摘要
目的 探讨 2型糖尿病者红细胞左旋精氨酸 -一氧化氮 (L- Arg- NO)通路的变化及其临床意义。方法 2型糖尿病患者 (19例 )与健康人 (10例 )对照。清晨空腹取静脉血 ,分离提纯红细胞 ,用放射同位素标记法测定 3H- L - Arg在红细胞转运的动力学特征 ;纯化红细胞一氧化氮合成酶 (NOS)并测定其含量及活性 ;测定血浆 NO产物 -硝酸盐和亚硝酸盐 (NOX)的含量。结果 2型糖尿病患者 (1)红细胞上 L- Arg跨膜总转运能力下降 ,最大转运速度 (Vmax)较对照组下降 2 1% (P <0 .0 1) ,米氏常数 (Km)较对照组增加 18% (P <0 .0 1)。经 Y+ 载体转运的 Vmax较对照组下降 2 8% (P <0 .0 1) ,而 Km与对照组差异无统计意义 (P >0 .0 5 )。经 Y+ L 转运的 Km较对照组增加 10 % (P <0 .0 1) ,Vmax无明显变化 (P>0 .0 5 )。 (2 )红细胞 NOS含量及活性分别较对照组下降 15 % (P<0 .0 1)及 34 % (P<0 .0 1)。 (3)血浆 NOX浓度与对照组相比降低了 17% (P <0 .0 5 )。结论 2型糖尿病时 ,红细胞 L - Arg- NO通路存在多环节障碍 ,可能导致 NO合成减少 ,使 NO介导的血管舒张受损 ,增加血小板的活性 ,促进血小板的聚集和粘附 。
Objective To investigate the changes in L Arginine Nitric oxide (L Arg NO) pathway of erythrocyte in patients with type 2 diabetes (DM). Methods Erythrocytes were isolated from venous blood taken from 19 patients with DM at admission and 10 normal controls. 3H L Arg transport was measured by radionuclide labeling. The content and activity of NO synthase (NOS) were measured after NOS had been isolated and purified, and the concentration of serum nitrate and nitrite (NO X) was measured.Results (1)The capacity of total L Arg transport in the DM group was lower than those in the control group maximum transport velocity (Vmax) decreased by 21%(P<0 01) and Michaelis constant (Km) increased by 18% (P<0 01). Compared with the control group, Vmax of system Y + L Arg transport decreased by 28% (P<0 01), and Km of the system Y +L L Arg transport increased by 10%(P<0 01) in the DM group. No significant difference was found with regard to Km of system Y + and Vmax of system Y +L in the two groups. (2)The content and activity of NOS in the DM group were lower than those in the control group (decreased by 15% and 34% respectively). (3)The concentration of serum NO X in the DM group was also found lower than that in the control group (decreased by 17%).Conclusion Multiple abnormal sites of L Arg NO pathway of erythrocytes were found in the patients with DM. The abnormality was able to decrease the production of NO, which may impair NO dependent vasodilation, increase the activity of platelets, accelerate the adhesion and aggregation of platelets, and promote the generation and development of diabetic angiopathy.
出处
《中国糖尿病杂志》
CAS
CSCD
2001年第5期266-270,共5页
Chinese Journal of Diabetes
