感染性休克下调大鼠血管内皮和血小板L-精氨酸／一氧化氮通路

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. NO2(superscript -)/NO3(superscript -) 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, NO2(superscript -)/NO3(superscript -) 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 (P＜0.01), but high-affinity L-arginine transport activity from the aorta intima and platelets was increased in early stage of septic shock (P＞0.05 and P ＜0.05), as compared with the sham group, respectively. The inhibitory effects of NO2(superscript -)/NO3(superscript -), NOS activity and the L-arginine transport showed a positive correlation between platelet and aortic intima (P＜0.01). CONCLUSION: Septic shock down-regulates endogenous L-arginine/NOS/NO pathway in aortic intima and platelet, up-regulates L-arginine/NOS/NO pathway of aortic media and adventitia. Detection of the alteration of endogenous L-arginine/NOS/NO pathway in platelet might act as an indirect method to assess the endothelial dysfunction involving the pathogensis of septic shock.