Greiff L, Wollmer P, Erjefält I, Andersson M, Pipkorn U, Persson C G
Department of Otorhinolaryngology, University Hospital of Lund, Sweden.
Thorax. 1993 Jun;48(6):651-5. doi: 10.1136/thx.48.6.651.
Topical application of nicotine and stimulation of tachykinin containing sensory nerves have been shown to produce mucosal exudation of plasma and derangement of the epithelial lining in guinea pig and rat airways. If this occurred in man these effects might contribute to the pathogenesis of airway disease. This study, performed in healthy volunteers without atopy, examined whether nicotine affects the plasma exudation response and the mucosal absorption permeability of the human nasal airway.
The acute effects of increasing topical doses of nicotine (0.08-2.0 mg) were examined (n = 8) on nasal symptoms (pain), mucosal exudation of plasma (albumin), mucosal secretion of mucin (fucose), and mucosal exudative responsiveness (histamine induced mucosal exudation of albumin). A separate placebo controlled study was carried out to determine whether frequent applications of the high dose of nicotine (2.0 mg given eight times daily for nine days) had any deleterious effects on the airway mucosa detectable as altered responses to histamine challenge. Both mucosal exudation of plasma (n = 12) and mucosal absorption of chromium-51 labelled EDTA (n = 8) were thus examined in nasal airways exposed to both nicotine and histamine.
Nicotine caused nasal pain and produced dose dependent mucosal secretion of fucose but failed to produce any mucosal exudation of albumin. The exudative responsiveness to histamine was, indeed, decreased when the challenge was performed immediately after administration of acute doses of nicotine, whereas the responsiveness was unaffected when histamine challenges were carried out during prolonged treatment with nicotine. The nasal mucosal absorption of 51Cr-EDTA in the presence of histamine did not differ between subjects receiving either placebo or nicotine treatment for nine days.
The results indicate that nicotine applied to the human airway mucosa produces pain and secretion of mucin, but inflammatory changes such as mucosal exudation of plasma and epithelial disruption may not be produced. Neurogenic inflammatory responses, which are so readily produced in guinea pig and rat airways, may not occur in human airways.
已表明在豚鼠和大鼠气道中，局部应用尼古丁以及刺激含速激肽的感觉神经会导致血浆黏膜渗出和上皮内衬紊乱。如果这种情况发生在人类身上，这些效应可能会导致气道疾病的发病机制。本研究在无特应性的健康志愿者中进行，旨在研究尼古丁是否会影响人鼻气道的血浆渗出反应和黏膜吸收通透性。
研究了递增局部剂量尼古丁（0.08 - 2.0毫克）的急性效应（n = 8），包括对鼻部症状（疼痛）、血浆黏膜渗出（白蛋白）、黏蛋白黏膜分泌（岩藻糖）以及黏膜渗出反应性（组胺诱导的白蛋白黏膜渗出）的影响。开展了一项单独的安慰剂对照研究，以确定频繁应用高剂量尼古丁（每天8次，每次2.0毫克，共9天）是否会对气道黏膜产生任何有害影响，可通过对组胺激发的反应改变来检测。因此，在暴露于尼古丁和组胺的鼻气道中，对血浆黏膜渗出（n = 12）和51铬标记的乙二胺四乙酸（51Cr - EDTA）的黏膜吸收（n = 8）进行了检测。
尼古丁导致鼻部疼痛，并产生剂量依赖性的岩藻糖黏膜分泌，但未引起白蛋白的任何黏膜渗出。当在急性剂量尼古丁给药后立即进行激发时，对组胺的渗出反应性确实降低，而在尼古丁长期治疗期间进行组胺激发时，反应性未受影响。在组胺存在的情况下，接受安慰剂或尼古丁治疗9天的受试者之间，51Cr - EDTA的鼻黏膜吸收没有差异。
结果表明，应用于人类气道黏膜的尼古丁会产生疼痛和黏蛋白分泌，但可能不会产生血浆黏膜渗出和上皮破坏等炎症变化。在豚鼠和大鼠气道中容易产生的神经源性炎症反应，在人类气道中可能不会发生。
