Grønbech J E, Lacy E R
Department of Cell Biology and Anatomy, Medical University of South Carolina, Charleston, USA.
Gastroenterology. 1996 Dec;111(6):1474-83. doi: 10.1016/s0016-5085(96)70008-2.
BACKGROUND & AIMS: Gastric mucosal hyperemia is a protective response mediated at least in part by the response of sensory afferent neurons to hydrogen ions. The aim of this study was to determine if other pathways to the hyperemic response are present and if these neurons have an effect exclusive of hyperemia on mucosal protection and repair.
Rat sensory afferent neurons were ablated by capsaicin treatment. Chambered stomachs were damaged by hypertonic saline followed by either acidic or neutral isotonic saline. Blood flow was measured by laser Doppler velocimetry, and mucosal morphology was quantitatively evaluated by microscopy.
Mucosal damage alone evoked a strong hyperemic response in both control and ablated rats. Ablated rats lost gastric protection despite this hyperemic response. Acid exposure after damage sustained the hyperemic response. Rapid epithelial restitution occurred faster (even over hemorrhagic lesions) in control rats.
The hyperemic response to mucosal damage alone is not mediated by sensory neurons. Protection of the stomach by sensory afferent neurons occurs by mechanisms also unrelated to their elicitation of hyperemia. Restitution during acid challenge is enhanced by the sustained hyperemic response mediated through sensory afferent neurons.
胃黏膜充血是一种至少部分由感觉传入神经元对氢离子的反应介导的保护性反应。本研究的目的是确定是否存在其他导致充血反应的途径,以及这些神经元对黏膜保护和修复是否具有除充血之外的其他作用。
通过辣椒素处理消融大鼠感觉传入神经元。用高渗盐水损伤有腔胃,随后分别给予酸性或中性等渗盐水。采用激光多普勒测速仪测量血流量,并用显微镜对黏膜形态进行定量评估。
仅黏膜损伤在对照大鼠和消融大鼠中均引发强烈的充血反应。尽管有这种充血反应,消融大鼠仍失去了胃保护作用。损伤后酸暴露使充血反应持续。对照大鼠中快速上皮修复(甚至在出血性病变上)发生得更快。
仅对黏膜损伤的充血反应并非由感觉神经元介导。感觉传入神经元对胃的保护作用是通过与它们引发充血无关的机制实现的。在酸刺激期间,通过感觉传入神经元介导的持续充血反应可增强修复作用。