Ludemann J P, Manoukian J, Shaw K, Bernard C, Davis M, al-Jubab A
Division of Pediatric Otolaryngology, Children's Memorial Hospital, Chicago, IL, USA.
J Otolaryngol. 1998 Jun;27(3):127-31.
Gastroesophageal reflux (GER) has been shown, clinically and experimentally, to cause inflammation of traumatized laryngeal mucosa. This study was performed to determine if GER causes inflammation of untraumatized laryngeal mucosa.
Sixteen adult New Zealand white rabbits underwent tube pharyngostomy under general anaesthesia without endotracheal intubation. After 7 days recovery, 1 mL/kg of normal saline or HCl (pH 1.5) with pepsin (0.3 mg/mL) was infused into the piriform sinus while the rabbit was under mild sedation: once, twice, or three times per day, for 14 consecutive days.
Rabbits that received HCl and pepsin exhibited various degrees of apnea and coughing. Eventually, most developed biphasic stridor on exertion. Histologically, the degree of laryngeal inflammation was greatest when GER was simulated three times per day. Glottic inflammation was greatest in one rabbit, which responded to GER simulation with paroxysmal coughing.
The mechanism of injury in GER laryngitis is postulated to be a combination of chemical trauma (due to HCl and pepsin) and mechanical trauma (due to an individually variable laryngeal chemoreflex). Further study of GER laryngitis in this new animal model is warranted.
临床及实验研究均已表明,胃食管反流(GER)可导致受损伤的喉黏膜发生炎症。本研究旨在确定GER是否会导致未受损伤的喉黏膜发生炎症。
16只成年新西兰白兔在全身麻醉且未行气管插管的情况下接受咽造瘘术。恢复7天后,在兔子轻度镇静状态下,将1 mL/kg的生理盐水或含胃蛋白酶(0.3 mg/mL)的盐酸(pH 1.5)注入梨状窝:每天1次、2次或3次,连续14天。
接受盐酸和胃蛋白酶的兔子出现了不同程度的呼吸暂停和咳嗽。最终,大多数兔子在用力时出现双相喘鸣。组织学检查显示,每天模拟GER 3次时喉炎程度最严重。一只兔子的声门炎症最严重,该兔子对GER模拟出现阵发性咳嗽。
GER性喉炎的损伤机制据推测是化学性创伤(由盐酸和胃蛋白酶引起)和机械性创伤(由个体差异的喉化学反射引起)的综合作用。有必要在这个新的动物模型中对GER性喉炎进行进一步研究。