NOS2 and Sepsis: Sepsis-related increase in bilirubin level, international normalized ratio, and lipid peroxidation in liver tissue were significantly attenuated by the early neuronal NO synthase (nNOS) and delayed iNOS blockade.[8] Additionally, H2S contributes to microcirculatory dysfunction in the systemic as well as hepatic microcirculations due to a differential vasoactive function on presinusoidal and sinusoidal sites within the liver.[9]