中华心血管病杂志
中華心血管病雜誌
중화심혈관병잡지
Chinese Journal of Cardiology
2014年
1期
48-52
,共5页
谢赟%刘奇良%徐佑龙%郜俊清%严鹏勇%张文全%孙剑光%王明瑜%金惠根
謝赟%劉奇良%徐祐龍%郜俊清%嚴鵬勇%張文全%孫劍光%王明瑜%金惠根
사빈%류기량%서우룡%고준청%엄붕용%장문전%손검광%왕명유%금혜근
心力衰竭,充血性%导管消融术%交感神经系统
心力衰竭,充血性%導管消融術%交感神經繫統
심력쇠갈,충혈성%도관소융술%교감신경계통
Heart failure,congestive%Catheter ablation%Sympathetic nervous system
目的 研究经导管射频消融去肾交感神经术(catheter-based renal sympathetic denervation,RDN)对右心室快速起搏导致的心力衰竭猪心功能的改善作用.方法 健康广西巴马小型猪12头,建立快速起搏致心力衰竭模型,以随机数字表法分为消融组(n=6,心室快速起搏1周后接受RDN术)和对照组(n=6,单纯心室快速起搏,不接受RDN术).12头猪分别于建模前及其后每周检查左心室舒张末期内径、左心室收缩末期内径、左心室射血分数(LVEF).建模后1周(RDN术前)及2周检测血肌酐和血肾素、醛固酮等的水平.RDN术后1周复查肾动脉造影.建模2周后处死猪,检查心肾组织病理、肾动脉病理及交感神经染色.结果 12头猪置入起搏器前LVEF平均值为(60.5±6.0)%,快速起搏后1周,平均值为(35.3±9.8)%,表明右心室快速起搏致心衰模型建立成功.随访2周,消融组LVEF高于对照组[(42.8±5.9)%比(33.4±9.7)%,P=0.001 8],左心室收缩末期内径明显小于对照组[(28.4±3.7)mm比(33.0±2.0) mm,P=0.001 6].消融组消融后肾素浓度较消融前下降[(170.75 ±68.94) ng/L比(216.25 ±83.73) ng/L,P=0.046 4],醛固酮水平无明显改变,对照组醛固酮水平则明显上升(P =0.048).消融组血压、肾功能均无明显下降,无肾动脉狭窄、夹层及血栓形成.肾动脉病理及免疫组织化学显示血管外膜交感神经元被破坏.结论 RDN可以显著改善心力衰竭猪的心脏收缩功能,逆转心室重构,抑制肾素-血管紧张素-醛固酮系统活性.
目的 研究經導管射頻消融去腎交感神經術(catheter-based renal sympathetic denervation,RDN)對右心室快速起搏導緻的心力衰竭豬心功能的改善作用.方法 健康廣西巴馬小型豬12頭,建立快速起搏緻心力衰竭模型,以隨機數字錶法分為消融組(n=6,心室快速起搏1週後接受RDN術)和對照組(n=6,單純心室快速起搏,不接受RDN術).12頭豬分彆于建模前及其後每週檢查左心室舒張末期內徑、左心室收縮末期內徑、左心室射血分數(LVEF).建模後1週(RDN術前)及2週檢測血肌酐和血腎素、醛固酮等的水平.RDN術後1週複查腎動脈造影.建模2週後處死豬,檢查心腎組織病理、腎動脈病理及交感神經染色.結果 12頭豬置入起搏器前LVEF平均值為(60.5±6.0)%,快速起搏後1週,平均值為(35.3±9.8)%,錶明右心室快速起搏緻心衰模型建立成功.隨訪2週,消融組LVEF高于對照組[(42.8±5.9)%比(33.4±9.7)%,P=0.001 8],左心室收縮末期內徑明顯小于對照組[(28.4±3.7)mm比(33.0±2.0) mm,P=0.001 6].消融組消融後腎素濃度較消融前下降[(170.75 ±68.94) ng/L比(216.25 ±83.73) ng/L,P=0.046 4],醛固酮水平無明顯改變,對照組醛固酮水平則明顯上升(P =0.048).消融組血壓、腎功能均無明顯下降,無腎動脈狹窄、夾層及血栓形成.腎動脈病理及免疫組織化學顯示血管外膜交感神經元被破壞.結論 RDN可以顯著改善心力衰竭豬的心髒收縮功能,逆轉心室重構,抑製腎素-血管緊張素-醛固酮繫統活性.
목적 연구경도관사빈소융거신교감신경술(catheter-based renal sympathetic denervation,RDN)대우심실쾌속기박도치적심력쇠갈저심공능적개선작용.방법 건강엄서파마소형저12두,건립쾌속기박치심력쇠갈모형,이수궤수자표법분위소융조(n=6,심실쾌속기박1주후접수RDN술)화대조조(n=6,단순심실쾌속기박,불접수RDN술).12두저분별우건모전급기후매주검사좌심실서장말기내경、좌심실수축말기내경、좌심실사혈분수(LVEF).건모후1주(RDN술전)급2주검측혈기항화혈신소、철고동등적수평.RDN술후1주복사신동맥조영.건모2주후처사저,검사심신조직병리、신동맥병리급교감신경염색.결과 12두저치입기박기전LVEF평균치위(60.5±6.0)%,쾌속기박후1주,평균치위(35.3±9.8)%,표명우심실쾌속기박치심쇠모형건립성공.수방2주,소융조LVEF고우대조조[(42.8±5.9)%비(33.4±9.7)%,P=0.001 8],좌심실수축말기내경명현소우대조조[(28.4±3.7)mm비(33.0±2.0) mm,P=0.001 6].소융조소융후신소농도교소융전하강[(170.75 ±68.94) ng/L비(216.25 ±83.73) ng/L,P=0.046 4],철고동수평무명현개변,대조조철고동수평칙명현상승(P =0.048).소융조혈압、신공능균무명현하강,무신동맥협착、협층급혈전형성.신동맥병리급면역조직화학현시혈관외막교감신경원피파배.결론 RDN가이현저개선심력쇠갈저적심장수축공능,역전심실중구,억제신소-혈관긴장소-철고동계통활성.
Objective This study investigated the effect of catheter-based renal sympathetic denervation (RDN) in pigs with rapid pacing induced heart failure.Methods Heart failure was induced by rapid right ventricular pacing in 12 pigs and pigs were randomly divided into RDN group(n =6):pacing + RDN at 7 days post pacing; control group (n =6):pacing only.Echocardiography examination (LVEF,LVEDD and LVESD) was performed before pacing and at 1 and 2 weeks post pacing.Serum biochemical markers including renin,aldosterone and creatinine were also measured at baseline,1 and 2 weeks after pacing.Repeated renal artery angiography was performed at 1 week after RDN.All pigs were sacrificed to examine the heart and renal pathology and renal artery sympathetic nerve staining at 2 weeks post pacing.Results LVEF decreased 1 week after rapid pacing from (60.5 ± 6.0) % to (35.3 ± 9.8) %.LVEF was significantly higher [(42.8 ± 5.9) % vs.(33.4 ± 9.7) %,P =0.001 8] while LVESD was significantly lower [(28.4 ±3.7) mm vs.(33.0 ±2.0) mm,P =0.001 6] in the RDN group than in the control group at 2 weeks post pacing.At 2 weeks after pacing,plasma concentrations of renin and aldersterone were significantly lower in RDN group compared to the control group (all P < 0.05).Kidney function and blood pressure were comparable between the two groups at 2 weeks post pacing.There were no signs of renal damages such as renal artery stenosis,dissection and thrombus in all pigs after 2 weeks pacing.Sympathetic neurons of adventitia were injured in RND group.Conclusion RDN could significantly improve cardiac function and attenuate left ventricular remodeling via inhibiting renin-angiotensin-aldosterone system in this pacing induced pig heart failure model.