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. Author manuscript; available in PMC: 2014 Jan 6.
Published in final edited form as: J Am Coll Cardiol. 2012 Mar 27;59(13):10.1016/j.jacc.2011.10.900. doi: 10.1016/j.jacc.2011.10.900

Figure 1. Mechanisms of hemolytic anemia in reducing NO bioavailability and association with vasculopathic sub-phenotypes of sickle cell disease.

Figure 1

Hemolysis releases cell-free plasma hemoglobin and arginase 1 into plasma, which catabolize NO and L-arginine. Activation of vascular oxidases, such as xanthine oxidase, NADPH oxidase and uncoupled eNOS, generate superoxide which scavenges NO. Hemolytic anemia and reduced NO bioavailability are associated with vasculopathic clinical complications in SCD patients.