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目的观察瑞舒伐他汀对自发性高血压大鼠(SHR)血压、肠系膜三级动脉血管结构和舒张功能的影响。方法 12周龄雄性SHR 32只,随机分为瑞舒伐他汀治疗组[SHR-R,10mg/(kg·d),n=16]和SHR组(SHR,n=16),对应周龄雄性Wistar Kyoto大鼠作为正常血压组(WKY,n=16)。采用无创尾袖法测量大鼠尾动脉血压;应用计算机图像分析计算血管管壁面积/管腔面积(W/L)、管壁厚度/管腔半径(WT/LR)。采用PowerLab生物信息采集系统分别检测离体肠系膜三级动脉对不同浓度血管活性物质的舒张反应。结果 SHR的收缩压明显高于同龄WKY大鼠(P<0.01)。瑞舒伐他汀治疗4、8周末,SHR-R的收缩压明显低于未治疗的SHR[治疗4周收缩压:SHR-R(180.0±14.6)比SHR(200.3±13.9)mm Hg;8周:SHR-R(180.1±13.5)比SHR(189.9±10.1)mm Hg,均P<0.01]。治疗4周,肠系膜三级动脉W/L和WT/LR组间差异无统计学意义(P>0.05)。治疗8周,SHR-R肠系膜三级动脉W/L及WT/LR明显降低[W/L:SHR-R 0.51±0.21比SHR 1.82±0.96;WT/LR:SHR-R 0.23±0.04比SHR 0.53±0.29,均P<0.01],且SHR-R与WKY大鼠的WT/LR相比,差异无统计学意义(P>0.05)。治疗4周,SHR-R的肠系膜三级动脉血管内皮依赖性舒张功能明显增强[最大舒张百分比(Emax):SHR-R(47.41±10.74)%比SHR(29.10±7.35)%,WKY(83.85±5.17)%;舒张反应敏感性(pD2):SHR-R 6.39±0.90比SHR5.96±0.58,WKY 8.34±0.21,均P<0.01],非内皮依赖性舒张功能也明显增强[Emax:SHR-R(75.23±20.10)%比SHR(46.13±11.45)%,WKY(96.28±2.68)%;pD2值:SHR-R 6.72±0.44比SHR 5.56±0.23,WKY 7.84±0.13,均P<0.01]。治疗8周与治疗4周比较,差异无统计学意义(P>0.05)。结论瑞舒伐他汀治疗可轻度降低SHR的血压,治疗4周即可改善血管舒张功能,治疗8周可抑制肠系膜三级动脉血管肥厚,并且舒张功能的改善先于血管结构的变化。
Objective To observe the effects of rosuvastatin on the blood pressure, the structure of the third mesenteric artery and the diastolic function in spontaneously hypertensive rats (SHR). Methods Thirty - two male SHRs at 12 weeks of age were randomly divided into three groups: rosuvastatin treatment group (SHR - R, 10 mg / (kg · d), n = 16] and SHR (n = 16) Wistar Kyoto rats were used as normotensive group (WKY, n = 16). The caudal artery blood pressure was measured by noninvasive tail cuff method. The vascular wall area / lumen area (W / L), wall thickness / lumen radius (WT / LR) were calculated by computer image analysis. PowerLab biological information acquisition system were used to detect the isolated mesenteric artery of three different concentrations of vasodilator response to relaxation. Results SHR systolic pressure was significantly higher than WKY rats of the same age (P <0.01). At 4 and 8 weeks of rosuvastatin treatment, the systolic blood pressure of SHR-R was significantly lower than that of untreated SHR [systolic blood pressure at 4 weeks of treatment: SHR-R (180.0 ± 14.6) vs SHR (200.3 ± 13.9) mm Hg; : SHR-R (180.1 ± 13.5) vs SHR (189.9 ± 10.1) mm Hg, all P <0.01]. After 4 weeks of treatment, there was no significant difference between W / L and WT / LR mesenteric tertiary arteries (P> 0.05). W / L: SHR-R 0.51 ± 0.21 vs SHR 1.82 ± 0.96; WT / LR: SHR-R 0.23 ± 0.04 vs SHR 0.53 after 8 weeks of treatment ± 0.29, all P <0.01]. There was no significant difference between SHR-R and WT / LR in WKY rats (P> 0.05). After 4 weeks of treatment, the superior mesenteric artery endothelium-dependent vasorelaxation of SHR-R was significantly enhanced [Emax]: SHR-R (47.41 ± 10.74)% vs SHR (29.10 ± 7.35)%, WKY 5.17)%; the diastolic response (pD2): SHR-R 6.39 ± 0.90 was higher than SHR 5.96 ± 0.58, WKY 8.34 ± 0.21, both P <0.01] R (75.23 ± 20.10)% vs SHR (46.13 ± 11.45)%, WKY (96.28 ± 2.68)%; pD2 values: SHR-R 6.72 ± 0.44 vs SHR 5.56 ± 0.23, WKY 7.84 ± 0.13, all P <0.01]. There was no significant difference between the 8-week treatment and 4-week treatment (P> 0.05). Conclusions Rosuvastatin can reduce the blood pressure of SHR slightly, improve the vasodilatation function after 4 weeks of treatment, inhibit the third grade arterial hypertrophy of mesenteric artery for 8 weeks and improve the diastolic function before vascular structure changes.