G. O'Grady: Auckland Bioengineering Institute, Private Bag 92019, Auckland 1142, New Zealand.
J Physiol. 2013 Sep 15;591(18):4567-79. doi: 10.1113/jphysiol.2013.254292. Epub 2013 May 27.
Gastrointestinal extracellular recordings have been a core technique in motility research for a century. However, the bioelectrical basis of extracellular data has recently been challenged by claims that these techniques preferentially assay movement artifacts, cannot reproduce the underlying slow wave kinetics, and misrepresent the true slow wave frequency. These claims motivated this joint experimental-theoretical study, which aimed to define the sources and validity of extracellular potentials. In vivo extracellular recordings and video capture were performed in the porcine jejunum, before and after intra-arterial nifedipine administration. Gastric extracellular recordings were recorded simultaneously using conventional serosal contact and suction electrodes, and biphasic and monophasic extracellular potentials were simulated in a biophysical model. Contractions were abolished by nifedipine, but extracellular slow waves persisted, with unchanged amplitude, downstroke rate, velocity, and downstroke width (P>0.10 for all), at reduced frequency (24% lower; P=0.03). Simultaneous suction and conventional serosal extracellular recordings were identical in phase (frequency and activation-recovery interval), but varied in morphology (monophasic vs. biphasic; downstroke rate and amplitude: P<0.0001). Simulations demonstrated the field contribution of current flow to extracellular potential and quantified the effects of localised depolarisation due to suction pressure on extracellular potential morphology. In sum, these results demonstrate that gastrointestinal extracellular slow wave recordings cannot be explained by motion artifacts, and are of a bioelectrical origin that is highly consistent with the underlying biophysics of slow wave propagation. Motion suppression is shown to be unnecessary as a routine control in in vivo extracellular studies, supporting the validity of the extant gastrointestinal extracellular literature.
胃肠道细胞外记录技术已经成为一个世纪以来运动研究的核心技术。然而,这些技术主要检测运动伪迹、不能重现潜在慢波动力学、以及错误表示真实慢波频率等观点,对细胞外数据的生物电基础提出了质疑。这些观点促使我们进行了这项联合实验-理论研究,旨在确定细胞外电位的来源和有效性。在猪空肠中进行了体内细胞外记录和视频捕获,在动脉内给予硝苯地平前后进行。同时使用传统的浆膜接触和抽吸电极记录胃细胞外记录,并在生物物理模型中模拟双相和单相细胞外电位。硝苯地平消除了收缩,但细胞外慢波仍然存在,幅度、下降速度、速度和下降宽度不变(所有 P>0.10),频率降低(低 24%;P=0.03)。同时进行的抽吸和传统浆膜细胞外记录在相位(频率和激活恢复间期)上是相同的,但在形态上有所不同(单相与双相;下降速度和幅度:P<0.0001)。模拟表明了电流流动对细胞外电位的场贡献,并量化了抽吸压力引起的局部去极化对细胞外电位形态的影响。总之,这些结果表明,胃肠道细胞外慢波记录不能用运动伪迹来解释,而是具有与慢波传播的潜在生物物理学高度一致的生物电起源。运动抑制被证明在体内细胞外研究中作为常规对照是不必要的,支持现有的胃肠道细胞外文献的有效性。