Background
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.
Methods
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+, Ca2+, 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.
Results
After six hours of decompression, the serum levels of K+ and urea increased and ST-segment elevated and heart rates decreased pronouncedly
over 48 h, CR increased and Ca2+ decreased considerably over 24 h. The serum levels of CK-MB and cTnI increased significantly from 6 h to 24 h and CK increased markedly from 0 h to 24 h after decompression and then decreased slowly. However, after 48 h 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 48 h, and changed significantly from 6 h to 48 h after decompression. The number of TUNEL-positive myocytes and caspase-3 protein
expression were higher from 6 h to 48 h after decompression. Moreover, the levels of K+, urea, CR, CK, CK-MB, cTnI and caspase-3 reached their highest values after 12 h 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.
Conclusions
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.
Keywords
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Article info
Publication history
Published online: December 17, 2012
Accepted:
November 8,
2012
Received in revised form:
November 5,
2012
Received:
October 10,
2012
Footnotes
☆This work was supported by a grant from the Department of Science and Technology in Guangdong province of China (No.: 2010B031000006).
Identification
Copyright
© 2012 Australian and New Zealand Society of Cardiac and Thoracic Surgeons (ANZSCTS) and the Cardiac Society of Australia and New Zealand (CSANZ). Published by Elsevier Inc. All rights reserved.
