期刊
PROCEEDINGS OF THE NATIONAL ACADEMY OF SCIENCES OF THE UNITED STATES OF AMERICA
卷 110, 期 24, 页码 9909-9913出版社
NATL ACAD SCIENCES
DOI: 10.1073/pnas.1301026110
关键词
redox; cardiovascular function; endotoxin
资金
- Medical Research Council UK
- British Heart Foundation
- Fondation Leducq
- UK Department of Health through the National Institute for Health Research comprehensive Biomedical Research Centre
- MRC [G0600785, G0700320, MR/K003232/1] Funding Source: UKRI
- British Heart Foundation [PG/10/98/28655, RG/12/12/29872, PG/10/44/28343] Funding Source: researchfish
- Medical Research Council [MR/K003232/1, G0700320, G0600785] Funding Source: researchfish
Sepsis is a common life-threatening clinical syndrome involving complications as a result of severe infection. A cardinal feature of sepsis is inflammation that results in oxidative stress. Sepsis in wildtype mice induced oxidative activation of cGMP-dependent protein kinase 1 alpha (PKG I alpha), which increased blood vessel dilation and permeability, and also lowered cardiac output. These responses are typical features of sepsis and their combined effect is a lowering of blood pressure. This hypotension, a hallmark of sepsis, resulted in underperfusion of end organs, resulting in their damage. A central role for PKG I alpha oxidative activation in injury is supported by oxidation-resistant Cys42Ser PKG I alpha knock-in mice being markedly protected from these clinical indices of injury during sepsis. We conclude that oxidative activation of PKG I alpha is a key mediator of hypotension and consequential organ injury during sepsis.
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