Key result
White muscle disease in lambs was associated with elevated mean cTnI (10.49 ng/ml), loss of cTnI expression, and augmented iNOS immunoreactivity in degenerated cardiac myocytes.
Case-Control (n=23)
cTnI elevation may mark cardiac injury in affected lambs; hypothesis-generating for iNOS in veterinary myopathy models.
White muscle disease (WMD) is a world-wide nutritional disease of all animal species characterised by degeneration of skeletal and cardiac muscles. In the present study we determined the cardiac troponin I (cTnI) and inducible nitric oxide synthase (iNOS) expression in hearts of the lambs with WMD (n = 15). Eight clinically healthy lambs served as control. Creatine kinase (CK), creatine kinase MB (CK-MB), aspartate aminotransferase (AST), and lactate dehydrogenase (LDH) activities were analysed for both groups. cTnI levels were measured by a commercially available ELISA kit. Mean cTnI (10.49 ± 0.25 ng/ml), CK (261.16 ± 38.61 U/l), CK-MB (214.16 ± 12.71 U/l), AST (125.83 ± 1.05), and LDH (228.77 ± 14.86 U/l) concentrations were higher in WMD cases. Immunohistochemistry revealed definitive loss of cTnI expression in all cases. None of the 8 controls showed loss of the cTnI expression. However, iNOS immunoreactivity was augmented in degenerated cardiac myocytes and macrophages infiltrating to the interstitium compared to controls. The results of the study suggested that cTnI antibody might successfully be used as a sensitive test in the diagnosis of myocardial injury. iNOS expression augments in cardiac myocytes in lambs with WMD, most likely through influencing the signalling pathways to iNOS induction.
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Tunca et al. (2009) conducted a case-control in White muscle disease (n=23). White muscle disease vs. Clinically healthy lambs was evaluated on Cardiac troponin I (cTnI) and inducible nitric oxide synthase (iNOS) expression. White muscle disease in lambs was associated with elevated mean cTnI (10.49 ng/ml), loss of cTnI expression, and augmented iNOS immunoreactivity in degenerated cardiac myocytes.
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