endothelin-1 and Crush-Syndrome

This study describes hematocrit values and quantitative changes in plasma endothelin-1 (ET-1) levels according to the severity of crush syndrome (CS) compression and decompression periods. The experiments were carried out on 50 randomly selected 200-250 gr mass Wistar rats with the use of the standard crush syndrome modeling method. The plasma level of ET-1 was determined by the immuneenzyme method with the use of ELISA REDEAR URIT 660. Hematocrit was determined using the standard method and measured according to tube column divisions. Our data show that ET-1 and hematocrit values rise commensurate with an increased duration of compression, and especially decompression periods. In CS, elevation of ET-1 concentrations and hematocrit values leads to significant microcirculation disturbances in parallel with longer and more severe compression and decompression periods. Specifically, the ET-1 concentration was significantly elevated, possibly in response to activation of surface endothelial В (ET-B) receptors located in the vessel endothelium. These receptors, in turn, have a vasodilative effect due to nitrogen oxide synthesis induction and vascular smooth muscle relaxation. The rise in hematocrit values during crush syndrome is associated with plasmorrhagia induced by trauma and toxic (rhabdomyolysis) shock.

Topics: Animals; Crush Syndrome; Endothelin-1; Hematocrit; Rats, Wistar; Rheology

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.

Topics: Animals; Atrial Natriuretic Factor; Calcium; Creatine Kinase; Creatinine; Crush Syndrome; Electrocardiography; Endothelin-1; Heart Injuries; Male; Muscle, Skeletal; Myocytes, Cardiac; Potassium; Rats; Rats, Sprague-Dawley; Time Factors; Troponin I