Myocardial electrotonic response to submaximal exercise in dogs with healed myocardial infarctions: evidence for β-adrenoceptor mediated enhanced coupling during exercise testing.
Myocardial electrotonic response to submaximal exercise in dogs with healed myocardial infarctions: evidence for β-adrenoceptor mediated enhanced coupling during exercise testing.
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DOI：
10.3389/fphys.2015.00025
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发表时间：
2015
影响因子：
4
通讯作者：
Billman GE
中科院分区：
文献类型：
--
作者：
Del Rio CL;Clymer BD;Billman GE
导言：心脏负荷试验中的自主神经激活是心肌梗死后(MI)患者公认的风险分层工具。然而，自主神经激活也可以调节心肌电紧张性偶联，这是一个已知的导致心律失常发生的因素。本研究验证了运动诱导的自主神经激活调节心肌梗死后易患或不耐受室颤(VF)动物的电紧张性耦合(由心肌电阻抗(MEI)测量)的假说。方法：25只心肌梗塞愈合后用于MEI测量的犬被训练在跑步机上跑步，并根据其对室颤的易感性进行分类(12只易感，9只抵抗)。在对照组和β-AR(β-AR)完全阻断(心得安)后进行6次运动试验(18min/次，峰值6.4 km/h@16%)，记录MEI和ECG，并在β-AR刺激(异丙肾上腺素)或超速起搏时记录MEI。结果：运动逐渐增加心率(HR)，降低心率变异性(HRV)。运动后MEI逐渐降低(电紧张性耦合增强)，运动高峰时MEI下降5.3±0.4%(或-23±1.8Ω，P<；0.001)。值得注意的是，运动介导的电紧张性变化由自主神经激活的程度线性预测，如心率或心率变异性的变化(P<；0.001)。事实上，阻断β-AR可减弱MEI对运动的反应，而直接刺激β-AR(静息时)可触发MEI的下降，与运动中观察到的结果相当；心室起搏对MEI没有显著影响。最后，易发生室颤的动物对运动的MEI反应明显更大。结论：这些数据表明，运动中β-AR的激活可以显著增强心肌的电紧张性偶联，特别是在易受缺血性室颤影响的狗身上。
Introduction: Autonomic neural activation during cardiac stress testing is an established risk-stratification tool in post-myocardial infarction (MI) patients. However, autonomic activation can also modulate myocardial electrotonic coupling, a known factor to contribute to the genesis of arrhythmias. The present study tested the hypothesis that exercise-induced autonomic neural activation modulates electrotonic coupling (as measured by myocardial electrical impedance, MEI) in post-MI animals shown to be susceptible or resistant to ventricular fibrillation (VF). Methods: Dogs (n = 25) with healed MI instrumented for MEI measurements were trained to run on a treadmill and classified based on their susceptibility to VF (12 susceptible, 9 resistant). MEI and ECGs were recorded during 6-stage exercise tests (18 min/test; peak: 6.4 km/h @ 16%) performed under control conditions, and following complete β-adrenoceptor (β-AR) blockade (propranolol); MEI was also measured at rest during escalating β-AR stimulation (isoproterenol) or overdrive-pacing. Results: Exercise progressively increased heart rate (HR) and reduced heart rate variability (HRV). In parallel, MEI decreased gradually (enhanced electrotonic coupling) with exercise; at peak exercise, MEI was reduced by 5.3 ± 0.4% (or -23 ± 1.8Ω, P < 0.001). Notably, exercise-mediated electrotonic changes were linearly predicted by the degree of autonomic activation, as indicated by changes in either HR or in HRV (P < 0.001). Indeed, β-AR blockade attenuated the MEI response to exercise while direct β-AR stimulation (at rest) triggered MEI decreases comparable to those observed during exercise; ventricular pacing had no significant effects on MEI. Finally, animals prone to VF had a significantly larger MEI response to exercise. Conclusions: These data suggest that β-AR activation during exercise can acutely enhance electrotonic coupling in the myocardium, particularly in dogs susceptible to ischemia-induced VF.
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DOI：
10.1016/0735-1097(93)90845-r
发表时间：
1993-07-01
影响因子：
24
作者：
DEFERRARI, GM;SALVATI, P;SCHWARTZ, PJ
通讯作者：
SCHWARTZ, PJ
影响因子：
--
作者：
COLLINS, MN;BILLMAN, GE
通讯作者：
BILLMAN, GE
影响因子：
10.8
作者：
BARNES, GE;HORWITZ, LD;BISHOP, VS
通讯作者：
BISHOP, VS
影响因子：
20.1
作者：
CASCIO, WE;YAN, GX;KLEBER, AG
通讯作者：
KLEBER, AG
结构异质性调节有效的难治期：局灶性心律不齐的机制。
影响因子：
3.7
作者：
Bishop MJ;Connolly A;Plank G
通讯作者：
Plank G