Evaluation of cardiac troponin I in serum and myocardium of rabbits with experimentally induced polymicrobial sepsis.

Autor: Tümer KÇ; Department of Internal Medicine, Faculty of Veterinary Medicine, Firat University, 23200, Elazığ, Turkey., Özdemİr H; Department of Internal Medicine, Faculty of Veterinary Medicine, Firat University, 23200, Elazığ, Turkey., Eröksüz H; Department of Pathology, Faculty of Veterinary Medicine, Firat University, 23200, Elazığ, Turkey.
Jazyk: angličtina
Zdroj: Experimental animals [Exp Anim] 2020 Jan 29; Vol. 69 (1), pp. 54-61. Date of Electronic Publication: 2019 Aug 29.
DOI: 10.1538/expanim.19-0046
Abstrakt: Sepsis is a potentially life-threatening condition, and it is frequently complicated by myocardial damage. Data on myocardial damage in rabbit caecal ligation and puncture (CLP) models are limited, although numerous animal models have been used to study sepsis-associated myocardial damage. This study aimed to investigate the effect of CLP on cardiac muscle by measuring serum cardiac troponin I (cTnI) concentrations and by detecting both histopathological changes and cTnI immunoreactivity in cardiomyocytes in rabbits. After CLP was performed in rabbits, blood samples were taken from the jugular vein at 0, 4, 8, and 12 h for haematological and biochemical analyses. At the end of the experiment, all of the rabbits were euthanised to examine the histopathological changes and the cTnI immunoreactivity in cardiac muscle tissue. No changes in serum cTnI concentration were observed in the experimental group (EG) or control group (CG) at 0 and 4 h. In EG, the mean serum cTnI concentrations were 0.230 ± 0.209 and 1.177 ± 0.971 ng/ml at 8 and 12 h, respectively. In CG, the mean serum cTnI concentrations were 0.032 ± 0.014 and 0.031 ± 0.021 ng/ml at 8 and 12 h, respectively. Moreover, cytoplasmic cTnI immunoreactivity decreased in EG compared with that in CG (P<0.01). The results demonstrated that CLP induced a systemic inflammatory response and caused myocardial damage in rabbits.
Databáze: MEDLINE