AIM: To investigate alteration and cross link of the aortic and platelet endogenous L-arginine/NOS/NO pathway induced by septic shock.METHODS: The septic shock model was made in rats by caecal ligation and puncture.NO-2 /NO-3 production released from aortic and platelet was measured with Greiss assay.NOS activity and L-arginine transport activity were detected by isotope tracer method.RESULTS: Both in early and late stage of septic shock,NO-2 /NO-3 production,NOS activity,and the L-arginine transport from the aorta intima and platelets were obviously decreased,while those of the aorta media and adventitia were obviously increased(P0.05 and P

Objective To investigate the effect of water-immersion restraint stress(WRS) on nitric oxide(NO) production and its mechanism in rat platelets.Methods Male SD rats underwent WIR stress for 2,4 and 8 hours.Ulcer index(UI) of stomach was chedsed by Guth method,nitrite production was measured by Greiss assay,nitric oxide synthase(NOS) activities and L-arginine transport rate were determined by isotope tracer method.ResultsAfter 2 h WRS,the NO production,the NOS activity and L-arginine transport rate in rat platelets obviously increased and then gradually decreased.After 8 h of WRS,these parameters were decreased as compared with the control group.The gastric ulcer appeared and got more serious after 4 h WIR stress.Conclusion Short-term WRS up-regulates L-arginine /NO pathway and increases nitric oxide production in the platelets but long-term WIR stress has the reversed effect.