High-Energy Pacing Inhibits Slow Wave Dysrhythmias in the Small Intestine

Nipuni D. Nagahawatte, Recep Avci, Niranchan Paskaranandavadivel, Leo K. Cheng
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Abstract

The motility of the gastrointestinal tract is coordinated in part by rhythmic slow waves, and disrupted slow wave patterns are linked to functional motility disorders. At present, there are no treatment strategies that primarily target slow wave activity. This study assessed the use of pacing to suppress glucagon-induced slow wave dysrhythmias in the small intestine. Slow waves in the jejunum were mapped in vivo using a high-resolution surface-contact electrode array in pigs (n=7). Glucagon was intravenously administered to induce hyperglycemia. Slow wave propagation patterns were categorized into antegrade, retrograde, collision, pacemaker and uncoupled activity. Slow wave characteristics such as period, amplitude and speed were also quantified. Post-glucagon infusion, pacing was applied at 4 mA and 8 mA and the resulting slow waves were quantified spatiotemporally. Antegrade propagation was dominant throughout all stages with a prevalence of 55 ± 38% at baseline. However, glucagon infusion resulted in a substantial and significant increase in uncoupled slow waves from 10 ± 8% to 30 ± 12% (p=0.004) without significantly altering the prevalence of other slow wave patterns. Slow wave frequency, amplitude and speed remained unchanged. Pacing, particularly at 8 mA, significantly suppressed dysrhythmic slow wave patterns and achieved more effective spatial entrainment (85%) compared to 4 mA (46%, p=0.039).This study defined the effect of glucagon on jejunal slow waves and identified uncoupling as a key dysrhythmia signature. Pacing effectively entrained rhythmic activity and suppressed dysrhythmias, highlighting the potential of pacing for gastrointestinal disorders associated with slow wave abnormalities.
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高能起搏抑制小肠慢波心律失常
胃肠道的蠕动部分是由节律性慢波协调的,慢波模式的紊乱与功能性蠕动障碍有关。目前,还没有主要针对慢波活动的治疗策略。本研究评估了使用起搏来抑制胰高血糖素诱发的小肠慢波节律失常。使用高分辨率表面接触电极阵列在猪体内绘制了空肠慢波图(7 头)。通过静脉注射胰高血糖素诱发高血糖。慢波传播模式分为前向、逆行、碰撞、起搏和非耦合活动。此外,还对慢波的周期、振幅和速度等特征进行了量化。输注胰高血糖素后,以 4 mA 和 8 mA 的电流起搏,并对由此产生的慢波进行时空量化。在所有阶段中,前向传播均占主导地位,基线发生率为 55 ± 38%。然而,输注胰高血糖素会导致非耦合慢波从 10 ± 8% 显著增加到 30 ± 12%(p=0.004),而不会显著改变其他慢波模式的发生率。慢波频率、振幅和速度保持不变。与 4 毫安(46%,p=0.039)相比,起搏(尤其是 8 毫安)可明显抑制节律失常的慢波模式,并实现更有效的空间抑制(85%)。该研究明确了胰高血糖素对空肠慢波的影响,并确定解偶联是关键的节律失常特征。起搏能有效控制节律活动并抑制节律失常,突出了起搏治疗与慢波异常相关的胃肠道疾病的潜力。
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