0521. A functional citrulline-arginine-no pathway and nos3 complex is essential to maintain microcirculatory function during endotoxemia

Introduction Sepsis is associated with high mortality rates as a result of the development of multiple organ failure (MOF). In MOF the competition for the amino acid arginine between the microcirculation and the inflammatory response is important. The endothelial nitric-oxide synthase (eNOS) uses arginine to produce nitric oxide (NO), which results in microcirculatory vasodilatation, whereas arginase and the inflammatory nitric-oxide synthase (iNOS) use arginine in the inflammatory response to produce acute phase proteins and to stimulate the host response. Enhanced arginine consumption combined with decreased arginine de novo synthesis from citrulline results in arginine deficiency for eNOS, eNOS uncoupling, and a decreased organ perfusion.