中华实验外科杂志
中華實驗外科雜誌
중화실험외과잡지
CHINESE JOURNAL OF EXPERIMENTAL SURGERY
2011年
10期
1753-1755
,共3页
周元%刘金平%连亦田%董念国%程龙献%孙宗全%刘坤%王玉
週元%劉金平%連亦田%董唸國%程龍獻%孫宗全%劉坤%王玉
주원%류금평%련역전%동념국%정룡헌%손종전%류곤%왕옥
房颤%乙酰胆碱%动作电位%频率适应性%电生理
房顫%乙酰膽堿%動作電位%頻率適應性%電生理
방전%을선담감%동작전위%빈솔괄응성%전생리
Atrial fibrillation%Acetylcholine%Action potential%Frequency adaptation%Electrophysiology
目的 观察房颤时人心房肌细胞动作电位变化及迷走神经递质乙酰胆碱(ACh)对离体人心房肌动作电位(AP)及有效不应期(ERP)的影响.方法 选择20例心脏瓣膜病患者分为两组,其中11例合并房颤者为房额组(AF),9例窦性心律者为对照组(SR),术中取右心耳组织,采用玻璃微电极技术,检测两组患者静息膜电位(RMP),动作电位复极达90%的时程(APD90),动作电位复极达50%的时程(APD50)及不同起搏频率下APD90的变化,同时观察给予Ach前后上述指标的变化.结果 Ach灌注前,AF组与SR组间RMP( 63.70±3.00) mV比(54.70 ±2.19) mV、APD90 (312.60±11.92) ms比(406.30±14.61) ms、APD50( 177.30±14.05) ms比(218.50±15.10) ms差异有统计学意义(P<0.05).Ach灌注后,AF与SR两组间RMP(67.8±2.0) mV比(61.4±1.8) mV、APD90 (263.60±13.38) ms比(316.20±15.40) ms、APD50( 173.60±16.82) ms 比(217.60±15.16) ms差异有统计学意义(P<0.05).与灌注前自身比较,两组RMP显著增高、APD90显著缩短(P<0.05).APD50差异无统计学意义(P>0.05).但在AF组患者,其APD90缩短程度( △APD90,%)较SR组小(P<0.05).结论 房颤时存在心房组织APD缩短,频率适应性降低等电重构,它促进了房颤的维持.Ach可加重重构作用,但在慢性房颤中这种作用减弱.这种改变可能是机体对抗房颤的一种调节机制.
目的 觀察房顫時人心房肌細胞動作電位變化及迷走神經遞質乙酰膽堿(ACh)對離體人心房肌動作電位(AP)及有效不應期(ERP)的影響.方法 選擇20例心髒瓣膜病患者分為兩組,其中11例閤併房顫者為房額組(AF),9例竇性心律者為對照組(SR),術中取右心耳組織,採用玻璃微電極技術,檢測兩組患者靜息膜電位(RMP),動作電位複極達90%的時程(APD90),動作電位複極達50%的時程(APD50)及不同起搏頻率下APD90的變化,同時觀察給予Ach前後上述指標的變化.結果 Ach灌註前,AF組與SR組間RMP( 63.70±3.00) mV比(54.70 ±2.19) mV、APD90 (312.60±11.92) ms比(406.30±14.61) ms、APD50( 177.30±14.05) ms比(218.50±15.10) ms差異有統計學意義(P<0.05).Ach灌註後,AF與SR兩組間RMP(67.8±2.0) mV比(61.4±1.8) mV、APD90 (263.60±13.38) ms比(316.20±15.40) ms、APD50( 173.60±16.82) ms 比(217.60±15.16) ms差異有統計學意義(P<0.05).與灌註前自身比較,兩組RMP顯著增高、APD90顯著縮短(P<0.05).APD50差異無統計學意義(P>0.05).但在AF組患者,其APD90縮短程度( △APD90,%)較SR組小(P<0.05).結論 房顫時存在心房組織APD縮短,頻率適應性降低等電重構,它促進瞭房顫的維持.Ach可加重重構作用,但在慢性房顫中這種作用減弱.這種改變可能是機體對抗房顫的一種調節機製.
목적 관찰방전시인심방기세포동작전위변화급미주신경체질을선담감(ACh)대리체인심방기동작전위(AP)급유효불응기(ERP)적영향.방법 선택20례심장판막병환자분위량조,기중11례합병방전자위방액조(AF),9례두성심률자위대조조(SR),술중취우심이조직,채용파리미전겁기술,검측량조환자정식막전위(RMP),동작전위복겁체90%적시정(APD90),동작전위복겁체50%적시정(APD50)급불동기박빈솔하APD90적변화,동시관찰급여Ach전후상술지표적변화.결과 Ach관주전,AF조여SR조간RMP( 63.70±3.00) mV비(54.70 ±2.19) mV、APD90 (312.60±11.92) ms비(406.30±14.61) ms、APD50( 177.30±14.05) ms비(218.50±15.10) ms차이유통계학의의(P<0.05).Ach관주후,AF여SR량조간RMP(67.8±2.0) mV비(61.4±1.8) mV、APD90 (263.60±13.38) ms비(316.20±15.40) ms、APD50( 173.60±16.82) ms 비(217.60±15.16) ms차이유통계학의의(P<0.05).여관주전자신비교,량조RMP현저증고、APD90현저축단(P<0.05).APD50차이무통계학의의(P>0.05).단재AF조환자,기APD90축단정도( △APD90,%)교SR조소(P<0.05).결론 방전시존재심방조직APD축단,빈솔괄응성강저등전중구,타촉진료방전적유지.Ach가가중중구작용,단재만성방전중저충작용감약.저충개변가능시궤체대항방전적일충조절궤제.
Objective To study the changes of action potential (AP) of atrial myocytes from patients with chronic atrial fibrillation (AF) and the electrophysiological effects of acetylcholine (Ach) on AP and effective refractory period (ERP) of atrial myocytes from AF patients.Methods Right atrial appendages were obtained from 11 patients with chronic AF and 9 patients matched as controls with sinus rhythm (SR).All patients were subjected to valve replacement surgery.Rest membrane potential (RMP),50% and 90% action potential duration ( APD50,APD90) of human atrial myocytes were recorded before and after administration of Ach by using standard intracellular microelectrode technique.APD90 and APD50 were also measured in different pacing rate.Results Before perfusion with Ach,RMP of atrial myocytes from patients with AF was more negative than in SR patients [ (63.70 ± 3.00) mV vs.(54.70 ±2.19) mV],P< 0.05.APD90 and APD50 in AF patients were shorter than in SR patients [ APD90(312.60±11.92) ms vs.(406.30±14.61) ms],APD50 (177.30±14.05) ms vs.(218.50±15.10)ms,P <0.05 ].Ach ( 10 μmol/L) made RMP more negative [ (67.8 ±2.0) mV vs.(61.4 ± 1.8) mV]and shortened APD90 [(263.60±13.38) ms vs.(316.20±15.40) ms],APD50 [(173.60±16.82)ms vs.(217.60 ± 15.16) ms] in both groups,P<0.05.APD50 had no significant change after perfusion with Ach,but the alterations of RMP and APD90 were more significant than those before perfusion respectively ( P < 0.05).The change of APD90 in SR patients is more remarkable than that in AF patients (P <0.05).Conclusion Patients with atrial fibrillation has the obvious decrease of frequency adaptation and more shortened APD,which contribute to the development and maintenance of atrial fibrillation.But it is not marked that these changes have been aggravated by Ach in patients with AF.Because the effect of Ach is decreased in these patients,this is possibly a regulative mechanism against AF.