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Intensive Care Medicine Experimental

, 5:15

First Online: 16 March 2017Received: 04 October 2016Accepted: 09 March 2017DOI: 10.1186-s40635-017-0130-9

Cite this article as: Constantino, L., Galant, L.S., Vuolo, F. et al. ICMx 2017 5: 15. doi:10.1186-s40635-017-0130-9


BackgroundExtracellular superoxide dismutase ECSOD protects nitric oxide NO bioavailability by decreasing superoxide levels and preventing peroxynitrite generation, which is important in maintaining renal blood flow and in preventing acute kidney injury. However, the profile of ECSOD expression after sepsis is not fully understood. Therefore, we intended to evaluate the content and gene expression of superoxide dismutase SOD isoforms in the renal artery and their relation to renal blood flow.

MethodsSepsis was induced in Wistar rats by caecal ligation and perforation. Several times after sepsis induction, renal blood flow 12, 24 and 48 h; the renal arterial content of SOD isoforms, nitrotyrosine, endothelial and inducible nitric oxide synthase e-NOS and i-NOS, and phosphorylated vasodilator-stimulated phosphoprotein pVASP; and SOD activity 3, 6 and 12 h were measured. The influence of a SOD inhibitor was also evaluated.

ResultsAn increase in ECSOD content was associated with decreased 3-nitrotyrosine levels. These events were associated with an increase in pVASP content and maintenance of renal blood flow. Moreover, previous treatment with a SOD inhibitor increased nitrotyrosine content and reduced renal blood flow.

ConclusionsECSOD appears to have a major role in decreasing peroxynitrite formation in the renal artery during the early stages of sepsis development, and its application can be important in renal blood flow control and maintenance during septic insult.

KeywordsSepsis Acute renal failure Superoxide Nitric oxide  Download fulltext PDF

Autor: Larissa Constantino - Letícia Selinger Galant - Francieli Vuolo - Karla Lorena Guarido - Luiza Wilges Kist - Giovanna Me

Fuente: https://link.springer.com/

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