Objective: Endogenous Ouabain (EO) is a cardiac glycoside secreted from the adrenal glands that plays a rolesodium homeostasis with hemodynamic and renal effects. It is considered a stress hormone. The role of EO duringcritical illness is unknown.Aim: to study 1. the time course of EO during cardio pulmonary bypass (CPB) and 2. the ability of renal replacementtherapy (RRT) to remove EO.Methods: in 11 patients undergoing mitral valve repair were performed an intraoperative time course with serialblood samples for EO, serum creatinine, NT-proBNP and cathecolamines. During surgery blood samples were repeatedevery 15 minutes. Then all these biomarkers were dosed at the end of surgery, 4 hours and 24 hours later. In the 15patients undergoing EO time course during RRT, EO plasma levels were measured when AKI (Acute Kidney Injury)occurred (at R of RIFLE and 24 hours after this moment).Results: In patients undergoing mitral valve repair EO levels increased 15 minutes after the beginning of CPBreaching the peak 4 hours after surgery (from 198±10 to 350±130 pmol/L, p<0.0001). Circulating catecholamine(Norepneephrine ad Epinephrine) levels increased immediately after CBP. NT-proBNP increased only 4 hours aftersurgery, reaching high plasma levels when EO decreased. Plasma EO and creatinine levels resulted significantlydirectly related (r=0.45, p=0.01) after surgery. Continuous RRT did not modified circulating EO in AKI patients.Conclusion: EO may be considered a stress hormone that changes rapidly during acute volume expansion andblood pressure fall during CPB.

Endogenous ouabain changes rapidly during cardiac pulmonary bypass

ZANGRILLO, ALBERTO;MANUNTA, PAOLO
2011-01-01

Abstract

Objective: Endogenous Ouabain (EO) is a cardiac glycoside secreted from the adrenal glands that plays a rolesodium homeostasis with hemodynamic and renal effects. It is considered a stress hormone. The role of EO duringcritical illness is unknown.Aim: to study 1. the time course of EO during cardio pulmonary bypass (CPB) and 2. the ability of renal replacementtherapy (RRT) to remove EO.Methods: in 11 patients undergoing mitral valve repair were performed an intraoperative time course with serialblood samples for EO, serum creatinine, NT-proBNP and cathecolamines. During surgery blood samples were repeatedevery 15 minutes. Then all these biomarkers were dosed at the end of surgery, 4 hours and 24 hours later. In the 15patients undergoing EO time course during RRT, EO plasma levels were measured when AKI (Acute Kidney Injury)occurred (at R of RIFLE and 24 hours after this moment).Results: In patients undergoing mitral valve repair EO levels increased 15 minutes after the beginning of CPBreaching the peak 4 hours after surgery (from 198±10 to 350±130 pmol/L, p<0.0001). Circulating catecholamine(Norepneephrine ad Epinephrine) levels increased immediately after CBP. NT-proBNP increased only 4 hours aftersurgery, reaching high plasma levels when EO decreased. Plasma EO and creatinine levels resulted significantlydirectly related (r=0.45, p=0.01) after surgery. Continuous RRT did not modified circulating EO in AKI patients.Conclusion: EO may be considered a stress hormone that changes rapidly during acute volume expansion andblood pressure fall during CPB.
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Utilizza questo identificativo per citare o creare un link a questo documento: https://hdl.handle.net/20.500.11768/1405
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