase-3 reached their highest values after 12h of decompression. There were significant correlations between the plasma ANP elevation and the myocardial ANP decline, between the plasma ANP elevation and the plasma ET-1 increase, and between the plasma ET-1 increase and the myocardial ET-1 decline.
Cardiomyocyte injury was induced by muscle crush injury at the early stage of decompression but not at compression. The most dangerous period of cardiomyocyte injury was at the 12th hour of decompression. Cardiomyocyte injury may partly relate to the changes of ANP and ET-1.
肌肉挤压伤常发生在地震、建筑物倒塌和 sjambok 鞭打之后，如果不及时治疗，常导致挤压综合征。挤压综合征的一般表现为肌红蛋白尿伴急性肾衰竭。然而，肌肉挤压伤后是否会引起心肌细胞损伤尚未得到研究。本研究旨在观察肌肉挤压伤对心肌细胞损伤的影响及其与大鼠肌肉挤压伤后心钠肽（ANP）和内皮素-1（ET-1）水平变化的关系。
采用雄性 Sprague-Dawley 大鼠制作肌肉挤压伤模型。将 48 只大鼠分为 6 组，记录心电图（ECG）变化。采用全自动生化分析仪和全自动化学发光仪分别检测血清钾（K(+））、钙（Ca(2+））、尿素、肌酐（CR）、肌酸激酶（CK）、肌酸激酶同工酶（CK-MB）和心肌肌钙蛋白 I（cTnI）水平。采用放射免疫法检测心肌和血浆中 ANP 和 ET-1 水平。采用 TUNEL 染色和 Western blot 定量分析心肌细胞凋亡和半胱氨酸天冬氨酸蛋白酶-3（caspase-3）蛋白表达。
减压 6 小时后，血清 K(+)和尿素水平升高，ST 段抬高，48 小时内心率明显下降，CR 显著升高，Ca(2+)明显降低。减压 6 小时至 24 小时 CK-MB 和 cTnI 水平明显升高，0 小时至 24 小时 CK 水平明显升高，然后缓慢下降。然而，减压 48 小时后，cTnI 血清水平仍高于对照组。减压后 48 小时内，血浆 ANP 和 ET-1 水平逐渐升高，心肌 ANP 和 ET-1 水平逐渐降低，减压后 6 小时至 48 小时变化显著。减压后 6 小时至 48 小时，TUNEL 阳性心肌细胞数和 caspase-3 蛋白表达增加。此外，K(+)、尿素、CR、CK、CK-MB、cTnI 和 caspase-3 的水平在减压 12 小时后达到最高。血浆 ANP 升高与心肌 ANP 下降、血浆 ANP 升高与血浆 ET-1 升高、血浆 ET-1 升高与心肌 ET-1 下降之间均存在显著相关性。
肌肉挤压伤早期可引起心肌细胞损伤，但在压迫期不会引起心肌细胞损伤。心肌细胞损伤最危险的时期是减压后的 12 小时。心肌细胞损伤可能部分与 ANP 和 ET-1 的变化有关。
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