Yapay Zeka Hızlı Bakış & Çıkarımlar
AI InsightThe median serum cTnI concentrations in the AG and the CG were 0.075 IQR; 0.017?0.077 and 0.015 ng/mL IQR; 0.01?0.02 at the 120-h mark, respectively P
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Abstract
Myocardial damage and increased circulating cardiac troponin I cTnI concentrations have been shown in various diseases that cause anemia in animals. Whether the acute anemia that occurs during these diseases directly contributes to myocardial damage and to the release of cTnI to the circulation still remains unclear. The objective of this study was to investigate the effect of acute anemia on myocardial damage and serum cTnI concentration using experimentally-induced acute normovolemic anemia. New Zealand rabbits were randomly separated into 2 groups: an acute anemia group AG, n = 8 and a control group CG, n = 6 . To induce acute anemia, repeated jugular phlebotomy was performed. Blood samples were collected before the experiment 0 and at 24, 48, 72, 96, and 120 h. Serum cTnI concentrations were measured using a human specific cTnI assay. After the last blood sample was taken, euthanasia was performed to evaluate the histopathological changes and the cTnI immunolabelling in cardiomyocytes. In the AG, the mean packed cell volume PCV was 13.1 ± 1.4% at 120 h. The median serum cTnI concentrations in the AG and the CG were 0.075 IQR; 0.017?0.077 and 0.015 ng/mL IQR; 0.01?0.02 at the 120-h mark, respectively P