CAJ | 학술논문

目的：观察热应激诱导心肌热休克蛋白（HSP ）70表达上调，对兔快速心房起搏致房颤心肌钙激活钾通道（KCa ）3.1表达的影响。方法：将24只新西兰大白兔随机分为假手术组（n＝8，仅植入电极而不起博）、起搏组（n＝8，以600次／min快速起搏右心房6h）和热应激起搏组（热应激组，n＝8，先行热应激预处理，再行与起搏组一样的快速起搏）。结果：与假手术组和起搏组比较，热应激组心脏各部位 HSP70mRNA和蛋白表达显著上调[HSP70蛋白，左房：（39.00±3.21）比（39.75±2.82）比（69.75±3.45），右房：（38.38±2.92）比（39.50±3.89）比（69.00±2.93），左心耳：（37.75±3.28）比（39.00±3.89）比（68.63±3.23），右心耳：（37.00±3.85）比（38.38±3.74）比（68.75±2.82）]， P均＜0.01，而起搏组和假手术组间无显著性差异（P＞0.05）；与起搏组KCa 3.1 mRNA和蛋白表达量显著下调比较，热应激组心脏各部位KCa 3.1 mRNA和蛋白表达量显著上调[KCa 3.1蛋白，左房：（21.25±1.67）比（24.00±2.62），右房：（21.13±1.96）比（23.75±1.83），左心耳：（21.00±2.07）比（23.75±1.67），右心耳：（20.88±2.03）比（23.50±2.45）]， P均＜0.05，且热应激组与假手术组间无显著差异（P＞0.05）。结论：热应激可诱导心房起搏心肌热休克蛋白（HSP）70表达上调，抑制KCa 3.1 mRNA和蛋白表达量显著下降。
목적：관찰열응격유도심기열휴극단백（HSP ）70표체상조，대토쾌속심방기박치방전심기개격활갑통도（KCa ）3.1표체적영향。방법：장24지신서란대백토수궤분위가수술조（n＝8，부식입전겁이불기박）、기박조（n＝8，이600차／min쾌속기박우심방6h）화열응격기박조（열응격조，n＝8，선행열응격예처리，재행여기박조일양적쾌속기박）。결과：여가수술조화기박조비교，열응격조심장각부위 HSP70mRNA화단백표체현저상조[HSP70단백，좌방：（39.00±3.21）비（39.75±2.82）비（69.75±3.45），우방：（38.38±2.92）비（39.50±3.89）비（69.00±2.93），좌심이：（37.75±3.28）비（39.00±3.89）비（68.63±3.23），우심이：（37.00±3.85）비（38.38±3.74）비（68.75±2.82）]， P균＜0.01，이기박조화가수술조간무현저성차이（P＞0.05）；여기박조KCa 3.1 mRNA화단백표체량현저하조비교，열응격조심장각부위KCa 3.1 mRNA화단백표체량현저상조[KCa 3.1단백，좌방：（21.25±1.67）비（24.00±2.62），우방：（21.13±1.96）비（23.75±1.83），좌심이：（21.00±2.07）비（23.75±1.67），우심이：（20.88±2.03）비（23.50±2.45）]， P균＜0.05，차열응격조여가수술조간무현저차이（P＞0.05）。결론：열응격가유도심방기박심기열휴극단백（HSP）70표체상조，억제KCa 3.1 mRNA화단백표체량현저하강。
Objective:To observe influence of up‐regulated expression of myocardial heat shock protein (HSP) 70 in‐duced by heat stress on myocardial calcium‐activated potassium channel (KCa ) 3.1 expression in rabbits with atrial fibrillation (AF) caused by rapid atrial pacing (RAP) .Methods :A total of 24 New Zealand white rabbits were ran‐domly divided into sham operation group (n=8 ,only implant electrode without pacing ) ,pacing group (n=8 ,right atrium (RA) received RAP at 600 times/min for 6h) and heat stress pacing group (heat stress group ,n=8 ,received heat stress preconditioning ,then the same RAP as pacing group ) .Results:Compared with sham operation group and pacing group ,there were significant up‐regulation of HSP70 mRNA and protein expression in different sites of heart [HSP70 protein ,left atrium (LA):(39.00 ± 3.21) vs .(39.75 ± 2.82) vs .(69.75 ± 3.45) ,RA: (38.38 ± 2.92) vs .(39.50 ± 3.89) vs .(69.00 ± 2.93) ,left atrial appendage (LAA):(37.75 ± 3.28) vs .(39.00 ± 3.89) vs . (68.63 ± 3.23) ,right atrial appendage (RAA): (37.00 ± 3.85) vs .(38.38 ± 3.74) vs .(68.75 ± 2.82)] in heat stress group , P<0. 01 all ,but there were no significant difference between pacing group and sham operation group , P>0.05 ;compared with pacing group with down‐regulation of KCa3.1 mRNA and protein expressions ,there were significant up‐regulation of KCa3.1 mRNA and protein expressions in different sites of heart [KCa3.1 protein ,LA:(21.25 ± 1.67) vs .(24.00 ± 2.62) ,RA :(21.13 ± 1.96) vs .(23.75 ± 1.83) ,LAA :(21.00 ± 2.07) vs .(23.75 ± 1.67) ,RAA:(20.88 ± 2.03) vs .(23.50 ± 2.45)] in heat stress group ,P<0.05 all ,and there were no significant difference between heat stress group and sham operation group , P>0. 05. Conclusion:Heat stress may induce up‐regulated expression of myocardial HSP 70 of myocardium ,and HSP 70 may inhibit down‐regulation of KCa 3. 1 mR‐NA and protein expressions in rabbits with atrial fibrillation.