肾去神经术对压力超负荷模型大鼠心血管系统重构的影响

Effects of renal denervation on cardiovascular structural remodeling in rats with pressure overload induced by transverse aortic constriction

目的研究肾去神经术(RDN)对主动脉弓缩窄术(TAC)建立的压力超负荷模型大鼠心血管系统重构的影响。方法50只SD大鼠随机分为TAC+RDN组(A组,20只)、TAC+假RDN组(B组,20只)和假TAC+假RDN组(C组,10只)。TAC及其假手术、RDN及其假手术分别在造模前和第6周实施。于造模前和实验第6周、10周和14周(处死前)分别对大鼠行超声心动图检查,测量左心房内径(LAD)、室间隔厚度(IVSTd)和左室后壁厚度(LVPWd)等指标。14周后处死大鼠,Masson染色检测主动脉血管结构变化。结果与B组比较,实验10周时A组LAD减小[(4.58±0.78)mm vs.(5.83±0.91)mm],IVSTd和LVPWd肥厚减弱[(2.00±0.12)mm vs.(2.26±0.21)mm和(2.07±0.14)mm vs.(2.33±0.21)mm](P<0.05)。与A、C组比较,B组大鼠主动脉中膜厚度变薄、内径增大,且主动脉中膜厚度/血管内径比值减小(P<0.05)。结论 RDN可改善TAC诱导的压力超负荷模型大鼠的左心房扩大、左心室肥厚及主动脉扩张,并延缓TAC模型大鼠心脏由代偿性肥厚向失代偿性心腔扩大的转变。

Objective To investigate the effects of renal denervation（RDN） on cardiovascular structural remodeling in SD rats with pressure overload induced by transverse aortic constriction （TAC）. Methods A total of 50 SD male rats was randomized into three groups of A（treated with TAC and RDN, 20 rats）, B（treated with TAC and sham RDN, 20 rats） and C（treated with sham TAC and sham RDN, 10 rats）. TAC and RDN（or sham operations） were carried out before TAC and in the 6th week, respectively. Echocardiography was performed before TAC, in the 6th, 10th, and 14th week to measure left atrial diameter（LAD）, interventricular septal thickness（IVSTd） ,left ventricular posterior wall in diastole （LVPWd）. The rats were killed in the 14th week and the aortic remodeling was evaluated by Masson staining. Results Echocardiography in the 10th week showed that LAD, IVSTd and LVPWd were significantly improved in group A than those in group B[（4. 58±0. 78） mm vs. （5.83±0.91） mm,（2.00±0.12） mm vs. （2.26±0.21） mm, and （2.07±0.14） mm vs. （2.33±0. 21） mm] （P〈0. 05）. Compared with groups of A and C, the media thickness of aorta was thinner, lumen diameter of aorta was enlarged and the ratio of media thickness to lumen diameter was decreased in group B（P〈0. 05）. Conclusion RDN can attenuate the left atrial enlargement, left ventricular hypertrophy and aortic dilatation, and delay the transformation of cardiac function status from compensatory hypertrophy to decompensated dilatation in TAC rats with pressure overload.