中华心血管病杂志
中華心血管病雜誌
중화심혈관병잡지
Chinese Journal of Cardiology
2011年
12期
1094-1100
,共7页
胡嘉禄%周祁娜%杨尚磊%陈华%张玲%颜彦%侯月梅
鬍嘉祿%週祁娜%楊尚磊%陳華%張玲%顏彥%侯月梅
호가록%주기나%양상뢰%진화%장령%안언%후월매
应激%心律失常%盐酸氟西汀
應激%心律失常%鹽痠氟西汀
응격%심률실상%염산불서정
Stress%Arrhythmia%Fluoxetine
目的 探讨精神应激大鼠的心律失常发生与胸1～5脊髓神经组织及心脏自主神经重构和心肌电重构的相关性.方法 30只SD雄性大鼠,体重180～220 g,随机分为对照组、应激组、应激+盐酸氟西汀组(简称氟西汀组)各10只.用Cronli方法建立后两组大鼠精神应激模型.观察各组:(1)心电图变化、心律失常发生;(2)胸1～5脊髓和心肌组织的场电位时程(FAPD)和场电位时程离散度(FAPDd)变化;(3)心肌组织免疫组化、电镜和激光共聚焦下的生长相关蛋白43( GAP-43)、乙酰胆碱酯酶(CHAT)、络氨酸羟化酶(TH)变化.结果 (1)应激组与对照组相比,体重、摄食量、水平运动、垂直运动得分、清洁动作次数等显著下降,粪便粒数显著增加.心电图出现P波、P-R间期、QRS间期及Q-T间期延长,并出现心率减慢、室性早搏(发生率为80％).胸1～5脊髓神经FAPD显著延长[( 144.25±12.63) ms比(79.56±8.01) ms],FAPDd显著增加[(13.3±9.11) ms比(9.36±7.01 )ms];左右心房及左右心室肌FAPD延长[左房(122.43±19.34) ms比(92.59±7.61)ms,右房(149.89±14.68) ms比(105.18±15.94)ms;左室(162.62±7.04) ms比(110.45±6.92)ms,右室( 152.21±30.49) ms比(131.06±12.04)ms],左右心房及左右心室肌的FAPDd也显著增加;心肌细胞排列紊乱、间质胶原纤维增生、中性粒细胞和淋巴细胞浸润;GAP-43、TH、CHAT心肌分布显著增加.(2)氟西汀组较应激组大鼠体重和摄食量增加,室性心律失常降低到20％,心电图各波段时间缩短.氟西汀组较应激组胸1～5脊髓神经的FAPD缩短[(134.32±11.23)ms比(144.25±12.63)ms],FAPDd降低[(12.74±10.11)ms比(13.3±9.11 )ms];左右心房及左右心室肌FAPD缩短[左房( 100.25±6.22)ms比(122.43±19.34)ms,右房(132.56±26.45) ms比(149.89±14.68) ms;左室(158.20±18.33)ms比(162.62±7.04)ms,右室(142.48±16.65)ms比(152.21±30.49) ms],左右心房及左右心室肌的FAPDd降低;心肌纤维化程度和生长相关蛋白43( GAP-43)、TH和CHAT分布降低.结论 大鼠精神应激产生了心脏自主神经和心肌电重构(心肌电激动传导异常),自主神经功能重构参与了大鼠应激性心肌电重构和室性心律失常的发生.氟西汀降低精神应激行为异常和有拮抗室性心律失常的作用,对其减少室性心律失常发生的机制有待进一步研究.
目的 探討精神應激大鼠的心律失常髮生與胸1～5脊髓神經組織及心髒自主神經重構和心肌電重構的相關性.方法 30隻SD雄性大鼠,體重180～220 g,隨機分為對照組、應激組、應激+鹽痠氟西汀組(簡稱氟西汀組)各10隻.用Cronli方法建立後兩組大鼠精神應激模型.觀察各組:(1)心電圖變化、心律失常髮生;(2)胸1～5脊髓和心肌組織的場電位時程(FAPD)和場電位時程離散度(FAPDd)變化;(3)心肌組織免疫組化、電鏡和激光共聚焦下的生長相關蛋白43( GAP-43)、乙酰膽堿酯酶(CHAT)、絡氨痠羥化酶(TH)變化.結果 (1)應激組與對照組相比,體重、攝食量、水平運動、垂直運動得分、清潔動作次數等顯著下降,糞便粒數顯著增加.心電圖齣現P波、P-R間期、QRS間期及Q-T間期延長,併齣現心率減慢、室性早搏(髮生率為80％).胸1～5脊髓神經FAPD顯著延長[( 144.25±12.63) ms比(79.56±8.01) ms],FAPDd顯著增加[(13.3±9.11) ms比(9.36±7.01 )ms];左右心房及左右心室肌FAPD延長[左房(122.43±19.34) ms比(92.59±7.61)ms,右房(149.89±14.68) ms比(105.18±15.94)ms;左室(162.62±7.04) ms比(110.45±6.92)ms,右室( 152.21±30.49) ms比(131.06±12.04)ms],左右心房及左右心室肌的FAPDd也顯著增加;心肌細胞排列紊亂、間質膠原纖維增生、中性粒細胞和淋巴細胞浸潤;GAP-43、TH、CHAT心肌分佈顯著增加.(2)氟西汀組較應激組大鼠體重和攝食量增加,室性心律失常降低到20％,心電圖各波段時間縮短.氟西汀組較應激組胸1～5脊髓神經的FAPD縮短[(134.32±11.23)ms比(144.25±12.63)ms],FAPDd降低[(12.74±10.11)ms比(13.3±9.11 )ms];左右心房及左右心室肌FAPD縮短[左房( 100.25±6.22)ms比(122.43±19.34)ms,右房(132.56±26.45) ms比(149.89±14.68) ms;左室(158.20±18.33)ms比(162.62±7.04)ms,右室(142.48±16.65)ms比(152.21±30.49) ms],左右心房及左右心室肌的FAPDd降低;心肌纖維化程度和生長相關蛋白43( GAP-43)、TH和CHAT分佈降低.結論 大鼠精神應激產生瞭心髒自主神經和心肌電重構(心肌電激動傳導異常),自主神經功能重構參與瞭大鼠應激性心肌電重構和室性心律失常的髮生.氟西汀降低精神應激行為異常和有拮抗室性心律失常的作用,對其減少室性心律失常髮生的機製有待進一步研究.
목적 탐토정신응격대서적심률실상발생여흉1～5척수신경조직급심장자주신경중구화심기전중구적상관성.방법 30지SD웅성대서,체중180～220 g,수궤분위대조조、응격조、응격+염산불서정조(간칭불서정조)각10지.용Cronli방법건립후량조대서정신응격모형.관찰각조:(1)심전도변화、심률실상발생;(2)흉1～5척수화심기조직적장전위시정(FAPD)화장전위시정리산도(FAPDd)변화;(3)심기조직면역조화、전경화격광공취초하적생장상관단백43( GAP-43)、을선담감지매(CHAT)、락안산간화매(TH)변화.결과 (1)응격조여대조조상비,체중、섭식량、수평운동、수직운동득분、청길동작차수등현저하강,분편립수현저증가.심전도출현P파、P-R간기、QRS간기급Q-T간기연장,병출현심솔감만、실성조박(발생솔위80％).흉1～5척수신경FAPD현저연장[( 144.25±12.63) ms비(79.56±8.01) ms],FAPDd현저증가[(13.3±9.11) ms비(9.36±7.01 )ms];좌우심방급좌우심실기FAPD연장[좌방(122.43±19.34) ms비(92.59±7.61)ms,우방(149.89±14.68) ms비(105.18±15.94)ms;좌실(162.62±7.04) ms비(110.45±6.92)ms,우실( 152.21±30.49) ms비(131.06±12.04)ms],좌우심방급좌우심실기적FAPDd야현저증가;심기세포배렬문란、간질효원섬유증생、중성립세포화림파세포침윤;GAP-43、TH、CHAT심기분포현저증가.(2)불서정조교응격조대서체중화섭식량증가,실성심률실상강저도20％,심전도각파단시간축단.불서정조교응격조흉1～5척수신경적FAPD축단[(134.32±11.23)ms비(144.25±12.63)ms],FAPDd강저[(12.74±10.11)ms비(13.3±9.11 )ms];좌우심방급좌우심실기FAPD축단[좌방( 100.25±6.22)ms비(122.43±19.34)ms,우방(132.56±26.45) ms비(149.89±14.68) ms;좌실(158.20±18.33)ms비(162.62±7.04)ms,우실(142.48±16.65)ms비(152.21±30.49) ms],좌우심방급좌우심실기적FAPDd강저;심기섬유화정도화생장상관단백43( GAP-43)、TH화CHAT분포강저.결론 대서정신응격산생료심장자주신경화심기전중구(심기전격동전도이상),자주신경공능중구삼여료대서응격성심기전중구화실성심률실상적발생.불서정강저정신응격행위이상화유길항실성심률실상적작용,대기감소실성심률실상발생적궤제유대진일보연구.
Objective The study aimed to investigate the relationship between arrhythmia occurrence and nerve remodeling of thoracic spinalcord 1-5 nerves as well as myocardial electrophysiological remodeling in a metal stress rat model.Methods Thirty SD rats (weight 180-250 g)were randomly divided into control group (n = 10),stress group (n = 10) and fluoxetine group (n = 10,10 mg/kg i.p.for 3 weeks).Stress model (given by unpredicted chronic mild stress) was established according to Cronli's protocol.Following parameters were observed:( 1 ) ECG waveform change and arrhythmias ; (2)tissue field action potential duration (FAPD) of thoracic spinal cord 1 - 5 and cardiac tissue mapped by microelectrode arrays ( MEA ) technique; ( 3 ) myocardial growth-associated protein ( GAP-43 ),tyrosine hydroxylase (TH),choline acetyltransferase (CHAT) distribution observed by immunofluorescence and confocal laser scanning microscope (LSCM).ResultsThree weeks later:(1) The body weight,food intake,consumption of sugar water,the horizontal and vertical movement score,cleaning action of rats were significantly decreased,and fecal grains significantly increased,P-wave,P-R interval,QRS-wave and Q-T interval were significantly prolonged and heart rate was significantly reduced in stress group compared with control group ( all P ＜0.05).Incidence of ventricular premature beat was 80％ in stress group and 0％ in control group (P ＜ 0.05 ).The FA PD of thoracic spinal cord 1 -5 nerves [ ( 144.25 ± 12.63 )ms vs (79.56 ±8.01 )ms ] and of cardiac tissue [ LA ( 122.43 ± 19.34)ms vs (92.59 ± 7.61 )ms,RA ( 149.89 ± 14.68 )ms vs (105.18 ± 15.94) ms,LV(162.62 ± 7.04) ms vs (110.45 ±6.92) ms,RV (152.21 ± 30.49) ms vs ( 131.06 ± 12.04) ms ] were significantly prolonged,FAPD dispersion (FAPDd) significantly increased [ thoracic spinal cord 1 - 5 ( 13.3 ± 9.11 ) ms vs ( 9.36 ± 7.01 ) ms ] in stress group compared with the control group.Disarrangement of myocardial cells,proliferation of collagen fiber,infiltration of neutrophil and lymphocytes in the cardiac tissue were also observed and distribution of GAP-43,TH and CHAT was significantly increased in stress group.(2) All these changes could be partly reversed by the treatment with fluoxetine.Conclusion Metal stress induced cardiac autonomic nerve and myocardial electrophysiological remodeling and ventricular arrhythmia in rats which could be significantly attenuated by fluoxetine in this model.
