Department of Biomedical Engineering, National University of Singapore, 4 Engineering Drive 3, Singapore, 117583, Singapore.
Med Biol Eng Comput. 2024 Oct;62(10):3151-3161. doi: 10.1007/s11517-024-03128-6. Epub 2024 May 24.
The gastrointestinal (GI) peristalsis is an involuntary wave-like contraction of the GI wall that helps to propagate food along the tract. Many GI diseases, e.g., gastroparesis, are known to cause motility disorders in which the physiological contractile patterns of the wall get disrupted. Therefore, to understand the pathophysiology of these diseases, it is necessary to understand the mechanism of GI motility. We present a coupled electromechanical model to describe the mechanism of GI motility and the transduction pathway of cellular electrical activities into mechanical deformation and the generation of intraluminal pressure (IP) waves in the GI tract. The proposed model consolidates a smooth muscle cell (SMC) model, an actin-myosin interaction model, a hyperelastic constitutive model, and a Windkessel model to construct a coupled model that can describe the origin of peristaltic contractions in the intestine. The key input to the model is external electrical stimuli, which are converted into mechanical contractile waves in the wall. The model recreated experimental observations efficiently and was able to establish a relationship between change in luminal volume and pressure with the compliance of the GI wall and the peripheral resistance to bolus flow. The proposed model will help us understand the GI tract's function in physiological and pathophysiological conditions.
胃肠道（GI）蠕动是 GI 壁的一种非自愿的波浪状收缩，有助于将食物沿消化道传播。许多胃肠道疾病，例如胃轻瘫，已知会导致运动障碍，其中壁的生理收缩模式会被打乱。因此，为了了解这些疾病的病理生理学，有必要了解 GI 运动的机制。我们提出了一个耦合的机电模型来描述 GI 运动的机制和细胞电活动向机械变形的转导途径，以及在胃肠道中产生腔内压力（IP）波。所提出的模型整合了平滑肌细胞（SMC）模型、肌动球蛋白相互作用模型、超弹性本构模型和 Windkessel 模型，以构建一个可以描述肠蠕动收缩起源的耦合模型。该模型的关键输入是外部电刺激，它在壁中转化为机械收缩波。该模型有效地再现了实验观察结果，并能够在 GI 壁的顺应性和对射流的外周阻力与管腔容积和压力变化之间建立关系。该模型将帮助我们了解 GI 道在生理和病理生理条件下的功能。
