Jiang Hongbo, Liao Donghua, Zhao Jingbo, Wang Guixue, Gregersen Hans
Key Laboratory for Biorheological Science and Technology of Ministry of Education, State and Local Joint Engineering Laboratory for Vascular Implants, Bioengineering College of Chongqing University, Chongqing, 400044, China.
GIOME, Bioengineering College of Chongqing University, Chongqing, 400044, China.
Biomech Model Mechanobiol. 2017 Jun;16(3):1065-1075. doi: 10.1007/s10237-017-0873-y. Epub 2017 Jan 23.
Significant stress softening recovery after potassium chloride (KCl) administration was previously demonstrated in the intact rat esophageal wall. The aim of this study is to investigate the effect of KCl activation on stress softening recovery in the separated mucosa-submucosa layer and muscle layer of rat esophagus. Three series of loading-unloading distensions were carried out on 10 rat esophagi where the two separated layers were distended at luminal pressure levels 0.5, 1.0 and 2.0 kPa. Numerous distension cycles were done in [Formula: see text]-free Krebs solution before and after activation with KCl (110 mmol) for 3 min in calcium-containing media. The diameter and luminal pressure were recorded for stress and strain calculation. During KCl activation, the muscle layer responded with a high-amplitude contraction, and the mucosa-submucosa layer responded with a longer-lasting low-amplitude contraction. The hysteresis loop areas from the muscle layer were significantly bigger than those from the mucosa-submucosa layer at distension pressures 1.0 and 2.0 kPa ([Formula: see text]). The calculated stiffness in the mucosa-submucosa layer was significantly higher than that in the muscle layer ([Formula: see text]). After activation with KCl, the stored energy and the stiffness after the stress and viscoelasticity softening increased in both layers, indicating that the reversible stress softening in esophagus after KCl activation is existed in both layers.
先前已证实在完整的大鼠食管壁中，给予氯化钾（KCl）后会出现显著的应力软化恢复。本研究的目的是探讨KCl激活对大鼠食管分离的黏膜 - 黏膜下层和肌层中应力软化恢复的影响。对10只大鼠食管进行了三组加载 - 卸载扩张实验，在管腔内压力水平为0.5、1.0和2.0 kPa的情况下，对两个分离的层进行扩张。在用含110 mmol KCl的含钙培养基激活3分钟前后，在无[公式：见原文]的Krebs溶液中进行了多次扩张循环。记录直径和管腔内压力以计算应力和应变。在KCl激活过程中，肌层出现高幅度收缩反应，黏膜 - 黏膜下层出现持续时间更长的低幅度收缩反应。在1.0和2.0 kPa的扩张压力下，肌层的滞后回线面积显著大于黏膜 - 黏膜下层的滞后回线面积（[公式：见原文]）。计算得出黏膜 - 黏膜下层的刚度显著高于肌层（[公式：见原文]）。用KCl激活后，两层中应力和粘弹性软化后的储能和刚度均增加，表明KCl激活后食管中两层均存在可逆的应力软化。
