Effects of nitric oxide in septic shock

被引:258
作者
Vincent, JL
Zhang, H
Szabo, C
Preiser, JC
机构
[1] Free Univ Brussels, Erasme Univ Hosp, Dept Intens Care, B-1070 Brussels, Belgium
[2] Univ Toronto, Mt Sinai Hosp, Div Resp Med, Toronto, ON M5G 1X5, Canada
[3] Childrens Hosp Med Ctr, Div Crit Care, Cincinnati, OH USA
关键词
D O I
10.1164/ajrccm.161.6.9812004
中图分类号
R4 [临床医学];
学科分类号
1002 ; 100602 ;
摘要
Nitric oxide (NO) is believed to play a key role in the pathogenesis of septic shock, although many aspects of NO's involvement remain poorly defined. Recent years have seen advances in our understanding of the production and effects of NO, but much of the work has been done in animal models and may not be directly relevant to the clinical situation. Differences between species and models can account for many of the apparently conflicting results obtained. Nevertheless, NO-directed strategies have been developed and tested clinically. However, NO can have both beneficial and detrimental effects on many organ systems in sepsis and attempts to nonselectively block all its actions may therefore not yield positive results on outcome. Further exploration and precision of the role of NO and development of techniques to assess the NO balance in individual patients is necessary before further progress can be made in this field.
引用
收藏
页码:1781 / 1785
页数:5
相关论文
共 50 条
[1]   Use of methylene blue in patients with refractory septic shock:: Impact on hemodynamics and gas exchange [J].
Andresen, M ;
Dougnac, A ;
Díaz, O ;
Hernández, G ;
Castillo, L ;
Bugedo, G ;
Alvarez, M ;
Dagnino, J .
JOURNAL OF CRITICAL CARE, 1998, 13 (04) :164-168
[2]   INHIBITION OF NITRIC-OXIDE SYNTHESIS CAUSES MYOCARDIAL-ISCHEMIA IN ENDOTOXEMIC RATS [J].
AVONTUUR, JAM ;
BRUINING, HA ;
INCE, C .
CIRCULATION RESEARCH, 1995, 76 (03) :418-425
[3]   Prolonged inhibition of nitric oxide synthesis in severe septic shock: A clinical study [J].
Avontuur, JAM ;
Nolthenius, RPT ;
van Bodegom, JW ;
Bruining, HA .
CRITICAL CARE MEDICINE, 1998, 26 (04) :660-667
[4]   Induction of diaphragmatic nitric oxide synthase after endotoxin administration in rats - Role on diaphragmatic contractile dysfunction [J].
Boczkowski, J ;
Lanone, S ;
UngureanuLongrois, D ;
Danialou, G ;
Fournier, T ;
Aubier, M .
JOURNAL OF CLINICAL INVESTIGATION, 1996, 98 (07) :1550-1559
[5]   INDUCTION OF N-G-MONOMETHYL-L-ARGININE UPTAKE - A MECHANISM FOR DIFFERENTIAL INHIBITION OF NO SYNTHASES [J].
BOGLE, RG ;
MACALLISTER, RJ ;
WHITLEY, GS ;
VALLANCE, P .
AMERICAN JOURNAL OF PHYSIOLOGY-CELL PHYSIOLOGY, 1995, 269 (03) :C750-C756
[6]   PROTECTIVE EFFECT OF S-NITROSO-N-ACETYL-PENICILLAMINE IN ENDOTOXIN-INDUCED ACUTE INTESTINAL DAMAGE IN THE RAT [J].
BOUGHTONSMITH, NK ;
HUTCHESON, IR ;
DEAKIN, AM ;
WHITTLE, BJR ;
MONCADA, S .
EUROPEAN JOURNAL OF PHARMACOLOGY, 1990, 191 (03) :485-488
[7]   NITRIC-OXIDE, AN ENDOTHELIAL-CELL RELAXATION FACTOR, INHIBITS NEUTROPHIL SUPEROXIDE ANION PRODUCTION VIA A DIRECT ACTION ON THE NADPH OXIDASE [J].
CLANCY, RM ;
LESZCZYNSKAPIZIAK, J ;
ABRAMSON, SB .
JOURNAL OF CLINICAL INVESTIGATION, 1992, 90 (03) :1116-1121
[8]   DIFFERENTIAL HEMODYNAMIC-EFFECTS OF L-NMMA IN ENDOTOXEMIC AND NORMAL DOGS [J].
COBB, JP ;
NATANSON, C ;
QUEZADO, ZMN ;
HOFFMAN, WD ;
KOEV, CA ;
BANKS, S ;
CORREA, R ;
LEVI, R ;
ELIN, RJ ;
HOSSEINI, JM ;
DANNER, RL .
AMERICAN JOURNAL OF PHYSIOLOGY-HEART AND CIRCULATORY PHYSIOLOGY, 1995, 268 (04) :H1634-H1642
[9]   Right ventricular overload causes the decrease in cardiac output after nitric oxide synthesis inhibition in endotoxemia [J].
Cohen, RI ;
Shapir, Y ;
Chen, L ;
Scharf, SM .
CRITICAL CARE MEDICINE, 1998, 26 (04) :738-747
[10]   Lipopolysaccharide-induced diaphragmatic contractile dysfunction in mice lacking the inducible nitric oxide synthase [J].
Comtois, AS ;
El-Dwairi, Q ;
Laubach, VE ;
Hussain, SNA .
AMERICAN JOURNAL OF RESPIRATORY AND CRITICAL CARE MEDICINE, 1999, 159 (06) :1975-1980