The Journal of otolaryngology · 1998
Effects of simulated gastroesophageal reflux on the untraumatized rabbit larynx.
СтатьяНазвание и аннотация: Перевод в очереди
Обработка статьи · этапы, ошибки и управление
Загрузка состояния…
Ошибки и ограничения
История · было → стало
Состояние обновляется каждые 5 секунд, пока блок открыт. Процент показывается только там, где известен объём работы. Пауза останавливает продолжение этапа; текущий запрос к источнику может завершиться.
Ludemann J P, Manoukian J, Shaw K, Bernard C, Davis M, al-Jubab A
Аннотация
OBJECTIVE: 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.
METHOD: 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.
RESULTS: 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.
CONCLUSION: 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.
METHOD: 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.
RESULTS: 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.
CONCLUSION: 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.