Why the study?
Does cTnI have higher specificity than CKMB in detecting isoproterenol-induced cardiotoxicity in rats?
Does cTnI have higher specificity than CKMB in detecting isoproterenol-induced cardiotoxicity in rats?
cTnI is more cardiospecific than CKMB in a rat model of isoproterenol-induced cardiotoxicity, supporting its use in preclinical testing.
Supports cTnI preference over CKMB in rat cardiotoxicity models; leaves open translation to clinical or other preclinical settings.
The aim of this study was to implement the determination of cardiac markers in preclinical research at our department. For this purpose, the pathophysiological model of acute cardiotoxicity induced by high doses of isoproterenol was used. Isoproterenol hydrochloride was intraperitoneally administrated to 42 Wistar male rats at a dose of 50 mg/kg body weight. Cardiac injury was determined by assessing the concentrations of the cardiac markers (cTnI - cardiospecific troponin I and CKMB - cardiac isoenzyme creatine kinase) in the blood at predetermined time-intervals (2, 4, 6, 12, 24 and 36 h), and confirmed by ECG. Isoproterenol hydrochloride caused an elevation in the plasma concentrations of both markers. The results showed a significant difference ( P < 0.01) in the concentrations of cTnI between the experimental and control groups at 2, 4, 6 and 24 h with a maximum peak between the fourth and sixth hour. However, the difference in the concentrations of CKMB between the experimental and control groups was non-significant. This experiment confirmed that cTnI is more cardiospecific than CKMB. It also revealed the possibility to use this marker in preclinical testing.
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Kolmanová et al. (2015) studied this question.
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