原发性高血压患者血管内皮功能失调与活性氧的关系及阿托伐他汀治疗的影响

Relationship between reactive oxygen species and endothelial dysfunction in hypertension and effects of atorvastatin therapy

目的观察高血压病患者血管内皮依赖性舒张功能与活性氧的关系及阿托伐他汀治疗的影响。方法将58例高血压病患者随机分为对照组(服用双氢克尿噻和倍他乐克)和实验组(另加用阿托伐他汀),检测两组治疗前后及28例正常人的血清超氧化物歧化酶(superoxide dism utase,SO D)水平、血管内皮依赖性舒张功能。结果高血压患者血清SO D水平降低,血管内皮依赖性舒张功能受损,两者显著正相关。治疗2个月后,两组血清SO D水平均升高,而实验组SO D升高更显著,且血管内皮依赖性舒张功能改善。结论活性氧是高血压血管内皮功能的主要影响因素,他汀类可通过减少活性氧保护血管内皮功能。

To observe the relationship between reactive oxide species(ROS) and endothelium-dependent vasodilation of patients with essential hypertension(EH) and effects of atorvastatin. 58 patients with EH were randomly divided into control group and experimental group. They were all treated with hydrochlorothiazide and betaloc for two months. Atorvastatin was added in experimental group. Levels of serum superoxide dismutase(SOD) and endothelium-dependent vasodilation were measured in the beginning and end of therapy. Levels of serum SOD were reduced and positively correlated with endothelium-dependent vasodilation in hypertensive subjects compared to normotensive subjects. Treatment with hydrochlorothiazide and betaloc for two months increased serum SOD. However, there was more significant increase of serum SOD and improve in endothelium-dependent vasodilation function in atorvastatin group. [Conclusions] ROS is an important factor of endothelium-dependent vasodilation function in EH and statins can reduce ROS and protect endothelial function.