Sepsis independently associated with HF, increased NOx, peripheral neutrophils, and fibrinogen levels, decreased prothrombin and the presence of the NOS3 (E298D) and NOS2A (exon 22) SNPs.
Endothelial nitric oxide synthase (eNOS) -786T→C and 894G→T polymorphisms have been associated with eNOS dysfunction, which might further compromise microcirculatory blood flow during sepsis and increase the risk of organ injury.
The eNOS gene polymorphism at position 894 (G>T, Glu298Asp) resulting in T allele has been studied in the context of vascular diseases, but its role in sepsis has not yet been explored.