Auris, nasus, larynx · 2020
Chronic REM-sleep deprivation induced laryngopharyngeal reflux in rats: A preliminary study.
СтатьяНазвание и аннотация: Перевод пока не подготовлен
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.
Zhang Yanping, Jiang Xingwang, Chen Hao, Li Heyun, Wang Zhenhua, Chen Yuankai, Li Li
Аннотация
OBJECTIVE: The aim of this study was to investigate the relationship of chronic REM-sleep deprivation with laryngopharyngeal reflux (LPR) and its mechanism.
METHODS: Forty healthy male SD rats (body weight 250-280 g) were randomly divided into four groups. The first three ones were test group, which underwent REM-sleep deprivation with different duration of time by modified multiplatform water surface method. The last group was the control one having normal sleep. All the animals were performed Dx-pH monitoring when finishing sleep deprivation, and sacrificed to study the gastric residual rate (GRR) and small intestine peristalsis (SPR) rate by charcoal meal method.
RESULTS: At prone position, the reflux incidence in the test groups fairly increased with the duration of sleep deprivation (p<0.05). The total number of reflux episodes at prone position in the test group rats with 3 months duration of sleep deprivation was significantly increased compared with that in the control ones (p<0.05). GRR in rats experiencing sleep deficiency for different duration all reduced significantly when compared to the control group (p<0.05). GRR and SPR presented continuous decline tendency with the duration of sleep deprivation (p>0.05).
CONCLUSIONS: It is suggested that chronic sleep deficiency could cause LPR in rats, which might result from the uncoordinated digestive tract motility caused by dysfunction of central nervous system after chronic REM-sleep deprivation. Our results implied that chronic REM-sleep deprivation might be one of the causes of LPR. Addressing sleep problems might help to decrease the prevalence of LPR and enhance its treatment efficacy.
METHODS: Forty healthy male SD rats (body weight 250-280 g) were randomly divided into four groups. The first three ones were test group, which underwent REM-sleep deprivation with different duration of time by modified multiplatform water surface method. The last group was the control one having normal sleep. All the animals were performed Dx-pH monitoring when finishing sleep deprivation, and sacrificed to study the gastric residual rate (GRR) and small intestine peristalsis (SPR) rate by charcoal meal method.
RESULTS: At prone position, the reflux incidence in the test groups fairly increased with the duration of sleep deprivation (p<0.05). The total number of reflux episodes at prone position in the test group rats with 3 months duration of sleep deprivation was significantly increased compared with that in the control ones (p<0.05). GRR in rats experiencing sleep deficiency for different duration all reduced significantly when compared to the control group (p<0.05). GRR and SPR presented continuous decline tendency with the duration of sleep deprivation (p>0.05).
CONCLUSIONS: It is suggested that chronic sleep deficiency could cause LPR in rats, which might result from the uncoordinated digestive tract motility caused by dysfunction of central nervous system after chronic REM-sleep deprivation. Our results implied that chronic REM-sleep deprivation might be one of the causes of LPR. Addressing sleep problems might help to decrease the prevalence of LPR and enhance its treatment efficacy.