中华心律失常学杂志
中華心律失常學雜誌
중화심률실상학잡지
CHINESE JOURNAL OF CARDIAC ARRHYTHMIAS
2013年
1期
60-62
,共3页
于胜波%代子玄%邹明辉%王徐乐%肖金平%赵庆彦%黄从新
于勝波%代子玄%鄒明輝%王徐樂%肖金平%趙慶彥%黃從新
우성파%대자현%추명휘%왕서악%초금평%조경언%황종신
心房颤动%肾交感神经%消融%肾素-血管紧张素-醛固酮系统
心房顫動%腎交感神經%消融%腎素-血管緊張素-醛固酮繫統
심방전동%신교감신경%소융%신소-혈관긴장소-철고동계통
Atrial fibrillation%Renal sympathetic nerve%Ablation%Renin-angiotensin-aldosterone system
目的 探讨经导管消融肾交感神经后对心房右前神经节(ARGP)刺激诱发心房颤动(房颤)的影响.方法 13只犬随机分为对照组(n=7)和消融组(n=6).对照组犬于右侧第4肋间开胸,采用不同电压高频刺激(20 Hz,0.1 ms) ARGP,观察心率减慢和房颤诱发情况;消融组犬先监测心房有效不应期(AERP),后行双侧经皮介入肾动脉消融,喂养6周后ARGP刺激同对照组.消融组犬在肾动脉消融前及后6周取静脉血检测血管紧张素Ⅱ(AngⅡ)及醛固酮水平.结果 消融组AERP在消融前及后6周差异无统计学意义[(134.4± 19.2) ms对(142.0±21.5) ms,P>0.05].与对照组相比,消融组犬ARGP刺激引起心率减慢50%所需电压[(3.5±1.6)V对(1.6±0.3)V,P=0.03]和诱发房颤的最低电压[(5.1±1.0)V对(2.1±0.7)V,P=0.03]明显升高.消融组犬消融6周后血清AngⅡ[(142.8±31.7) pg/ml对(91.7±23.8)pg/ml,P=0.01]和醛固酮水平[(272.2±37.4) pg/ml对(156.3±17.6)pg/ml,P<0.01]明显降低.结论 肾去交感神经可抑制ARGP刺激对房颤的诱发,其机制可能与肾去交感神经后肾素-血管紧张素-醛固酮系统活性降低有关.
目的 探討經導管消融腎交感神經後對心房右前神經節(ARGP)刺激誘髮心房顫動(房顫)的影響.方法 13隻犬隨機分為對照組(n=7)和消融組(n=6).對照組犬于右側第4肋間開胸,採用不同電壓高頻刺激(20 Hz,0.1 ms) ARGP,觀察心率減慢和房顫誘髮情況;消融組犬先鑑測心房有效不應期(AERP),後行雙側經皮介入腎動脈消融,餵養6週後ARGP刺激同對照組.消融組犬在腎動脈消融前及後6週取靜脈血檢測血管緊張素Ⅱ(AngⅡ)及醛固酮水平.結果 消融組AERP在消融前及後6週差異無統計學意義[(134.4± 19.2) ms對(142.0±21.5) ms,P>0.05].與對照組相比,消融組犬ARGP刺激引起心率減慢50%所需電壓[(3.5±1.6)V對(1.6±0.3)V,P=0.03]和誘髮房顫的最低電壓[(5.1±1.0)V對(2.1±0.7)V,P=0.03]明顯升高.消融組犬消融6週後血清AngⅡ[(142.8±31.7) pg/ml對(91.7±23.8)pg/ml,P=0.01]和醛固酮水平[(272.2±37.4) pg/ml對(156.3±17.6)pg/ml,P<0.01]明顯降低.結論 腎去交感神經可抑製ARGP刺激對房顫的誘髮,其機製可能與腎去交感神經後腎素-血管緊張素-醛固酮繫統活性降低有關.
목적 탐토경도관소융신교감신경후대심방우전신경절(ARGP)자격유발심방전동(방전)적영향.방법 13지견수궤분위대조조(n=7)화소융조(n=6).대조조견우우측제4륵간개흉,채용불동전압고빈자격(20 Hz,0.1 ms) ARGP,관찰심솔감만화방전유발정황;소융조견선감측심방유효불응기(AERP),후행쌍측경피개입신동맥소융,위양6주후ARGP자격동대조조.소융조견재신동맥소융전급후6주취정맥혈검측혈관긴장소Ⅱ(AngⅡ)급철고동수평.결과 소융조AERP재소융전급후6주차이무통계학의의[(134.4± 19.2) ms대(142.0±21.5) ms,P>0.05].여대조조상비,소융조견ARGP자격인기심솔감만50%소수전압[(3.5±1.6)V대(1.6±0.3)V,P=0.03]화유발방전적최저전압[(5.1±1.0)V대(2.1±0.7)V,P=0.03]명현승고.소융조견소융6주후혈청AngⅡ[(142.8±31.7) pg/ml대(91.7±23.8)pg/ml,P=0.01]화철고동수평[(272.2±37.4) pg/ml대(156.3±17.6)pg/ml,P<0.01]명현강저.결론 신거교감신경가억제ARGP자격대방전적유발,기궤제가능여신거교감신경후신소-혈관긴장소-철고동계통활성강저유관.
Objective To investigate the effect of renal sympathetic denervation on inducibility of atrial fibrillation(AF) by anterior right ganglionic plexi (ARGP)stimulation.Methods Thirteen dogs were used for the study as follows:control group(n =7) and renal artery ablation (RAA) group (n =6).In control group,after right thoracotomy,high-frequency electrical stimulation(20 Hz,0.1 ms duration)was applied to the ARGP for 1 minute by incremental voltages up to the voltage that induced AF.In RAA group,after atrial effective refractory period (AERP) measured,each renal artery was ablated and dogs were raised for 6 weeks.The procedure of ARGP stimulation was same as in the control group.Blood was collected before and after ablation 6 weeks to measure the levels ofangiotensin Ⅱ(Ang Ⅱ)and aldosterone(ALD) in RAA dogs.Results AERP had no significant change before and after renal artery ablation 6 weeks [(134.4±19.2) ms vs (142.0±21.5) ms,P>0.05].Compared with that in control group,dogs had higher voltage in the sinus rate slowing response induced by ARGP stimulation in RAA group[(3.5±1.6)V vs(1.6±0.3)V,P=0.03].Furthermore,the lowest voltage that induce AF was higher in RAA group than that in control group[(5.1±1.0)V vs(2.1±0.7)V,P=0.03].The plasma Ang Ⅱ and aldosterone concentration showed a greatly decreasing after RAA 6 weeks in RAA group [Ang Ⅱ:(142.8±31.7) pg/ml vs(91.7±23.8)pg/ml,P=0.01 ; Aldosterone:(272.2±37.4) pg/ml vs(156.3±17.6)pg/ml,P<0.01].Conclusions Renal sympathetic denervation inhibited the inducibility of AF during ARGP stimulation.This effect might have relationship with decreased activity of renin-angiotensin-aldosterone system(RAAS).