title: Revisiting the hyperhemolysis paradigm.
abstract: In this issue of Blood, 2 articles test fundamental hypotheses relating intravascular hemolysis to sickle cell disease (SCD) pathogenesis. Detterich et al confirm a role for hemolysis and cell-free plasma hemoglobin (Hb) in pulmonary and systemic endothelial dysfunction in humans. Almeida et al show in mice that hemolysis induces inflammation that is caused by nitric oxide (NO) scavenging and ameliorated by NO donors and the NO-donor properties of hydroxyurea (HU).
authors.affiliation: UNIVERSITY OF PITTSBURGH.
authors.forename: Mark T
authors.initials: MT
authors.lastname: Gladwin
mesh_terms: D000755:Anemia, Sickle Cell / Q000503:physiopathology*; D000818:Animals; D001803:Blood Transfusion; D001916:Brachial Artery / Q000503:physiopathology*; D003497:Cyclic N-Oxides / Q000494:pharmacology*; D005260:Female; D016166:Free Radical Scavengers / Q000494:pharmacology*; D006454:Hemoglobins / Q000378:metabolism*; D006801:Humans; D006918:Hydroxyurea / Q000494:pharmacology*; D006976:Hypertension, Pulmonary / Q000503:physiopathology*; D007093:Imidazoles / Q000494:pharmacology*; D007962:Leukocytes / Q000187:drug effects*; D008168:Lung / Q000503:physiopathology*; D008297:Male; D009569:Nitric Oxide / Q000378:metabolism*; D014262:Tricuspid Valve Insufficiency / Q000503:physiopathology*
chemical_list: D003497:Cyclic N-Oxides; D016166:Free Radical Scavengers; D006454:Hemoglobins; D007093:Imidazoles; D009569:Nitric Oxide; D006918:Hydroxyurea