Mark T. Gladwin, Alan N. Schechter, James H. Shelhamer, Lewis K. Pannell, Deirdre A. Conway, Borys W. Hrinczenko, James S. Nichols, Margaret E. Pease-Fye, Constance T. Noguchi, Griffin P. Rodgers, Frederick P. Ognibene
J Clin Invest.
1999;
104(7):937–945
doi:10.1172/JCI7637
This article Copyright © 1999, The American Society for Clinical Investigation
Abstract
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N
itric oxide (NO) inhalation has been reported to increase the oxygen affinity of sickle cell erythrocytes. Also, proposed allosteric mechanisms for hemoglobin, based on S-nitrosation of β-chain cysteine 93, raise the possibilty of altering the pathophysiology of sickle cell disease by inhibiting polymerization or by increasing NO delivery to the tissue. We studied the effects of a 2-hour treatment, using varying concentrations of inhaled NO. Oxygen affinity, as measured by P50, did not respond to inhaled NO, either in controls or in individuals with sickle cell disease. At baseline, the arterial and venous levels of nitrosylated hemoglobin were not significantly different, but NO inhalation led to a dose-dependent increase in mean nitrosylated hemoglobin, and at the highest dosage, a significant arterial-venous difference emerged. The levels of nitrosylated hemoglobin are too low to affect overall hemoglobin oxygen affinity, but augmented NO transport to the microvasculature seems a promising strategy for improving microvascular perfusion.
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