肾动脉射频消融对远期高血压及心脏重构的影响

Effects of renal sympathetic denervation on long-term hypertension and cardiac remodeling in rabbits

目的观察肾动脉射频消融(renal sympathetic denervation,RSD)对远期高血压以及心脏重构的影响。方法采用腹主动脉缩窄建立压力负荷性高血压兔模型,建模2个月进行RSD,术后2个月测定血压、左室质量指数(LVMI)、心肌胶原容积分数,以及血浆中去甲肾上腺素(NE)、精氨酸血管加压素(AVP)、血管紧张素Ⅱ(AngⅡ)、醛固酮(Ald)的变化。结果 RSD 2个月后,高血压+射频组的血压低于高血压组(P<0.05)。与假手术组比较,高血压组左室后壁厚度(LVPWT)、室间隔厚度(IVST)、LVMI明显增加(P<0.05),与高血压组比较,高血压+射频组上述数值明显下降(P<0.05)。心肌胶原容积分数(CVF)在高血压组是升高的,经消融后也得以降低(P<0.05)。高血压组NE、AngⅡ、Ald和AVP较假手术组明显升高(P<0.05),RSD后NE、AVP较高血压组明显下降(P<0.05),但Ald、AngⅡ无显著差异。结论 RSD可以降低压力负荷导致的血压升高,降低了心脏的肥厚程度和心肌纤维化。

AIM To observe the effects of renal sympathetic denervation （RSD） on long-term hypertension and cardiac remodeling. METHODS We established rabbit models of pressure overload hypertension by abdominal aortic constriction. After 2 months, abdominal RSD was carried out with radiofrequency ablation catheter. Two months after RSD, blood pressure values were measured by carotid artery intubation. For evaluation of the cardiac remodeling, left ventricular myocardial index was measured by weighing and calculating, ventricular wall thickness was measured by cardiac uhrasonography and myocardial fibrosis index was measured by Sirius scarlet staining method. Changes of NE, AVP, Ang Ⅱ and Ald were also detected by ELISA. RESULTS Two months after RSD, blood pressure in hypertension ＋ ablation group was lower than in hypertension group （P 〈 0. 05 ）, but no significant difference was observed between control ＋ ablation group and control group. Left ventricular posterior wall thickness （LVPWT）, interventricular septum thickness （IVST） and left ventricular mass index （LVMI） increased significantly in hypertension group and control group （P 〈 0. 05）. However, these values declined after ablation. Measurement of collagen content found that myocardial collagen volume fraction （CVF） was elevated in the hypertensive group but it also decreased after ablation, indicating that the level of cardiac remodeling was reduced. NE, Ang Ⅱ, Aid and AVP in the hypertensive group were significantly higher （ P 〈 0. 05 ） but NE and AVP decreased in hypertension ＋ ablation group （P 〈 0. 05 ） after RSD. No significant difference was observed in Ald and Ang Ⅱ. CONCLUSION RSD can reduce blood pressure caused by pressure-overload and can also reduce cardiac hypertrophy and cardiac fibrosis. The effects of RSD on long-term hypertension and cardiac remodeling may result from reducing the sympathetic ganglion of renal arteries.