Lundberg J M, Brodin E, Hua X, Saria A
Acta Physiol Scand. 1984 Feb;120(2):217-27. doi: 10.1111/j.1748-1716.1984.tb00127.x.
The occurrence of neurogenic inflammation as indicated by Evans blue extravasation was studied in various organs of the guinea-pig. Electrical stimulation of the trigeminal nerve caused Evans blue extravasation due to increased vascular permeability in the nasal mucosa and gingiva. Vagal stimulation induced extravasation in the epiglottis, larynx, trachea, bronchial tree and esophagus. Splanchnic stimulation induced Evans blue extravasation in the gall bladder, bile ducts and superior mesenteric artery. Stimulation of the inferior mesenteric ganglion caused a marked extravasation in the upper and middle part of both ureters, while pelvic activation induced a reaction in the lower ureter, urinary bladder, urethra and vagina. I.v. substance P (SP) (3 nmol X kg11) or capsaicin (1 mumol X kg-1) both induced extravasation in many tissues including those in which nerve stimulation produced a response. The extravasation responses to SP, capsaicin or nerve stimulation all had similar border-line zones, such as esophagus to stomach, bile ducts to duodenum, rectum to anal mucosa, pulmonary artery to heart and vagina to uterus. Quantitative determinations showed especially large permeability effects in the trachea, umbilical ligament and ureter. The permeability effect of capsaicin and nerve stimulation was abolished in capsaicin-pretreated animals, while the response to SP was still present. Capsaicin pretreatment caused an almost total loss of SP in several visceral organs including the respiratory and urinary tracts. The SP content in these tissues was correlated (r = 0.97) to the Evans blue extravasation following nerve stimulation or i.v. capsaicin. SP and capsaicin caused contractions in vitro of the esophagus, ureter, urinary bladder, trachea and gall bladder. The capsaicin-induced contraction of the trachea was resistant to tetrodotoxin pretreatment. The non-cholinergic, non-adrenergic contraction of the urinary bladder upon field stimulation was still present in capsaicin-pretreated animals. In conclusion, neurogenic inflammation occurs in several organs with a highly region-specific distribution, which is accompanied by the presence of capsaicin-sensitive SP neurons. Both parasympathetic and sympathetic pathways contain capsaicin-sensitive afferent fibres which mediate an increase in vascular permeability most likely by releasing SP. In addition, both capsaicin and SP cause smooth muscle contraction in several visceral organs.
通过伊文思蓝外渗来指示的神经源性炎症在豚鼠的各个器官中的发生情况得到了研究。三叉神经的电刺激会导致伊文思蓝外渗，这是由于鼻黏膜和牙龈中的血管通透性增加所致。迷走神经刺激会在会厌、喉、气管、支气管树和食管中诱发外渗。内脏神经刺激会在胆囊、胆管和肠系膜上动脉中诱发伊文思蓝外渗。刺激肠系膜下神经节会在双侧输尿管的上中部引起明显的外渗，而盆腔激活会在输尿管下段、膀胱、尿道和阴道中诱发反应。静脉注射P物质（SP）（3 nmol·kg⁻¹）或辣椒素（1 μmol·kg⁻¹）都会在许多组织中诱发外渗，包括那些神经刺激会产生反应的组织。对SP、辣椒素或神经刺激的外渗反应都有类似的边界区域，如食管与胃、胆管与十二指肠、直肠与肛门黏膜、肺动脉与心脏以及阴道与子宫。定量测定表明，在气管、脐韧带和输尿管中通透性效应尤为显著。在辣椒素预处理的动物中，辣椒素和神经刺激的通透性效应被消除，而对SP的反应仍然存在。辣椒素预处理导致包括呼吸道和泌尿道在内的几个内脏器官中SP几乎完全丧失。这些组织中的SP含量与神经刺激或静脉注射辣椒素后的伊文思蓝外渗相关（r = 0.97）。SP和辣椒素在体外会引起食管、输尿管、膀胱、气管和胆囊的收缩。辣椒素诱发的气管收缩对河豚毒素预处理具有抗性。在辣椒素预处理的动物中，场刺激时膀胱的非胆碱能、非肾上腺素能收缩仍然存在。总之，神经源性炎症在几个器官中发生，具有高度的区域特异性分布，同时伴有对辣椒素敏感的SP神经元的存在。副交感神经和交感神经通路都含有对辣椒素敏感的传入纤维，它们最有可能通过释放SP来介导血管通透性的增加。此外，辣椒素和SP都会在几个内脏器官中引起平滑肌收缩。
