高脂血症对大鼠心肌一氧化氮水平的影响

Effect of hyperlipidemia on nitric oxide levels of blood and myocardial tissues in rats

目的 :探讨高脂血症时血管活性物质的变化特点及调脂药物吉非罗齐对内皮依赖的舒张功能的影响机制。方法 :建立高脂血症模型 ,检测其血脂、一氧化氮、血中血管紧张素Ⅱ和血管内皮生长因子和心肌组织一氧化氮、血管紧张素Ⅱ水平及其在吉非罗齐治疗 1 6周后的变化。结果 :高脂血症组血和组织一氧化氮水平低于正常对照组、血VEGF高于正常对照组 ,但血管紧张素Ⅱ、血压和心脏重量与对照组无显著差异。第 2 0周时治疗组的TG、LDL -C显著低于非治疗组 ,且血一氧化氮、VEGF和组织一氧化氮浓度高于非治疗组。结论 :高脂血症会抑制血管内皮分泌一氧化氮的功能 ,心肌组织局部的一氧化氮产量也明显减少 ,而吉非罗齐可逆转此改变 。

AIM: To study the impact of hyperlipidemia on vasoactive substances and the mechanism of gemfibrozil in regulating the endothelial function. METHODS: The hyperlipidemic model was established with rats. The serum levels of lipid, NO, angiotensin Ⅱ (Ang Ⅱ), vascular endothelial growth factor(VEGF) and levels of NO, AngⅡ in myocardial tissues were measured. RESULTS: Hyperlipidemic rats had lower level of NO and higher level of VEGF than control subjects. Significant correlation had been shown between serum levels of lipid and NO. Administration of gemfibrozil significantly elevated serum VEGF, NO and myocardial tissue NO levels. CONCLUSIONS: Hyperlipidemia not only reduced serum NO level but also reduced myocardial NO content, which could cause endothelial dysfunction. Gemfibrozil reversed the above changes induced by hyperlipidemia, which might have relevance to VEGF.