Increased arterial and tissue NOx previously reported in this sepsis model [2] are suspected to result from NO oxidation reactions and the scavenging effects of oxy- and deoxyhemoglobin on NO [53, 54]; however, previous EPR (Electron paramagnetic resonance) spectroscopy studies in our model have shown an accumulation of hemoglobin-NO [22] in the septic RBC suggesting that NO could be accumulating within the RBC or regenerated by the RBC itself [46], although the extent and effect of such a reaction in the context of tissue iNOS/NO upregulation and overproduction [2] is unclear. This evidence concerns the gene NOS2 and Sepsis.