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幼龄动物和人类婴儿胃食管反流及气道保护反应的生理学研究。

Physiological studies of gastro-oesophageal reflux and airway protective responses in the young animal and human infant.

作者信息

Jeffery H E, Page M, Post E J, Wood A K

机构信息

Department of Perinatal Medicine, University of Sydney, New South Wales, Australia.

出版信息

Clin Exp Pharmacol Physiol. 1995 Aug;22(8):544-9. doi: 10.1111/j.1440-1681.1995.tb02064.x.

Abstract
  1. The mechanisms that underlie the Sudden Infant Death Syndrome (SIDS) must explain its two unique features; age at death and death during apparent sleep. 2. The occurrence of gastro-oesophageal reflux (GOR) during active sleep in infants presenting with apparent life threatening episodes (ALTE) and their similar age distribution to SIDS infants, suggested that reflux could be a cause of asphyxia. 3. Sleep related GOR was found to be a physiological and not a pathological event in normal, healthy term infants. 4. In healthy term infants, those infants that were formula-fed (who have a higher incidence of SIDS) had significantly longer oesophageal clearance times for acid reflux and significantly more active sleep compared with breast fed infants. 5. In very preterm infants (who are at increased risk for SIDS), both the frequency and duration of reflux during active sleep was significantly less at term equivalent age compared with healthy term infants, suggesting additional factors must operate to promote an ALTE. 6. One mechanism which may explain the pathogenesis of GOR could be that the reflux reaches the level of the pharynx and this, in turn, stimulates laryngeal receptors to produce apnoea. 7. Simulated reflux to the level of the pharynx in the sleeping piglet evoked airway protective responses, namely swallow, arousal and occasionally expectoration, but neither apnoea nor oxygen desaturation. 8. In the same piglets treated with pentobarbitone sodium, swallowing was impaired and arousal depressed. Simulated reflux to the pharynx produced significant apnoea and oxygen desaturation and death in two of five piglets.(ABSTRACT TRUNCATED AT 250 WORDS)
摘要
  1. 婴儿猝死综合征(SIDS)的潜在机制必须解释其两个独特特征:死亡年龄和在看似睡眠期间死亡。2. 在出现明显危及生命事件(ALTE)的婴儿的活跃睡眠期间发生胃食管反流(GOR),且其年龄分布与SIDS婴儿相似,这表明反流可能是窒息的一个原因。3. 在正常、健康的足月儿中,与睡眠相关的GOR被发现是一种生理而非病理事件。4. 在健康足月儿中,与母乳喂养的婴儿相比,人工喂养的婴儿(SIDS发病率较高)酸反流的食管清除时间明显更长,且活跃睡眠明显更多。5. 在极早产儿(SIDS风险增加)中,与健康足月儿相比,在相当于足月年龄时,活跃睡眠期间反流的频率和持续时间明显更少,这表明必须有其他因素起作用来引发ALTE。6. 一种可能解释GOR发病机制的机制可能是反流到达咽部水平,进而刺激喉部感受器产生呼吸暂停。7. 对睡眠中的仔猪模拟反流至咽部水平会引发气道保护反应,即吞咽、觉醒,偶尔还有咳痰,但不会引发呼吸暂停或氧饱和度下降。8. 在用戊巴比妥钠治疗的同一批仔猪中,吞咽功能受损,觉醒受到抑制。模拟反流至咽部会导致五头仔猪中的两头出现明显的呼吸暂停、氧饱和度下降并死亡。(摘要截断于250字)

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