参七脉心通胶囊对颈动脉硬化患者血清NO及ET的影响

目的观察参七脉心通胶囊对颈动脉硬化并高脂血症患者的血脂、血清一氧化氮（NO）、血浆内皮素（ET）水平的影响,进一步探讨参七脉心通胶囊抗动脉粥样硬化的机制。方法将70例高脂血症并颈动脉硬化患者随机分为参七脉心通胶囊中药组（中药组）及阿托伐他汀西药组（西药组）,每组35例,分别给予参七脉心通胶囊及阿托伐他汀口服治疗12周。于清晨空腹抽取服药前、服药后及停药2周后的静脉血,检测血总胆固醇（TC）、三酰甘油（TG）、高密度脂蛋白（HDL）、低密度脂蛋白（LDL）、NO、ET水平。结果治疗12周后两组患者TC、TG、LDL及ET明显降低,血清NO及HDL水平明显升高,与治疗前相比显差异有统计学意义（P〈0.01）,其中西药组优于治疗组（P〈0.05）;停药2周后西药组所有患者TC、TG和LDL水平较治疗后升高,NO水平明显降低,与服药前无明显差异（P＞0.05）;而ET水平则明显回升,甚至高于服药前水平（P〈0.05）。在中药组却未出现这种趋势。结论参七脉心通胶囊对高脂血症并颈动脉硬化患者的血管内皮功能有明显保护作用,从而防治动脉硬化的进一步发展。

Effect of Shenqi Maixintong Capsule on Serum NO and ET in Patients with Carotid Artery Atherosclerosis

Objective To observe the effect of Shenqi Maixintong capsule（SMC）on the lipid,serum nitric oxide（NO）,and plasma endothelin（ET）.Methods Seventy patients with carotid atherosclerosis and hyperlipidemia were randomly divided into two groups：Chinese medicine group（n=35）treated by SMC,and the western medicine group（n=35）treated by atorvastatin orally for 12weeks.The fasting venous blood was collected before and after treatment,2weeks after the drug withdrawal,to test the level of total cholesterol（TC）,triglyceride（TG）,high density lipoprotein cholesterol（HDL）,low density lipoprotein cholesterol（LDL）,NO,and ET.Results After treatment of 12weeks,the levels of TC,TG,LDL and ET-1in two groups were decreased significantly,while the level of NO and HDL were increased significantly,there was significant difference compared with before treatment（P〈0.01）.The effect in western medicine group was better than that in Chinese medicine group（P〈0.05）.After 2weeks of withdrawal,the level of TC,TG and LDL in western medicine group was increased compared with that after treatment（P〉0.05）.The level of NO was decreased significantly,there was no significantly difference compared with that before treatment（P〉0.05）,and the level of ET was increased and it was higher than that before treatment（P〈0.05）.Conclusion The SMC had protective effect on vascular endothelial in patients with carotid atherosclerosis and hyperlipidemia.It might prevent the further development of atherosclerosis.