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1 Department of Intensive Care, and 2 Department of Pathology, Erasme University Hospital, Free University of Brussels, B-1070 Brussels, Belgium
Received 14 January 1997; accepted in final form 2 June 1997.
Zhang, Haibo, Peter Rogiers, Nadia Smail, Ana Cabral,
Jean-Charles Preiser, Marie-Odile Peny, and Jean-Louis Vincent.
Effects of nitric oxide on blood flow distribution and
O2 extraction capabilities during
endotoxic shock. J. Appl. Physiol.
83(4): 1164-1173, 1997.
The effects of the nitric oxide (NO)
synthase inhibitor
NG-monomethyl-L-arginine
(L-NMMA) and the NO donor
3-morpholinosydnonimine (SIN-1) were tested in 18 endotoxic dogs. L-NMMA infusion
(10 mg · kg
1 · h1)
increased arterial and pulmonary artery pressures and systemic and
pulmonary vascular resistances but decreased cardiac index, left
ventricular stroke work index, and blood flow to the hepatic, portal,
mesenteric, and renal beds. SIN-1 infusion (2 µg · kg1 · min1)
increased cardiac index; left ventricular stroke work index; and
hepatic, portal, and mesenteric blood flow. It did not significantly influence arterial and pulmonary artery pressures but decreased renal
blood flow. The critical O2
delivery was similar in the L-NMMA group and in the control
group (13.3 ± 1.6 vs. 12.8 ± 3.3 ml · kg1 · min1)
but lower in the SIN-1 group (9.1 ± 1.8 ml · kg1 · min1,
both P < 0.05). The critical
O2 extraction ratio was also
higher in the SIN-1 group than in the other groups (58.7 ± 10.6 vs.
42.2 ± 7.6% in controls, P < 0.05; 43.0 ± 15.5% in
L-NMMA group,
P = not significant). We conclude that
NO is not implicated in the alterations in
O2 extraction capabilities
observed early after endotoxin administration.
cardiac output; hypotension; organ perfusion; oxygen delivery; sepsis; endothelium-derived relaxing factor; nitrite; tumor necrosis
factor-
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