中华心血管病杂志
中華心血管病雜誌
중화심혈관병잡지
Chinese Journal of Cardiology
2015年
11期
975-981
,共7页
祖克拉·吐尔洪%周祁娜%王红丽%周贤惠%李耀东%张宇%李晋新%张疆华%邢强
祖剋拉·吐爾洪%週祁娜%王紅麗%週賢惠%李耀東%張宇%李晉新%張疆華%邢彊
조극랍·토이홍%주기나%왕홍려%주현혜%리요동%장우%리진신%장강화%형강
心房颤动%心肌梗死%肾上腺素能纤维
心房顫動%心肌梗死%腎上腺素能纖維
심방전동%심기경사%신상선소능섬유
Atrial fibrillation%Myocardial infarction%Adrenergic fibers
目的 建立急性心肌梗死(AMI)后新发心房颤动犬模型,并探讨新发心房颤动与交感神经重构的关系.方法 采用随机数字表法将成年比格犬分为4组,A组结扎左回旋支(n=6),B组结扎左回旋支、右房前支和右房中间支(n=6),C组结扎前室间支(n=6),D组为假手术组(n=6).测定心肌梗死前、梗死后30min、2h和4h的心房颤动诱发率、心房颤动持续时间、有效不应期(ERP)、心肌酪氨酸羟化酶(TH)和去甲肾上腺素转运蛋白(NET)阳性神经纤维密度.结果 (1)右心房和左心耳Burst刺激后,B组的心房颤动诱发率最高分别为96.7%(58/60)和95.0%(57/60),A组最高分别为81.7%(49/60)和38.3%(23/60),C组最高分别为28.3%(17/60)和35.0%(21/60),D组最高分别为20.0%(12/60)和33.3%(20/60).(2)梗死后4h,B组左心耳心房颤动持续时间为(193.5±54.7)s,均长于A组的(53.8±9.4)s、C组的(45.0±19.5)s和对照组的(16.7±4.5)s(P均<0.05).(3)B组梗死后30min的左心耳ERP为(173.8±8.0)ms,长于梗死前的(162.5±6.4)ms(P<0.05);梗死后2和4h的左心耳ERP分别为(145.0±6.1)ms和(137.2±6.3)ms,均较梗死前缩短(P均<0.05).(4)左心房和左心耳TH阳性神经纤维密度A组分别为(3485±694)μm2/mm2和(2645±454)μm2/mm2,B组分别为(7873±1159)μm2/mm2和(3070±605)μm2/mm2,均分别高于C组的(1474±475)μm2/mm2和(1177±277)μm2/mm2及对照组的(678±206) μm2/mm2和(489±125)μm2/mm2(P均<0.05),且B组右心房、右心耳的TH阳性神经纤维密度均高于A组(P均<0.05);左心房和左心耳NET阳性神经纤维密度A组分别为(476±75)μm2/mm2和(414±52)μm2/mm2,B组分别为(527±81)μm2/mm2和(429±85)μm2/mm2,均分别低于C组的(1044±105)μm2/mm2和(867±67)μm2/mm2及对照组的(1438±60)μm2/mm2和(1027±119)μm2/mm2(P均<0.05).结论 同时结扎犬的左回旋支、右房前支和右房中间支,可明显提高AMI后新发心房颤动的建模成功率和心房颤动持续时间;AMI后的心脏交感神经重构可能与心房颤动的触发和持续有关.
目的 建立急性心肌梗死(AMI)後新髮心房顫動犬模型,併探討新髮心房顫動與交感神經重構的關繫.方法 採用隨機數字錶法將成年比格犬分為4組,A組結扎左迴鏇支(n=6),B組結扎左迴鏇支、右房前支和右房中間支(n=6),C組結扎前室間支(n=6),D組為假手術組(n=6).測定心肌梗死前、梗死後30min、2h和4h的心房顫動誘髮率、心房顫動持續時間、有效不應期(ERP)、心肌酪氨痠羥化酶(TH)和去甲腎上腺素轉運蛋白(NET)暘性神經纖維密度.結果 (1)右心房和左心耳Burst刺激後,B組的心房顫動誘髮率最高分彆為96.7%(58/60)和95.0%(57/60),A組最高分彆為81.7%(49/60)和38.3%(23/60),C組最高分彆為28.3%(17/60)和35.0%(21/60),D組最高分彆為20.0%(12/60)和33.3%(20/60).(2)梗死後4h,B組左心耳心房顫動持續時間為(193.5±54.7)s,均長于A組的(53.8±9.4)s、C組的(45.0±19.5)s和對照組的(16.7±4.5)s(P均<0.05).(3)B組梗死後30min的左心耳ERP為(173.8±8.0)ms,長于梗死前的(162.5±6.4)ms(P<0.05);梗死後2和4h的左心耳ERP分彆為(145.0±6.1)ms和(137.2±6.3)ms,均較梗死前縮短(P均<0.05).(4)左心房和左心耳TH暘性神經纖維密度A組分彆為(3485±694)μm2/mm2和(2645±454)μm2/mm2,B組分彆為(7873±1159)μm2/mm2和(3070±605)μm2/mm2,均分彆高于C組的(1474±475)μm2/mm2和(1177±277)μm2/mm2及對照組的(678±206) μm2/mm2和(489±125)μm2/mm2(P均<0.05),且B組右心房、右心耳的TH暘性神經纖維密度均高于A組(P均<0.05);左心房和左心耳NET暘性神經纖維密度A組分彆為(476±75)μm2/mm2和(414±52)μm2/mm2,B組分彆為(527±81)μm2/mm2和(429±85)μm2/mm2,均分彆低于C組的(1044±105)μm2/mm2和(867±67)μm2/mm2及對照組的(1438±60)μm2/mm2和(1027±119)μm2/mm2(P均<0.05).結論 同時結扎犬的左迴鏇支、右房前支和右房中間支,可明顯提高AMI後新髮心房顫動的建模成功率和心房顫動持續時間;AMI後的心髒交感神經重構可能與心房顫動的觸髮和持續有關.
목적 건립급성심기경사(AMI)후신발심방전동견모형,병탐토신발심방전동여교감신경중구적관계.방법 채용수궤수자표법장성년비격견분위4조,A조결찰좌회선지(n=6),B조결찰좌회선지、우방전지화우방중간지(n=6),C조결찰전실간지(n=6),D조위가수술조(n=6).측정심기경사전、경사후30min、2h화4h적심방전동유발솔、심방전동지속시간、유효불응기(ERP)、심기락안산간화매(TH)화거갑신상선소전운단백(NET)양성신경섬유밀도.결과 (1)우심방화좌심이Burst자격후,B조적심방전동유발솔최고분별위96.7%(58/60)화95.0%(57/60),A조최고분별위81.7%(49/60)화38.3%(23/60),C조최고분별위28.3%(17/60)화35.0%(21/60),D조최고분별위20.0%(12/60)화33.3%(20/60).(2)경사후4h,B조좌심이심방전동지속시간위(193.5±54.7)s,균장우A조적(53.8±9.4)s、C조적(45.0±19.5)s화대조조적(16.7±4.5)s(P균<0.05).(3)B조경사후30min적좌심이ERP위(173.8±8.0)ms,장우경사전적(162.5±6.4)ms(P<0.05);경사후2화4h적좌심이ERP분별위(145.0±6.1)ms화(137.2±6.3)ms,균교경사전축단(P균<0.05).(4)좌심방화좌심이TH양성신경섬유밀도A조분별위(3485±694)μm2/mm2화(2645±454)μm2/mm2,B조분별위(7873±1159)μm2/mm2화(3070±605)μm2/mm2,균분별고우C조적(1474±475)μm2/mm2화(1177±277)μm2/mm2급대조조적(678±206) μm2/mm2화(489±125)μm2/mm2(P균<0.05),차B조우심방、우심이적TH양성신경섬유밀도균고우A조(P균<0.05);좌심방화좌심이NET양성신경섬유밀도A조분별위(476±75)μm2/mm2화(414±52)μm2/mm2,B조분별위(527±81)μm2/mm2화(429±85)μm2/mm2,균분별저우C조적(1044±105)μm2/mm2화(867±67)μm2/mm2급대조조적(1438±60)μm2/mm2화(1027±119)μm2/mm2(P균<0.05).결론 동시결찰견적좌회선지、우방전지화우방중간지,가명현제고AMI후신발심방전동적건모성공솔화심방전동지속시간;AMI후적심장교감신경중구가능여심방전동적촉발화지속유관.
Objective To establish the canine model of new-onset atrial fibrillation (AF) after acute myocardial infarction (AMI),and explore the relationship between new-onset AF and sympathetic neural remodeling in this model Methods Twenty four adult mongrel dogs were randomly divided into 4 groups by applying random number table.Group A (n=6):ligate the left circumflex artery (LCX).Group B (n=6):ligate the LCX and right atrial anterior artery and right atrial middle artery.Group C (n=6):ligate left anterior descending artery.Group D(n=6):sham operation.Sequential electrophysiology study was performed in all dogs to determine the AF induction rate,AF duration,effective refractory period (ERP),the density of tyrosine hydroxylase (TH) and norepinephrine transporter (NET) before AMI or sham operation,and at 30 min,2 hours and 4 hours after AMI or sham operation.Results (1) The highest AF induction rate of right atrium and left auricle was 96.7% (58/60) and 95.0% (57/60) in group B,81.7% (49/60) and 38.3% (23/60) in group A,28.3% (17/60) and 35.0% (21/60) in group C,20.0% (12/60) and 33.3% (20/60) in group D.(2) At 4 hours after AMI,AF duration was significantly prolonged in group B (193.50±54.67) s,compared with group A (53.83±9.37) s,group C (45.00±19.50) s,and group D (16.67±4.50) s (all P<0.05).(3) In group B,the ERP of AF was prolonged at 30 minutes after AMI and shortened at 2 hours and 4 hours after AMI compared with baseline level(all P<0.05).(4) The TH density of left atrium ((3485±694)μm2/mm2) and left auricle ((2645±454) μm2/mm2) in group A and the TH density of left atrium ((7873±1159)μm2/mm2) and left auricle ((3070±605)μm2/mm2) in group B were significantly higher than those in group C ((1474±475) μm2/mm2,(1177±277)μm2/mm2) and group D ((678±206)μm2/mm2,(489±125)μm2/mm2) (all P<0.05),and the TH density of right atrium and right auricle in group B were higher than group A (all P<0.05).The NET density of left atrium ((476±75)μm2/mm2) and left auricle ((414±52) μm2/mm2) in group A and the NET density of left atrium((527±81)μm2/mm2) and left auricle((429±85)μm2/mm2) in group B were lower than that in group C ((1044±105)μm2/mm2,(867±67) μm2/mm2) and group D ((1438±60)μm2/mm2,(1027±119)μm2/mm2) (all P<0.05).Conclusions Ligating the LCX,right atrial anterior artery and right atrial middle artery at the same time can significantly increase the success rate in establishing the canine model of new-onset atrial fibrillation after acute myocardial infarction and can also increase the AF duration.Cardiac sympathetic remodeling after acute myocardial infarction is associated with induction and duration of AF.