叶酸、维生素B_(12)对冠心病患者血清同型半胱氨酸、一氧化氮水平的影响

Effects of folic acid and vitamin B_(12) on homocysteine and nitric oxide (NO) levels in CHD patients with hyperhomocysteinemia

目的:探讨叶酸、维生素B12对冠心病伴高同型半胱氨酸(Hcy)血症患者的血清Hcy、一氧化氮(NO)水平的影响。方法:采用酶联免疫法测定冠心病组(98例)患者和正常对照组(57例)空腹血清Hcy水平,应用亚硝酸盐还原酶法测定其血清NO水平。69例高Hcy血症的冠心病患者(Hcy≥15μmol/L)随机分为对照组(30例,仅服用硝酸酯类、他汀类及阿司匹林等基础药物)、干预组(39例,除基础用药外加用叶酸5mg/d、维生素B12500μg/d口服),治疗前及治疗4周后测定患者空腹血清Hcy、NO水平。结果:冠心病组患者血清Hcy水平明显高于正常对照组(P<0.01),NO水平明显低于正常对照组(P<0.05),冠心病组血清Hcy水平与NO水平呈明显负相关(r=-0.72,P<0.05),干预组患者治疗4周后Hcy水平平均降低了36.4%,治疗前、后Hcy水平差异有统计学意义(P<0.01),NO水平与服药前相比明显升高(P<0.05),治疗4周后对照组Hcy及NO水平亦有变化,但差异无统计学意义(P>0.05)。结论:冠心病患者Hcy水平升高,NO水平降低,口服叶酸、维生素B12可明显降低冠心病患者高Hcy血症者的血浆Hcy水平,改善冠心病患者内皮功能。

Objective： To study the effects of folic acid and vitamin B12 on serum homocysteine（Hcy） and nitric oxide （NO） levels in CHD patients with hyperhomoeysteinemia. Methods： Serum Hey levels were determined by ELISA, and appllication of Nitrite reduetase determination of the concentration NO in CHD patients and controls. The patients whose serum Hey levels were higher than 15 μmol/L were divided into therapy group and control group. The patients in therapy group were given folie acid 5 mg,vitamin B12 0.5 mg per day,while the patients in control group were not given. Hey and NO levels were all examined four weeks later again. Results： Mean serum Hey level was significantly higher in coronary patients than in controls, while the content of NO was lower in observed group than in control group and the difference were significant in contrast （ P 〈 0.01 ）. There was negative correlation between the decreasing extent of Hcy levels and NO concentrations（ r = -0.72 ,P 〈 0.05）. Hcy levels of the patients in therapy group were decreased by 36.4% four weeks later. There was significant difference between the levels before and after therapy（ P 〈 0.01 ）. Gonclusions： Hey levels in CHD patients were markedly higher than those in control group. Supplement of folie acid, vitamin B12 can decrease serum Hey levels in CHD patients with hyperhomoeysteinemia. The mechanism could be improved endothelial function in CHD patients.