Letter by Stamler et al Regarding Article, “Nitrite and S-Nitrosohemoglobin Exchange Across the Human Cerebral and Femoral Circulation: Relationship to Basal and Exercise Blood Flow Responses to Hypoxia”
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To the Editor:
We read with interest the article by Bailey et al.1 Based on measuring nitrite (NO2–), iron-nitrosyl hemoglobin (HbFeNO), and S-nitrosohemoglobin (SNO-Hb) in volunteers’ blood during hypoxia and exercise, they concluded that deoxyhemoglobin-mediated NO2– reduction to form HbFeNO is “…the dominant mechanism underlying hypoxic vasodilation,” with no role for SNO-Hb. We are concerned that this conclusion likely reflects confusion about the role of these species in blood flow regulation and limitations of the methodology used to measure them.
Classic experiments by Furchgott and Ignarro showed that hemoglobin scavenged endogenous nitric oxide (NO) by forming HbFeNO. This implied, paradoxically, that hemoglobin in red blood cells would impair tissue blood flow. It was shown subsequently that red blood cells actually dilate blood vessels at the lower …