| Abjectives:The discovery of an endothelium-derived relaxing factor (EDRF) and its later identification as nitric oxide (NO) have to be considered as one of the most exciting discoveries in medicine in the 1980s.In the consequence,NO was nominated 'molecule of the year'in 1992.NO is a small uncharged gas molecule that is a highly reactive free radical. It have been found that a lot of cell or tissue has L-arginine/Nitric Oxide (L-arg/NO) system in our body.The nitric oxide is synthesized from the essential amino acid L-arginine by a family of enzymes,most of which are cytosolic,known as the nitric oxide synthase (NOS). It is produced in the platelet. Platelet NO release could be mediated by an intraplatelet L-arg/NO pathway, and it can be modify by platelet NOS . L-arginine transporter activity was measured using radioisotope tracer studies.The Na+-independent system y+ is the main transport way in platelet ,which is a high-affinity,but a lower capacity. Intraplatelet L-arginine and oxygen produce NO and L-citrulline with NADPH, FMN, FAD,BH4 and Fe. Intraplatlet NO spread around tissue,which actived Guanylate cyclase (GS),which triggers the formation of cyclic guanosine monophosphate (cGMP),seems to be the most relevant target of NO at low concentrations. cGMP is an important cellular messenger regulating intracellular calcium concentrations, which mediate physiological functions of NO such as platelet aggregation. Intraplatelet NO play more important role in the physiology of decreacing platlet aggregation than plasma NO,especially in endothelial dysfunction.Platelet activition in vivo and vitro is enhanced in normal pregnancy as part of a generalized coagulopathy resulting in an increased risk of thrombosis.Furthermore,platelet activition is thought to contribute to the pathogenesis of severe pregnancy induced hypertension (PIH) and preeclampsia, which may result in hemodynamic changes, platelet aggregation, endothelial injury and vasoconstriction, and so generates or amplifies progressive damage to the maternal vasculature as described in preeclampsia. Severe PIH is a common complication of pregnancy,which is a leading cause of maternal morbidity and fetal death in developed countries and is associated with premature delivery and intrauterine growth restriction. However,the mechanism mediating the increase in platelet reactivity in PIH is still unclear.To verify the hypothesized derangement of the L-arg/NO pathway in severe PIH,we measured platelet-rich plasma levels of L-arg transport, NOS activity,cGMP and NO production . Methods 1 PIH criterion was in according with the latest Director of editorial committee is Yue Jie). Twelve third-trimester pregnant women and twelve severe PIH were enrolled for this study. They were no other compliments besides hypertension. The study group was no significant difference compared with the control group in the year, generation, weight of mother, et al. 2 The platelet L-arg transport were measured throught the marker 3H-L-arg. 3 The NOS activity were measured throught the marker 3H-L-arg. 4 The cGMP production were measured using radioisotope tracer studies.5 NO production were measured the concentration of the anions NO2- and NO3- in PRP.The reaction was followed by the colorimetric detection at 540 nm of the azo dye product of the Griess reaction .Results 1 The levers of L-arg transport were increased with the increasing L-arg concentration in study group and control group.But control group were increased significantly compared with study group in every L-arg concentration. 2 NOS activity were decreaced in study group compared with control group(5.36±1.45 pmol/108pt·min-1 vs 6.73±1.27 pmol/108pt·min-1) (P<0.05).3 cGMP production were decreaced in study group compared with control group(0.26±0.09 nmol/108 pt vs 0.36±0.12 nmol/108 pt) (P<0.05). 4 NO production were decreaced in study group compared with control group(0.18±0.02 nmol/108 pt vs 0.24±0.07 nmol/108 pt )(P<0.01).Conc...
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