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Am J Physiol Heart Circ Physiol (August 5, 2004). doi:10.1152/ajpheart.00310.2004
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Submitted on March 29, 2004
Accepted on July 26, 2004

Pulmonary vascular effects of red blood cells containing S-nitrosated hemoglobin

Steven Deem1*, Seong Su Kim2, Jin-Hye Min3, Randy Eveland4, Jennifer Moulding5, Sabrina Martyr6, Xunde Wang6, Erik R Swenson4, and Mark T Gladwin6

1 Anesthesiology, University of Washington, Seattle, WA, USA; Medicine, University of Washington, Seattle, WA, USA
2 Anesthesiology, University of Ulsan, Kangnung, Korea, Republic of
3 Anesthesiology, Myongji Hospital, Kwangdon University, Korea, Republic of
4 Medicine, University of Washington, Seattle, WA, USA
5 Anesthesiology, University of Washington, Seattle, WA, USA
6 Critical Care Medicine, National Institutes of Health, Bethesda, MD, USA

* To whom correspondence should be addressed. E-mail: sdeem{at}u.washington.edu.

The role of S-nitrosated hemoglobin (SNO-Hb) in the regulation of blood flow is a central and controversial question in cardio-pulmonary physiology. In the current study, we investigate whether intact human red blood cells (RBCs) synthesized to contain high SNO-Hb levels are able to export nitric oxide bioactivity and vasodilate the pulmonary circulation, and whether SNO-Hb dependent vasodilation occurs secondary to an intrinsic oxygen-linked, allosteric function of hemoglobin. RBCs containing supraphysiologic concentrations (100-1000 x normal) of SNO-Hb (SNO-RBCs) were synthesized and added to isolated, perfused rat lungs during anoxic or normoxic ventilation, and during normoxic ventilation with pulmonary hypertension induced by the thromboxane mimetic U-46619. SNO-RBCs produced dose-dependent pulmonary vasodilation compared to control RBCs during conditions of both normoxic (U-46619) and hypoxic pulmonary vasoconstriction. These effects were associated with a simultaneous, rapid, and temperature-dependent loss of SNO from Hb. Both vasodilatory effects and the rate of SNO-Hb degradation were independent of oxygen tension and hemoglobin oxygen saturation. Furthermore, these effects were not affected by inhibition of the erythrocyte membrane band 3 protein (anion exchanger-1), a putative membrane facilitator of NO export from RBCs. While these data support observations by multiple groups that synthesized SNO-Hb can vasodilate, this effect is not under intrinsic oxygen-dependent allosteric control, nor likely to be relevant in the pulmonary circulation at normal physiological concentrations.




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P. Sonveaux, I. I. Lobysheva, O. Feron, and T. J. McMahon
Transport and Peripheral Bioactivities of Nitrogen Oxides Carried by Red Blood Cell Hemoglobin: Role in Oxygen Delivery
Physiology, April 1, 2007; 22(2): 97 - 112.
[Abstract] [Full Text] [PDF]


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