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- W2131703092 abstract "Background Cardiac dysfunction after brain death (BD) limits donors for cardiac transplantation. Glucocorticoids ameliorate brain death–induced donor heart dysfunction. We hypothesized that glucocorticoid therapy alleviates myocardial depression through altering the balance between pro- and anti-inflammatory mediators via the nuclear factor-kappaB (NF-κB)/inhibitor of kappaB-alpha (IκBα) pathway and/or by preserving beta-adrenergic receptor (βAR) signaling in the heart. Methods Crossbred pigs (25 to 35 kg) were randomly assigned to the following groups (n = 5/treatment): sham (Group 1); BD (Group 2); and BD with glucocorticoids (30 mg/kg methylprednisolone), either 2 hours before (Group 3) or 1 hour after BD (Group 4). Tumor necrosis factor-alpha (TNF-α) levels were measured in plasma at baseline and 1 hour and 6 hours after BD. Protein levels were measured in left ventricular homogenates procured 6 hours after BD. Results Pro-inflammatory proteins (TNF-α) and interleukin-6 were lower in Group 3 and Group 4 compared with Group 2 at 6 hours after BD (p < 0.01). Intracellular adhesion molecule-1 was also lower in Group 4 compared with Group 2 (p = 0.001). Interleukin-10, an anti-inflammatory mediator, was lower in Group 4 than in Group 2 (p < 0.001), but not different between Groups 2 and 3. At 6 hours after BD, neither NF-κB activity nor basal adenylate cyclase activity differed between Groups 3 and 4 compared with Group 2. Conclusions Glucocorticoids maintained myocardial function and shifted the balance of pro- and anti-inflammatory mediators after BD. The mechanisms by which glucocorticoids preserve myocardial function, however, do not appear to involve the NF-κB pathway or βAR signaling. Cardiac dysfunction after brain death (BD) limits donors for cardiac transplantation. Glucocorticoids ameliorate brain death–induced donor heart dysfunction. We hypothesized that glucocorticoid therapy alleviates myocardial depression through altering the balance between pro- and anti-inflammatory mediators via the nuclear factor-kappaB (NF-κB)/inhibitor of kappaB-alpha (IκBα) pathway and/or by preserving beta-adrenergic receptor (βAR) signaling in the heart. Crossbred pigs (25 to 35 kg) were randomly assigned to the following groups (n = 5/treatment): sham (Group 1); BD (Group 2); and BD with glucocorticoids (30 mg/kg methylprednisolone), either 2 hours before (Group 3) or 1 hour after BD (Group 4). Tumor necrosis factor-alpha (TNF-α) levels were measured in plasma at baseline and 1 hour and 6 hours after BD. Protein levels were measured in left ventricular homogenates procured 6 hours after BD. Pro-inflammatory proteins (TNF-α) and interleukin-6 were lower in Group 3 and Group 4 compared with Group 2 at 6 hours after BD (p < 0.01). Intracellular adhesion molecule-1 was also lower in Group 4 compared with Group 2 (p = 0.001). Interleukin-10, an anti-inflammatory mediator, was lower in Group 4 than in Group 2 (p < 0.001), but not different between Groups 2 and 3. At 6 hours after BD, neither NF-κB activity nor basal adenylate cyclase activity differed between Groups 3 and 4 compared with Group 2. Glucocorticoids maintained myocardial function and shifted the balance of pro- and anti-inflammatory mediators after BD. The mechanisms by which glucocorticoids preserve myocardial function, however, do not appear to involve the NF-κB pathway or βAR signaling." @default.
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- W2131703092 date "2007-01-01" @default.
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- W2131703092 title "Glucocorticoids Alter the Balance Between Pro- and Anti-inflammatory Mediators in the Myocardium in a Porcine Model of Brain Death" @default.
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- W2131703092 doi "https://doi.org/10.1016/j.healun.2006.10.011" @default.
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