{"title":"The hemoglobin-nitric oxide axis: implications for transfusion therapeutics","authors":"J. R. Lancaster, A. Hutchings, J. Kerby, R. Patel","doi":"10.1111/J.1778-428X.2007.00084.X","DOIUrl":null,"url":null,"abstract":"SUMMARY Understanding mechanisms that regulate nitric oxide (NO) function in the vascular compartment is critical in the context of transfusion-based therapeutics. The role of hemoglobin (Hb), either cell-free or encapsulated within the erythrocyte, has received much attention owing largely to the rapid rate of reactions between NO and either oxy- or deoxyheme. In this review, we discuss the different mechanisms proposed by which NO reactions with Hb are controlled under physiological conditions and which involve both preventing NO-scavenging by Hb and erythrocyte (and Hb)-dependent stimulation of NO-signaling. How these mechanisms may be utilized therapeutically in the design and application of Hb-based oxygen carrier therapeutics is also discussed.","PeriodicalId":90375,"journal":{"name":"Transfusion alternatives in transfusion medicine : TATM","volume":null,"pages":null},"PeriodicalIF":0.0000,"publicationDate":"2007-12-01","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"https://sci-hub-pdf.com/10.1111/J.1778-428X.2007.00084.X","citationCount":"6","resultStr":null,"platform":"Semanticscholar","paperid":null,"PeriodicalName":"Transfusion alternatives in transfusion medicine : TATM","FirstCategoryId":"1085","ListUrlMain":"https://doi.org/10.1111/J.1778-428X.2007.00084.X","RegionNum":0,"RegionCategory":null,"ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":null,"EPubDate":"","PubModel":"","JCR":"","JCRName":"","Score":null,"Total":0}
引用次数: 6
Abstract
SUMMARY Understanding mechanisms that regulate nitric oxide (NO) function in the vascular compartment is critical in the context of transfusion-based therapeutics. The role of hemoglobin (Hb), either cell-free or encapsulated within the erythrocyte, has received much attention owing largely to the rapid rate of reactions between NO and either oxy- or deoxyheme. In this review, we discuss the different mechanisms proposed by which NO reactions with Hb are controlled under physiological conditions and which involve both preventing NO-scavenging by Hb and erythrocyte (and Hb)-dependent stimulation of NO-signaling. How these mechanisms may be utilized therapeutically in the design and application of Hb-based oxygen carrier therapeutics is also discussed.