• S N Hussain, M N Abdul-Hussain, and Q el-Dwairi.
• Critical Care Division, Royal Victoria Hospital, Montreal, Quebec, Canada.
• J Crit Care. 1996 Dec 1; 11 (4): 167-75.

PurposeThe main aim of this study was to assess the correlation between exhaled nitric oxide (NO) and serum NO concentrations during the course of endotoxemia. We also assessed whether or not the inducible isoform of NO synthase is responsible for the increase in NO production in endotoxemia animals.Materials And MethodsAnesthetized and mechanically ventilated dogs were injected with either saline (control) or Escherichia coli endotoxin (LPS [Lipopolysaccharides]), and the animals were sacrificed 150 minutes later. We measured hemodynamics, exhaled NO, and serum arterial and mixed venous NO concentrations. Western blotting was performed on lung, pulmonary artery, aorta, and kidney tissue samples using anti-inducible NO synthase antibody.ResultsArterial pressure, cardiac output, and pulmonary arterial pressure in the control group remained unchanged, whereas a significant decline in these parameters was observed in the LPS group. Exhaled NO and serum arterial NO concentrations rose significantly within 30 minutes of endotoxin injection and remained higher than baseline values, whereas mixed venous serum NO did not change from baseline values. There was a significant linear relationship between exhaled NO and arterial serum NO concentrations. By comparison, exhaled NO, and arterial and mixed venous serum NO levels remained unchanged in the control group. Western blotting showed no expression of inducible NO synthase (iNOS) isoform in the control or LPS groups.ConclusionsThese results suggest that exhaled NO accurately reflects changes in arterial serum NO concentration and that the source of enhanced NO release in acute endotoxemia is not the iNOS isoform.

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