Van Lunteren Erik, Moyer Michelle, Pollarine Jennifer
Department of Pulmonary Medicine, Louis Stokes Cleveland Department of Veterans Affairs Medical Center, Cleveland, Ohio 44106, USA.
Muscle Nerve. 2008 Dec;38(6):1616-22. doi: 10.1002/mus.21045.
Blocking K(+) channels with aminopyridines enhances muscle contractile performance in vitro, but the improvements are relatively short-lasting during fatigue-inducing stimulation. We hypothesized that in vivo inotropic actions persist over long periods of fatigue-inducing stimulation. The effects of 3,4-diaminopyridine (DAP) were evaluated for rat extensor digitorum longus (EDL) muscle. DAP increased twitch force by 105%. There was a significant leftward shift in the force-frequency relationship, with force values being increased at frequencies up to and including 20 HZ. During repetitive fatigue-inducing 20-HZ stimulation, DAP-induced force increases were large and persisted significantly for at least 30 minutes. Thus, DAP substantially improves contractile performance of EDL muscle in vivo for much longer periods during fatigue-inducing contractions than in vitro. These data provide support for a potential role for aminopyridines as inotropic agents in applications such as functional electrical stimulation, in which low to medium stimulation frequencies are typically utilized.
用氨基吡啶阻断钾通道可增强体外肌肉收缩性能，但在诱导疲劳的刺激过程中，这种改善相对短暂。我们假设在体内，变力作用在长时间诱导疲劳的刺激过程中持续存在。评估了3,4-二氨基吡啶（DAP）对大鼠趾长伸肌（EDL）的影响。DAP使抽搐力增加了105%。力-频率关系显著向左偏移，在高达并包括20赫兹的频率下，力值增加。在重复性诱导疲劳的20赫兹刺激过程中，DAP诱导的力增加幅度很大，并且至少持续30分钟。因此，与体外情况相比，DAP在体内能在更长时间内显著改善EDL肌肉在诱导疲劳收缩过程中的收缩性能。这些数据为氨基吡啶在诸如功能性电刺激等应用中作为变力剂的潜在作用提供了支持，在功能性电刺激中通常使用低至中等刺激频率。
