alexa Endogenous Ouabain Changes Rapidly During Cardiac Pulmonary by Pass | OMICS International | Abstract
ISSN: 2157-7536

Journal of Steroids & Hormonal Science
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Research Article

Endogenous Ouabain Changes Rapidly During Cardiac Pulmonary by Pass

Elena Bignami2, Nunzia Casamassima1, Elena Frati2, Elisabetta Messaggio1, Laura Corno2, Alberto Zangrillo2 and Paolo Manunta1*

1Nephrology and Dialysis Unit, San Raffaele Scientific Institute, Università Vita Salute San Raffaele, Milan, Italy

2Anesthesia and Intensive Care Unit, San Raffaele Scientific Institute, Università Vita Salute San Raffaele, Milan, Italy

*Corresponding Author:
Dr. Paolo Manunta MD
Chair of Nephrology
San Raffaele Scientific Institute
Università Vita Salute San Raffaele
Via Olgettina 60, 20132 Milan, Italy
Tel: ++39 02 26433890/5330
Fax: ++39 02 26432384
E-mail: [email protected]

Received date: November 02, 2011; Accepted date: December 24, 2011; Published date: December 27, 2011

Citation: Bignami E, Casamassima N, Frati E, Messaggio E, Corno L, et al. (2011) Endogenous Ouabain Changes Rapidly During Cardiac Pulmonary by Pass. J Steroids Hormon Sci S3:002. doi:10.4172/2157-7536.S3-002

Copyright: © 2011 Bignami E, et al. This is an open-access article distributed under the terms of the Creative Commons Attribution License, which permits unrestricted use, distribution, and reproduction in any medium, provided the original author and source are credited.

Abstract

 Objective: Endogenous Ouabain (EO) is a cardiac glycoside secreted from the adrenal glands that plays a role sodium homeostasis with hemodynamic and renal effects. It is considered a stress hormone. The role of EO during critical illness is unknown. 

Aim: to study 1. the time course of EO during cardio pulmonary bypass (CPB) and 2. the ability of renal replacement therapy (RRT) to remove EO. Methods: in 11 patients undergoing mitral valve repair were performed an intraoperative time course with serial blood samples for EO, serum creatinine, NT-proBNP and cathecolamines. During surgery blood samples were repeated every 15 minutes. Then all these biomarkers were dosed at the end of surgery, 4 hours and 24 hours later. In the 15 patients 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 CPB reaching 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 after surgery, reaching high plasma levels when EO decreased. Plasma EO and creatinine levels resulted significantly directly 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 and blood pressure fall during CPB.

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