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目的:探讨氟伐他汀(HMG-CoA还原酶抑制剂)对自发性高血压大鼠阻力血管结构和功能的影响。方法:8周龄雄性SHR大鼠,氟伐他汀20mg·kg~(-1)·d~(-1)灌胃治疗。计算血管壁腔比作为阻力血管结构变化指标;应用离体主动脉和肠系膜动脉环对硝普钠和去甲肾上腺素反应的敏感性,观察治疗后血管的功能变化。结果:8周后,治疗组血管的壁腔比低于对照的SHR(0.44±0.09 vs 0.79±0.09,P<0.05);氟伐他汀能增加SHR主动脉对硝普钠舒张的敏感性,EC_(50)[(4.9 vs 190)pmol·L(-1)P<0.05];减弱主动脉和肠系膜动脉对去甲肾上腺素收缩的敏感性,EC_(50)[主动脉:(0.20 vs 0.02)nmol·L~(-1),P<0.05;肠系膜动脉:(1.46 vs 0.72)nmol·L~(-1),P<0.05]。结论:短期氟伐他汀治疗,改善SHR大鼠阻力血管的舒缩功能,同时也抑制了SHR大鼠在血压发展过程中伴随的血管壁肥厚现象。
Objective: To investigate the effect of fluvastatin (HMG-CoA reductase inhibitor) on the structure and function of resistance vessels in spontaneously hypertensive rats. Methods: 8-week-old male SHR rats were treated with fluvastatin 20 mg · kg -1 · d -1. The ratio of vascular wall to lumen was calculated to be the index of resistance vascular structure. The sensitivity of isolated aorta and mesenteric artery rings to nitroprusside and norepinephrine reaction was observed and the changes of vascular function were observed. Results: After 8 weeks, the vessel wall ratio of the treated group was lower than that of the control SHR (0.44 ± 0.09 vs 0.79 ± 0.09, P <0.05). Fluvastatin increased the sensitivity of the aorta of SHR to diastolic sodium nitroprusside, EC_ (50 vs [49 vs 190, pmol·L (-1), P <0.05]; attenuated the sensitivity of the aorta and mesenteric arteries to norepinephrine contraction; nmol·L -1, P <0.05; mesenteric artery: (1.46 vs 0.72) nmol·L -1, P <0.05]. Conclusion: Short-term fluvastatin treatment can ameliorate the systolic and diastolic function of resistance vessels in SHR rats and inhibit the vascular wall hypertrophy associated with the development of blood pressure in SHR rats.