Nitric oxide (NO) plays an important role in the modulation of hypoxic pulmonary vasoconstriction; in turn, red blood cells (RBCs) augment HPV by hemoglobin-mediated oxidation and inactivation of NO. In addition, scavenging of reactive oxygen species by RBCs may play a role in augmentation of HPV. NO delivery and/or production by RBCs does not appear to be important in the control of pulmonary vasomotor tone. This review will discuss regulation of HPV by RBCs with an emphasis on hemoglobin-NO interactions. In addition, the review will discuss how biologic (S-nitrosation) or pharmacologic (cross-linking) modification of hemoglobin may affect pulmonary circulatory-hemoglobin interactions.
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http://dx.doi.org/10.1007/978-0-387-34817-9_19 | DOI Listing |
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