机构地区:[1]成都上锦南府医院暨四川大学华西医院上锦分院心脏外科,成都610000 [2]中国人民解放军总医院第七医学中心心内科,100700 [3]河北燕达医院心内科,廊坊065000 [4]山西医科大学第二临床医院心脏外科,太原030000 [5]中国人民解放军总医院超声科,北京100700 [6]北京大学北大医院心内科,北京100000 [7]四川大学华西医院心脏大血管外科,成都610000
出 处:《中国循证心血管医学杂志》2020年第2期182-187,共6页Chinese Journal of Evidence-Based Cardiovascular Medicine
基 金:2017年度河北省重点研发计划大健康服务和生物医药专项(172777106D);国家自然科学基金(81671777)。
摘 要:目的阐明持续训练相关性心房颤动(AF)的机制,可能为制定新的治疗方法和选择训练方法提供信息。本研究旨在评估兔动物模型中持续训练诱发房颤的机制。方法33只新西兰大耳兔随机分为三组(每组11只):对照组(Group C)、中强度耐力运动训练组(Group M)及高强度耐力运动训练组(Group H),于训练前、训练后8周、12周分别检测各组兔固有心率(IHR);全部训练结束后,各组随机各取6只,共18只兔采用离体心脏Langendorff系统进行1μm/L乙酰胆碱(Ach)+不同浓度阿托品溶液(0 mg/ml^0.002 mg/ml)灌注冠脉,在左心耳置入的电极分别记录相应的心房有效不应期(AERP)及90%动作电位时程(APD90);给予心房早搏程序刺激(S1S2)诱发房颤。灌流完后剪取兔左心房,经PT-PCR技术检测心房肌组织IKAch通道Kir3.1、Kir3.4的mRNA表达。取剩余各组5只实验兔,共15只运用全细胞膜片钳技术,记录心房肌细胞IKAch电流密度。结果长期高强度的耐力运动训练16周后,Group H兔IHR明显低于其他两组;1μm/L Ach背景下,相同剂量阿托品作用下,随着运动强度的增加APD90、AERP相应缩短有统计学差异(Group H vs.Group C and M,P<0.001);同一组内,随着阿托品剂量的增加APD90、AERP相应延长,房颤发生率降低有统计学差异(P<0.05);Group H心房肌细胞IKAch电流密度高于其他两组(Group H vs.Group C、M,P<0.05),Group H心房组织Kir3.1、Kir3.4的mRNA表达量高于其他两组(Group H vs.Group C、M,P<0.05)。结论长期的高强度耐力运动训练促进运动试验兔房颤发生。Objective Elucidating the mechanisms of continuous training-related atrial fibrillation(AF)may provide information for the development of new treatments and the selection of training methods.This study aimed to evaluate the mechanism of continuous training-induced atrial fibrillation in rabbit animal models.Methods 33 New Zealand big eared rabbits were randomly divided into three groups(11 in each group):the control group(Group C),the medium-endurance endurance training group(Group M)and the high-intensity endurance training group(Group H)The rabbit's intrinsic heart rate(IHR)was measured before,8 and 12 weeks after training.After all training,6 rats were randomly taken from each group.A total of 18 rabbits were perfused with 1μm/L acetylcholine(Ach)+atropine solution(0 mg/ml^0.002 mg/ml)in the coronary heart using the Langendorff system of isolated heart.The electrodes placed in the left atrial appendage recorded the corresponding atrial effective refractory period(AERP)and 90%action potential duration(APD90).Premature atrial premature beat stimulation(S1S2)was used to induce atrial fibrillation.After perfusion,the left and right atriums of rabbits were cut,and the mRNA expression of Kir3.1 and Kir3.4 in IKAch channels of atrial muscle tissue was detected by PT-PCR.The remaining 5 experimental rabbits in each group used the whole-cell patch-clamp technique to record the IKAch current density of atrial muscle cells.Results After 16 weeks of long-term high-intensity endurance training,the IHR of Group H rabbits was significantly lower than the other two groups.Under the background of 1μm/L Ach,under the same dose of atropine,the APD90 and AERP shortened correspondingly with the increase of exercise intensity(Group H vs.Group C and M,P<0.001).In the same group,with the increase of atropine dose,APD90 and AERP were prolonged,and the incidence of atrial fibrillation decreased statistically(P<0.05).The IKAch current density of Group H atrial muscle cells was higher than those of the other two groups(Group H vs.Group
关 键 词:心房颤动 耐力运动训练 IKAch kir3.1 kir3.4
分 类 号:R541.75[医药卫生—心血管疾病]
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