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Inhaled bromine has deleterious cardiac signs, according to our reports. Mechanisms of delayed cardiac effects in the survivors of a single bromine exposure in this paper. With increased LV end-diastolic pressure and LV end-diastolic wall tension, as a result of increased LV fibrosis, a rise in right ventricular and left ventricular end-diastolic pressure and LV end-diastolic pressure and LV end-diast fibrosis was noted. At both time points, TEM images demonstrated myofibrillar damage, cytoskeletal dysfunction, and mitochondrial damage at both time points. Myofibrillar injury and increased LV wall strain were among the causes of rises in cardiac troponin I and N-terminal pro brain natriuretic peptide and elevated LV wall tensions. As a result of rising LV end-systolic wall strain, LV shortening slowed, and was accompanied by greater sarcoendoplastic reticulum calcium ATPase activation and a striking dephosphorylation of phospholamban, a cause of decreased LV shortening. Therefore, bromine-induced persistent cardiac dysfunction is dependent on oxidative stress-induced persistent myocardial disease, as well as phospholamban dephosphorylation. These results in our preclinical model will educate physicians and public health workers, as well as provide useful endpoints to analyze therapies.
Source link: https://doi.org/10.1007/s00204-020-02919-8
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