Time course of liver nitric oxide concentration in early septic shock by cecal ligation and puncture in rats

被引：10

作者：

Eyenga, P. ^{[1
,2
]}

Lhuillier, F. ^{[1
,2
]}

Morel, J. ^{[2
,3
]}

Roussel, D. ^{[4
]}

Sibille, B. ^{[4
]}

Letexier, D. ^{[4
]}

Cespuglio, R. ^{[5
]}

Duchamp, C. ^{[4
]}

Goudable, J. ^{[2
]}

Bricca, G. ^{[2
]}

Viale, J. P. ^{[1
,2
]}

机构：

[1] Hop Croix Rousse, Hosp Civils Lyon, Serv Anesthesie Reanimat, F-69317 Lyon, France

[2] UCBLyon1, INSERM, EA4173 ERI 22, F-69008 Lyon, France

[3] Hop Nord St Etienne, CHU St Etienne, F-42055 St Etienne, France

[4] CNRS, Lab Physiol Cellulaire & Mol, UMR 5123, F-69100 Villeurbanne, France

[5] UCBLyon1, INSERM, EA4170, F-69008 Lyon, France

来源：

NITRIC OXIDE-BIOLOGY AND CHEMISTRY | 2010年 / 23卷 / 03期

关键词：

Nitric oxide; Septic shock; Cecal ligation and puncture; Experimental model; LASER-DOPPLER FLOWMETRY; IN-VIVO; SYNTHASE INHIBITION; HEPATIC PERFUSION; ENDOTOXIN; EXPRESSION; INJURY; MICE; SEPSIS;

D O I：

10.1016/j.niox.2010.06.002

中图分类号：

Q5 [生物化学]; Q7 [分子生物学];

学科分类号：

071010 ; 081704 ;

摘要：

An overwhelming nitric oxide (NO) production is a crucial step in the circulatory events as well as in the cellular alterations taking place in septic shock. However, evidences of this role arise from studies assessing the NO production on an intermittent basis precluding any clear evaluation of temporal relationship between NO production and circulatory alterations. We evaluated this relationship by using a NO specific electrode allowing a continuous measurement of NO production. Septic shock was induced by a cecal ligation and puncture (CLP) in a first group of anesthetized rats. After the same CLP, a second group received a selective iNOS inhibitor (L-NIL). Control rats were sham operated or sham operated with L-NIL administration. While NO concentration was measured every 2 min by a NO-sensitive electrode over 7 h following CLP, the liver microcirculation was recorded by a laser-Doppler flowmeter. CLP induced a severe septic shock with hypotension occurring at a mean time of 240 min after CLP. At the same time, an increase in liver NO concentration was observed, whereas a decrease in microvascular liver perfusion was noted. In the septic shock group, L-NIL administration induced an increase in arterial pressure whereas the liver NO concentration returned to baseline values. In addition, shock groups experienced an increase in iNOS mRNA. These data showed a close temporal relationship between the increase in liver NO concentration and the microvascular alteration taking place in the early period of septic shock induced by CLP. The iNOS isoform is involved in this NO increase. (C) 2010 Elsevier Inc. All rights reserved.

引用

页码：194 / 198

页数：5

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