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目的:研究新型AT_1受体拮抗剂坎替沙坦对大鼠去窦弓神经(SAD)引起的心血管肥大的作用及其可能机制.方法:长期治疗时,大鼠SAD术后从食物中给予坎替沙坦(6 mg·kg~(-1)·d~(-1))16周.急性治疗时,大鼠 SAD术后第 30大经胃内单次给坎替沙坦 3 mg/kg.结果:SAD大鼠坎替沙坦治疗组的左心室和主动脉肥厚指数明显低于未治疗组,相当于或低于正常水平.SAD引起的心肌肥大、纤维化、心肌内小动脉和主动脉管壁增厚以及血管内弹力膜破坏几乎被坎替沙坦完全抑制.治疗后血浆血管紧张素Ⅱ浓度明 显升高,与心血管肥厚指数呈负相关.坎替沙坦单次给药后3小时观察期内,SAD大鼠血压及其波动性维持在较低水平.结论:坎替沙坦能有效抑制SAD引起的心血管肥厚.这种心血管保护作用除与已知机制有关外,还可能与其上调循环血管紧张素Ⅱ和稳定血压有关.
Objective: To investigate the effect of canonasartan, a novel AT1 receptor antagonist, on cardiovascular hypertrophy induced by sinusoidal aortic arch (SAD) in rats and its possible mechanism.Methods: After long-term treatment, rats were given SAD (6 mg · kg -1 · d -1) for 16 weeks.Acute treatment, rats in the 30th SAD after intragastric administration of canisartan 3 mg / kg.Results: The left ventricular and aortic hypertrophy index in canisartan-treated group was significantly lower than that of untreated group, and the level of SAD-induced cardiac hypertrophy, fibrosis, Aortic wall thickening and vasospastic membrane destruction almost completely inhibited by canisartan.After treatment, the plasma concentration of angiotensin Ⅱ was significantly increased, and was negatively correlated with cardiovascular hypertrophy index.Canostatam single administration During the 3-hour observation period, the blood pressure and its volatility in SAD rats were kept at a low level.Conclusion: Canisartan can effectively inhibit cardiovascular hypertrophy induced by SAD, except for the known mechanism of cardiovascular protection , May also be related to its up-regulation of circulating angiotensin Ⅱ and stable blood pressure.