Published online before print January 22, 2004, doi: 10.1161/01.RES.0000117771.63140.D6
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Submitted on June 6, 2003
Revised on January 6, 2004
Accepted on January 9, 2004
Enhanced S-Nitroso-Albumin Formation From Inhaled NO During Ischemia/Reperfusion
Ella S.M. Ng ;
From the Department of Physiology and Biophysics (E.S.M.N., D.K., P.K.), Immunology Research Group, University of Calgary, Calgary, Alberta, Canada; Center for Cardiovascular Sciences (D.J.), Albany Medical College, Albany, NY; and Webb-Waring Institute (J.M.M., D.H., M.Y.), University of Colorado Health Sciences Center, Denver, Colo.
* To whom correspondence should be addressed. E-mail: pkubes{at}ucalgary.ca.
In the present study, we investigated whether inhaled nitric oxide (NO) was transported by plasma proteins, such as S-nitroso-albumin (SNO-Alb), in the feline circulation and whether this molecule delivers NO to the periphery under conditions of stress, specifically ischemia/reperfusion (I/R). A flow probe was interposed between the femoral and superior mesenteric artery for blood flow measurements, and a branch of the superior mesenteric vein was cannulated for arterial-venous sampling. In animals breathing room air, SNO-Alb was below detection level in arterial or venous blood. NO inhalation resulted in a significant arterial-venous gradient for SNO-Alb. Concomitant with this loss of SNO-Alb across the intestinal vasculature was an increase in nitrite (NO2-). However, this release of NO was not sufficient to alter intestinal blood flow. I/R during NO inhalation caused a very large increase in arterial SNO-Alb that permitted a 5-fold increase in SNO-Alb consumption and significant generation of NO2- within the postischemic intestinal vasculature. The increased SNO-Alb consumption was sufficient to dramatically improve intestinal blood flow. The very large burst of arterial SNO-Alb during I/R was completely blocked by the administration of superoxide dismutase, suggesting that oxidative stress contributed to the increased SNO-Alb formation. Our data suggest that inhaled NO can increase nitrosothiol production and these molecules may be a functional NO delivery system during cardiovascular disease.
Key words: S-nitroso-albumin • oxidative stress • postischemic vasculature
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