Yanping Zhang1, Xingwang Jiang2, Hao Chen2, Heyun Li3, Zhenhua Wang3, Yuankai Chen2, Li Li2. 1. Department of Otolaryngology, the 8th Medical Center of Chinese PLA General Hospital, Beijing 100091, China; College of Otolaryngology Head and Neck Surgery, Chinese PLA General Hospital, Beijing 100048, China; National Clinical Research Center for Otolaryngology Diseases, Beijing 100853, China. Electronic address: yanping309@yahoo.com. 2. Department of Otolaryngology, the 8th Medical Center of Chinese PLA General Hospital, Beijing 100091, China; College of Otolaryngology Head and Neck Surgery, Chinese PLA General Hospital, Beijing 100048, China; National Clinical Research Center for Otolaryngology Diseases, Beijing 100853, China. 3. Basic Medical College of Air Force Military Medical University, Xi'an 710032, China.
Abstract
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.
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.