Mayer E A, Raybould H, Koelbel C
Department of Medicine, Harbor-UCLA Medical Center, Torrance 90509.
Dig Dis Sci. 1988 Mar;33(3 Suppl):71S-77S. doi: 10.1007/BF01538134.
Neurogenic inflammation is a reaction which includes vasodilation, plasma extravasation, and smooth muscle contraction elicited by activation of and release of mediators from unmyelinated afferent nerve endings. Further release of inflammatory mediators follows activation of axon collaterals associated with these afferent nerve endings as axon reflexes. Substance P, somatostatin, vasoactive intestinal polypeptide, and calcitonin gene-related peptide are candidate mediators. Recent evidence suggests that several of these peptides may be colocalized either with one or more other peptides or with acetylcholine or noradrenalin. Communicating pathways exist between nerves within the mucosa and the muscle layers. Both long and short visceral reflexes occur. Inflammatory, mechanical, or chemical stimuli reaching the mucosa may release peptides from peripheral nerve endings. Thus neurogenic inflammation may be an important factor in inflammatory bowel disease.
神经源性炎症是一种反应,包括由无髓传入神经末梢激活并释放介质所引发的血管舒张、血浆外渗和平滑肌收缩。随着轴突反射激活与这些传入神经末梢相关的轴突侧支,炎症介质会进一步释放。P物质、生长抑素、血管活性肠多肽和降钙素基因相关肽是候选介质。最近的证据表明,这些肽中的几种可能与一种或多种其他肽或与乙酰胆碱或去甲肾上腺素共定位。黏膜内神经与肌层之间存在沟通途径。长、短内脏反射均会发生。到达黏膜的炎症、机械或化学刺激可能会从外周神经末梢释放肽。因此,神经源性炎症可能是炎症性肠病的一个重要因素。