Interplay of the red blood cell and vascular endothelial nitric oxide synthase system to combat cardiac complications of anemia

Figures

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  Fig. 1. Scheme illustrating the mechanisms of cardioprotection by nitric oxide or the aggravation of ischemic cardiac damage by impaired nitric oxide signaling. Nitric oxide confers known cardioprotective effects and attenuates I/R cardiac damage (as observed in STEMI and NSTEMI [17]). The protective effects are lost by genetic or pharmacological eNOS inhibition. Implications for the novel findings on interplay of red blood cell/vascular eNOS for cardioprotection in a model of anemia are described [28]. In principle, anemic patients have a worse prognosis after AMI or ACS due to dysfunctional RBC ·NO signaling, but upregulation of eNOS activity in the heart and vessels of anemic patients provides compensatory protection that is lost upon genetic or pharmacological eNOS inhibition. GTPCH-1 GTP-cyclohydrolase-1, GTN glycerol trinitrate (nitroglycerin), STEMI ST-elevation myocardial infarction, NSTEMI non-STEMI. Contains images from Servier Medical Art by Servier, licensed under a Creative Commons Attribution 3.0 Unported License