Nitric Oxide Scavenging by Red Blood Cell Microparticles and Cell-Free Hemoglobin as a Mechanism for the Red Cell Storage Lesion
Author(s) -
Chenell Donadee,
Nicolaas J.H. Raat,
Tamir Kanias,
Jesús Tejero,
Janet Lee,
Eric E. Kelley,
Xuejun Zhao,
Chen Liu,
Hannah Reynolds,
Ivan Azarov,
Sheila Frizzell,
E. Michael Meyer,
Albert D. Donnenberg,
Lirong Qu,
Darrel Triulzi,
Daniel B. Kim–Shapiro,
Mark T. Gladwin
Publication year - 2011
Publication title -
circulation
Language(s) - English
Resource type - Journals
SCImago Journal Rank - 7.795
H-Index - 607
eISSN - 1524-4539
pISSN - 0009-7322
DOI - 10.1161/circulationaha.110.008698
Subject(s) - hemolysis , hemoglobin , nitric oxide , red blood cell , vasoconstriction , red cell , vasodilation , medicine , methemoglobin , lesion , endothelium , oxidative stress , pharmacology , biochemistry , chemistry , immunology , pathology
Intravascular red cell hemolysis impairs nitric oxide (NO)-redox homeostasis, producing endothelial dysfunction, platelet activation, and vasculopathy. Red blood cell storage under standard conditions results in reduced integrity of the erythrocyte membrane, with formation of exocytic microvesicles or microparticles and hemolysis, which we hypothesized could impair vascular function and contribute to the putative storage lesion of banked blood.
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