NOS2 and serum lipopolysaccharide activity: Interestingly, intravital microscopy studies have revealed that iNOS-deficient mice have greater leucocyte-endothelial cell interactions than wild type mice during lipopolysaccharide (LPS)-induced endotoxemia, without altering the expression level of adhesion molecules (27), thus, indicating that the iNOS/NO axis participates in the regulation of inflammation-mediated endothelial cell function.