Molecular pathological study on vascular lesions due to ischemic heart diseases and related diseases

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After short (<30 min) and long (>45 min) time of ischemia conferred by coronary artery occlusion of the rats, reperfusion caused dilatation and constriction of arterioles, respectively. The vascular diameter was correlated with phosphorylation of Akt and serine 1177 residue of eNOS. Reactive oxygen species (ROS) generation and PKC activation contribute to the vasoconstriction through inhibition of eNOS phosphorylation. In the blood of Lipopolysaccaride-injected rat, monocyte NADPH generate ROS, thereby promoting HNE production, as detected by the highly sensitive immunoassay that we have developed.We have developed a time-resolved fluoroimmunoassay for a lipid peroxide 4-hydroxynonenal (HNE), which is 100-fold more sensitive than conventional ELISA. By this assay, we found that a low dose bacterial lipo-polysaccharide (LPS) increased serum HNE, with a peak at 20 min. LPS increased HNE in vitro in the monocyte-enriched plasma, which was inhibited by a specific NADPH oxidase inhibitor. These data suggest that monocyte NADPH oxidase is involved in the lipid peroxidation (HNE formation) in the LPS-challenged rat.