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- W1969132236 abstract "Major burn injury promotes an increase in myocardial intracellular sodium level ([Na+]i) which is thought to promote myocyte calcium accumulation, cellular injury and myocardial dysfunction. Since burn injury increases myocardial PKC activity, which in turn reduces Na-K-ATPase activity, we hypothesized that post burn inhibition of PKC would increase Na-K-ATPase activity, reduce burn-related Na+accumulation and improve myocardial performance. Adult Sprague Dawley rats were divided to receive: burn over 40% TBSA and fluid resuscitation (Group 1); burn treated with calphostin (0.1 mg/kg 30 min, 6 hrs, and 21 hrs post burn) + fluid (Group 2); sham burn given vehicle (Group 3); sham burn + calphostin (Group 4). Na-K-ATPase and PKC activities were determined (biochemical analyses). Myocyte [Na+]i was determined using a fluorescent indicator (SBFI); myocyte secretion of cytokines was measured by ELISA; myocardial function was studied in vitro (Langendorff). Burn injury promoted a..." @default.
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- W1969132236 date "2006-03-01" @default.
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- W1969132236 title "Calphostin Increases Myocardial Na-K-ATPase Activity and Reduces Myocyte Sodium Overload After Burn Injury" @default.
- W1969132236 doi "https://doi.org/10.1097/01253092-200603001-00159" @default.
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