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作 者:金朝[1] 丛玉隆[2] 殷周健[2] 李宾[3] 周春喜[3] 李楠[3] 陆庆国[3]
机构地区:[1]空军第四研究所第五研究室,北京100036 [2]解放军总医院临床检验科,北京100853 [3]解放军总医院基础所仪器中心,北京100853
出 处:《标记免疫分析与临床》2002年第3期153-156,共4页Labeled Immunoassays and Clinical Medicine
摘 要:为观察口服左旋精氨酸对正常人血小板胞浆内钙离子浓度的影响并探讨其作用机制 ,选择了 10名至少 2周内未服用任何药物 ,不吸烟、喝酒的健康男性志愿者。受试者服药前做 1次检测 ,然后口服左旋精氨酸 4天 ,前 3天每天服 2 0克 ,分 3次服用 ,第 4天服用 1次 ,服 7克 ,3小时后抽血测试。结果表明 ,服用左旋精氨酸后 ,血小板胞浆内cGMP浓度 (1.91± 0 .2 0pmol/ 10 9血小板vs 2 .14± 0 .34pmol/ 10 9血小板 ,P <0 .0 5 )、血清一氧化氮代谢产物NO-3 浓度 (32 .6 6± 14 .31μmol/Lvs 4 9.0 2± 9.75 μmol/L ,P <0 .0 5 )升高。ADP诱导的血小板[Ca2 + ]i 升高幅度 (A/B值 0 .4 5± 0 .14vs 0 .32± 0 .0 9,P <0 .0 1)降低。研究结果表明 ,口服左旋精氨酸可以通过促进血管内皮细胞和血小板合成NO来降低血小板胞浆内钙离子浓度的升高 。To study the effect of oral take L-arginine on [Ca 2+ ] i of human platelet, ten male volunteers were selected to tade L-arginine for 4 days (20g/three times/a day, the 4th day took about 7g). They are neither smokers nor drinkers and no drugs were taken by them during 2 weeks before study. Tests were performed before and after taking L-arginine. Before and after taking L-arginine, platelet intracellular cGMP were 1.91 ±0.20 vs 2.14±0.34pmol/10 9 platelets, P <0.05, and elevation of [Ca 2+ ] i (A/B value: 0.32±0.09 vs 0.45±0.14) were inhibited. The results has showed that oral take L-arginine could inhibit platelet activation. This inhibition should be ascribed to such two points: (1) The amount of NO released by endothelial cells has increased. A basal release of NO has been found to regulate the blood vessel intensity and inhibit platelet adhesion. After taking L-arginine, the endothelial cells released more NO and the plasma NO - 3 level also increased. (2) The platelet has synthesized more NO. There is an L-arginine/NO pathway in platelet and platelet could synthesize NO from L-rginine to inhibit its activation. Taking L-arginine has enhanced the negative effect of this pathway by producing more NO. The study will be helpful to further study on the possibility of oral take L-arginine to avoid thrombotic and hemorrhagic diseases.
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