Lee Il-Woo, Goh Eui-Kyung, Roh Hwan-Jung, Lee Chang-Hoon, Chung Brian J, Chon Kyong-Myong
Department of Otolaryngology, College of Medicine, Pusan National University, Busan, Korea.
Otol Neurotol. 2006 Apr;27(3):433-40. doi: 10.1097/00129492-200604000-00023.
It is generally accepted that cigarette smoke is a major risk factor for middle ear disease. However, the literature is void of articles addressing the direct relationship between cigarette smoke exposure and middle ear disease. Furthermore, there are many conflicting opinions concerning the role of cigarette smoke in the pathogenesis of middle ear disease. The purpose of this study was to evaluate the effects of cigarette smoke on the Eustachian tube mucosa.
Thirty healthy 150 to 230 g Sprague Dawley rats with normal middle ears were used. The animals were divided into six groups of five. Five experimental groups (N=5 each) were exposed to a domestic cigarette (This, tar 7.0 mg, nicotine 0.75 mg) every 30 minutes (total 2.5 hours, 5 cigarettes total) on a daily basis in a smoking chamber for 1, 2, 4, 6, or 8 weeks. A control group (N=5) was placed in the same chamber without exposure to cigarette smoke. After exposure, the animals were sacrificed and cross sections of the Eustachian tubes were prepared. Histologic changes of the Eustachian tube mucosa were observed through light and electron microscopes.
Loss of cilia, goblet cell depletion, and squamous metaplasia of the Eustachian tube mucosa were observed following exposure to smoke. The one- and two-week exposure groups demonstrated the greatest decrease in goblet cell counts. The eight-week exposure group showed recovery from this decrease. Squamous metaplasia was observed in all experimental groups and was most prominent in the eight-week exposure group.
These findings suggest that cigarette smoke directly affects Eustachian tube mucosa in the early stages of exposure. Some of the mucosal changes, however, were reversed during the latter stages of exposure. A mechanism different from that which occurs in the nasal cavity and trachea may be activated in the Eustachian tube after exposure to passive smoke. The protective function of the Eustachian tube may play some role in this mechanism.
人们普遍认为香烟烟雾是中耳疾病的主要危险因素。然而，文献中缺乏探讨香烟烟雾暴露与中耳疾病直接关系的文章。此外，关于香烟烟雾在中耳疾病发病机制中的作用存在许多相互矛盾的观点。本研究的目的是评估香烟烟雾对咽鼓管黏膜的影响。
使用30只体重150至230克、中耳正常的健康斯普拉格-道利大鼠。将动物分为六组，每组五只。五个实验组（每组n = 5）每天在吸烟室内每隔30分钟暴露于一支国产香烟（焦油7.0毫克，尼古丁0.75毫克）（共2.5小时，总计5支香烟），持续1、2、4、6或8周。一个对照组（n = 5）置于同一室内，不暴露于香烟烟雾。暴露后，处死动物并制备咽鼓管的横断面。通过光学显微镜和电子显微镜观察咽鼓管黏膜的组织学变化。
暴露于烟雾后，观察到咽鼓管黏膜纤毛丧失、杯状细胞减少和鳞状化生。一至两周暴露组杯状细胞计数下降最为明显。八周暴露组显示出这种下降的恢复。所有实验组均观察到鳞状化生，在八周暴露组中最为显著。
这些发现表明，香烟烟雾在暴露早期直接影响咽鼓管黏膜。然而，一些黏膜变化在暴露后期得到逆转。暴露于被动吸烟后，咽鼓管可能激活了一种不同于鼻腔和气管的机制。咽鼓管的保护功能可能在这一机制中发挥了一定作用。
