中华心律失常学杂志
中華心律失常學雜誌
중화심률실상학잡지
CHINESE JOURNAL OF CARDIAC ARRHYTHMIAS
2008年
4期
292-297
,共6页
李悦%李俭强%李为民%公永太%盛力%邵群%张莉%单鸿波%刘洁%于江波%刘巍%韩薇
李悅%李儉彊%李為民%公永太%盛力%邵群%張莉%單鴻波%劉潔%于江波%劉巍%韓薇
리열%리검강%리위민%공영태%성력%소군%장리%단홍파%류길%우강파%류외%한미
心房颤动%钙激活蛋白酶%血管紧张素%结构重构%犬
心房顫動%鈣激活蛋白酶%血管緊張素%結構重構%犬
심방전동%개격활단백매%혈관긴장소%결구중구%견
Atrial fibrillation%Calpains%Angiotensin%Structural remodehng%Dog
目的 观察西拉普利和缬沙坦对心房颤动(房颤)犬心房肌钙激活蛋白酶(calpairIs)mR-NA和蛋白表达及心房结构重构的影响.方法 27只犬随机分为假手术组、对照组、西拉普利组和缬沙坦组.对照组、西拉普利组和缬沙坦组犬以400次/min心房快速起搏6周,建立房颤犬模型.假手术组犬埋植起搏器后不起搏.测量左心房容积及收缩功能变化,记录房颤诱发及维持情况,检测心房肌calpains mRNA和蛋白表达,观察心房肌病理组织学和超微结构改变.结果 西拉普利组和缬沙坦组犬心房肌calpain I mRNA和蛋白表达较假手术组增多(P＜0.05),但较对照组显著减少(P＜0.01).各组犬心房肌calpain I蛋白表达与肌溶解高度相关(r=0.89,P＜0.01).各组犬心房肌calpainⅡmRNA和蛋白表达差异无统计学意义.与对照组相比,西拉普利组和缬沙坦组犬心房肌病理组织学和超微结构改变显著减轻,左心房及左心耳容积明显减小,左心房收缩功能显著增强,房颤诱发率和持续时间明显降低.结论 房颤犬心房肌calpain I mRNA和蛋白表达显著上调.西拉普利和缬沙坦能明显抑制房颤犬心房肌ealpain I表达,防治心房结构重构,减少房颤发生.
目的 觀察西拉普利和纈沙坦對心房顫動(房顫)犬心房肌鈣激活蛋白酶(calpairIs)mR-NA和蛋白錶達及心房結構重構的影響.方法 27隻犬隨機分為假手術組、對照組、西拉普利組和纈沙坦組.對照組、西拉普利組和纈沙坦組犬以400次/min心房快速起搏6週,建立房顫犬模型.假手術組犬埋植起搏器後不起搏.測量左心房容積及收縮功能變化,記錄房顫誘髮及維持情況,檢測心房肌calpains mRNA和蛋白錶達,觀察心房肌病理組織學和超微結構改變.結果 西拉普利組和纈沙坦組犬心房肌calpain I mRNA和蛋白錶達較假手術組增多(P＜0.05),但較對照組顯著減少(P＜0.01).各組犬心房肌calpain I蛋白錶達與肌溶解高度相關(r=0.89,P＜0.01).各組犬心房肌calpainⅡmRNA和蛋白錶達差異無統計學意義.與對照組相比,西拉普利組和纈沙坦組犬心房肌病理組織學和超微結構改變顯著減輕,左心房及左心耳容積明顯減小,左心房收縮功能顯著增彊,房顫誘髮率和持續時間明顯降低.結論 房顫犬心房肌calpain I mRNA和蛋白錶達顯著上調.西拉普利和纈沙坦能明顯抑製房顫犬心房肌ealpain I錶達,防治心房結構重構,減少房顫髮生.
목적 관찰서랍보리화힐사탄대심방전동(방전)견심방기개격활단백매(calpairIs)mR-NA화단백표체급심방결구중구적영향.방법 27지견수궤분위가수술조、대조조、서랍보리조화힐사탄조.대조조、서랍보리조화힐사탄조견이400차/min심방쾌속기박6주,건립방전견모형.가수술조견매식기박기후불기박.측량좌심방용적급수축공능변화,기록방전유발급유지정황,검측심방기calpains mRNA화단백표체,관찰심방기병리조직학화초미결구개변.결과 서랍보리조화힐사탄조견심방기calpain I mRNA화단백표체교가수술조증다(P＜0.05),단교대조조현저감소(P＜0.01).각조견심방기calpain I단백표체여기용해고도상관(r=0.89,P＜0.01).각조견심방기calpainⅡmRNA화단백표체차이무통계학의의.여대조조상비,서랍보리조화힐사탄조견심방기병리조직학화초미결구개변현저감경,좌심방급좌심이용적명현감소,좌심방수축공능현저증강,방전유발솔화지속시간명현강저.결론 방전견심방기calpain I mRNA화단백표체현저상조.서랍보리화힐사탄능명현억제방전견심방기ealpain I표체,방치심방결구중구,감소방전발생.
Objective The present study was designed to evaluate the effects of eilazapril and Valsar-tan on the mRNA and protein expressions of atrial ealpain I and calpain Ⅱ,and atrial structural remodeling in dogs with atrial fibrillation(AF)induced by chronic,rapid atrial pacing.Methods Twenty-seven dogs were randomly divided into the sham-operated group(n=6),control group(n=7),eilazapril group(n=7)and val-sartan group(n=7).The dogs in the control group,cilazapril group and valsartan group were subjected to rapid atrial pacing at 400 bpm for 6 weeks,whereas the pacemakers in the sham-operated group were not operational.The dogs in the cilazapril and valsartan groups were given cilazapril(1 mg·kg-1·d-1)or valsartan(30 mg·kg-1·d-1)respectively from 1 week before pacing until pacing Was stopped.Transthoracie and transoesopha-geal echocardiographic examinations were performed to detect the changes in left atrium volume and contractile function.The inducibility and duration of AF were measured in all groups.The mRNA expressions of atrial calpain I and ealpain Ⅱ were semi-quantified by reverse transcription polymerase chain reaction.The pro-tein levels of calpain I and calpain Ⅱ in atrial myocardium were measured by Western-blot method.Patho-histological and ultrastructural changes in atrial tissue were assessed by light and electron microscopy.Results After 6-week pacing,the mRNA and protein expressions of ealpain 1 were up-regulated dramatically in the control group compared to those in the sham-operated group,and the protein expressions of ealpain I in all groups correlated closely with the myolysis(r=0.89,P＜0.01).Cilazapril and valsartan could significantly inhibit the mRNA and protein expressions of calpain I.No differences were found in the mRNA and protein ex-pressions of calpain Ⅱ among the groups.Compared with the control group,dramatically smaller loft atrium and left atrial appendage volumes and markedly improved atrial contractile function were observed in the cilazapril and valsartan groups.Compared with atrial myoeytes obtained from the sham-operated group dogs,atrial myo-cytes from the control group dogs showed a reduced number of sarcomeres,a significantly higher myolytic area of atria(24.3%vs.3.1%,P＜0.01),increased vacuolization and dissolution.Cilazapril and valsartan could ef-fectively prevent the pathohistological and uhrastructural changes induced by chronic rapid atrial pacing,dra-matically decreased the area of myolysis(P＜0.05)and significantly reduced the inducibility and duration of AF.Conclusions Cilazapril and valsartun could inhibit ealpain I up-regulation,suppress atrial structural re-modding,and prevent the induction and maintenance of AF in chronic,rapid atrial pacing dogs.
