2009Critical CareOpen access

Endothelial nitric oxide synthase deficiency and inducible nitric oxide synthase inhibition in the setting of septic cardiomyopathy

Annette van de Sandt, Rainer Windler, Axel Gödecke, Jan Ohlig, Stefanie Becher, Ernst van Faassen, Tienush Rassaf, Jürgen Schrader, Malte Kelm, Marc W. Merx

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Abstract

Nitric oxide (NO) plays a central role in the pathogenesis of septic cardiomyopathy. However, the relative contribution of inducible nitric oxide synthase (iNOS) and endothelial nitric oxide synthase (eNOS) remains unclear. The aim of this study is to elucidate the influence of eNOS and iNOS on cardiac function, NO production rate and survival in the clinically relevant polymicrobial cecum ligation and puncture (CLP) model of sepsis.

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What this paper is about

Nitric oxide (NO) plays a central role in the pathogenesis of septic cardiomyopathy. However, the relative contribution of inducible nitric oxide synthase (iNOS) and endothelial nitric oxide synthase (eNOS) remains unclear. The aim of this study is to elucidate the influence of eNOS and iNOS on cardiac function, NO production rate and survival in the clinically relevant polymicrobial cecum ligation and puncture (CLP) model of sepsis.

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Available abstract

Nitric oxide (NO) plays a central role in the pathogenesis of septic cardiomyopathy. However, the relative contribution of inducible nitric oxide synthase (iNOS) and endothelial nitric oxide synthase (eNOS) remains unclear. The aim of this study is to elucidate the influence of eNOS and iNOS on cardiac function, NO production rate and survival in the clinically relevant polymicrobial cecum ligation and puncture (CLP) model of sepsis.

Key concepts: Medicine, Nitric oxide synthase, Endothelial nitric oxide synthase, Nitric oxide, ATP synthase, Cardiomyopathy, Microbiology, Pharmacology

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