摘要
目的通过耐力运动训练兔动物模型探索运动相关性心房颤动(AF)的发生机制。方法 36只新西兰大耳兔随机分为对照组、中强度耐力训练组、高强度耐力训练组(每组12只):对照组不做任何耐力训练处理;耐力运动训练组每周训练5 d,每天1 h或一次性力竭(不足1 h),共持续16周(中强度耐力训练组:坡度0度,速度15 m/min;高强度耐力训练组:坡度0度,速度30 m/min)。训练完成后,各组随机各取6只,共18只兔采用离体心脏Langendorff系统进行灌流,将1μmol/L乙酰胆碱(Ach)+不同浓度的氯化钡(BaCl2)溶液(0、0.1、0.5、1、3、6μmol/L)灌入冠脉内,开始持续给药过程中电生理指标的测定及记录。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)、并给予心脏期前程序刺激(S1S2)诱发房颤,记录并计算房颤发生率。灌流完后剪取兔左心房,经实时荧光定量(qRT)-PCR技术检测心房肌组织内向整流钾电流/通道(IK1)kir2.1、kir2.2、胶原蛋白Ⅰ和胶原蛋白Ⅲ的mRNA表达量。取各组剩余6只实验兔,共18只取左心房组织标本,应用Masson染色进行组织学检查,测定心肌组织胶原容积分数。结果长期高强度的运动训练16周后,不同组间,Ach背景相同,BaCl2剂量相同作用下,随着运动强度的增加,APD90、AERP相应缩短,房颤发生率增加,BaCl2取0~6μmol/L时,高强度耐力训练组与其余两组间比较差异均有统计学意义(P<0.001),而其余两组之间差异无统计学意义。同一组内,Ach背景相同,随着BaCl2剂量的增加,APD90、AERP相应延长,房颤发生率降低,3组组内比较,差异均有统计学意义(P<0.05)。随着运动量的增加,兔左心房kir2.1、kir2.2、胶原蛋白Ⅰ和胶原蛋白Ⅲ的mRNA表达量均增加,胶原容积分数增加,高强度耐力训练组>中强度耐力训练组>对照组,差异有统计学意义(P<0.05)。结论长期的高强度耐力运动训练可通过增加实验兔心房组织纤维化程度、心肌细胞IK1数量和(或)功能,改变心电传导,促使实验兔房颤发生和维持。
Objective This study was aimed to assess mechanisms underlying continuous training induced atrial fibrillation(AF) in an animal model. Methods Healthy New Zealand rabbits were divided into three groups(n=12 each): control group(C), moderate intensity group(M), and high intensity group(H). The intensity of continuous training was adjusted according to the treadmill speed. After 12 weeks of training, with a Langendorff perfusion system,AF was induced by S1 S2 stimulation and the incidence was recorded. Changes in atrial kir2.1, kir2.2, type Ⅰ and Ⅲcollagen protein mRNA expressions were assessed by quantitative real-time PCR. Masson staining was used to assess the extracellular collagen volume fraction(CVF). Results After 12 weeks, comparing with group C, groups M and H had greater(P<0.05): CVF, incidence of AF(P<0.05, also between Groups H and M), and atrial inward rectifier potassium current/channel(IK1). In Group H, kir2.1, kir2.2, type Ⅰ and Ⅲ collagen protein mRNA expressions in the left atrium were increased(P<0.05, compared with Groups C and M). Conclusion Long-term and high-intensity treadmill running could increase AF incidence in rabbits.
作者
袁斗
谭琛
姚建民
李丹
黄思慧
武忠
YUAN Dou;TAN Chen;YAO Jian-min;LI Dan;HUANG Si-hui;WU Zhong(Department of Cardiovascular Surgery,Chengdu Shang Jin Nan Fu Hospital,West China Hospital,Sichuan University,Chengdu 611743,China;Department of Cardiology,Hebei Yan Da Hospital,Sanhe 065200,China;Department of Cardiovascular Surgery,Second Hospital of Shanxi Medical University,Taiyuan 030000,China;Department of Ultrasound,PLA General Hopsital,Beijing 100000,China;Department of Cardiology,Peking University First Hospital,Beijing 100000,China;Department of Cardiovascular Surgery,West China Hospital,Sichuan University,Chengdu 610041,China)
出处
《四川大学学报（医学版）》
CAS
CSCD
北大核心
2020年第2期213-218,共6页
Journal of Sichuan University(Medical Sciences)
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(No.172777106D)
四川省科技计划项目(No.2017HH0108)资助。
