• Jérôme Morel, Jacques Yuan Li, Pierre Eyenga, Anne Meiller, Marie Paule Gustin, Giampiero Bricca, Serge Molliex, and Jean Paul Viale.
• Département d'anesthésie réanimation, Centre hospitalier universitaire de Saint-Etienne, 42055 Saint-Etienne Cedex 02, France; Unité de recherche EA 4174, Hémostase, Inflammation et Sepsis, UCB Lyon 1, 69008 Lyon, France. Electronic address: jerome.morel@chu-st-etienne.fr.
• Microvasc. Res. 2013 Nov 1; 90: 187-91.

AbstractNitric oxide (NO) is believed to play a key role in adverse microvascular changes during sepsis. A deficit in NO has been evoked as a potential mechanism of microcirculatory deterioration in the early phase of septic shock. The aim of this study was to evaluate simultaneously and continuously both hepatic microcirculation and local NO production during early experimental sepsis. Wistar male rats were divided into two groups: a sepsis group undergoing cecal ligation and puncture (CLP) peritonitis and a control group undergoing sham surgery. Hepatic microcirculation was continuously monitored using a laser Doppler probe and local nitric oxide (NO) production by means of a specific electrode. Constitutive and inducible NO synthase production was assessed 2h after surgery, at onset of shock, and at 2 and 3h after shock. In control animals, hepatic microcirculatory perfusion and NO production remained stable throughout the experiment. In septic animals, whereas a fall in microcirculatory perfusion was noted as early as 2h after CLP, NO concentration remained stable and further increased after the onset of shock. At this time, inducible NO synthase was the only isoform significantly elevated. In this non-resuscitated experimental model of sepsis, an absolute liver deficit of NO could not explain the early adverse changes in the local microvascular system.© 2013.

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