Pickens D L, Schefft G, Thach B T
Edward Mallinckrodt Department of Pediatrics, Washington University School of Medicine, St. Louis, MO 63110.
Am Rev Respir Dis. 1988 Jan;137(1):113-8. doi: 10.1164/ajrccm/137.1.113.
We examined the hypothesis that most idiopathic prolonged apneic spells in preterm infants originate as a form of upper airway protective reflex. We elicited a previously described upper airway reflex in 10 sleeping preterm infants with apnea of prematurity by instilling physiologic saline into the oropharynx and recording respiration, heart rate, and swallowing. Immediately after a small pharyngeal bolus of warm saline, one or more of several characteristic airway reflex responses occurred with most stimulus trials. These responses included brief central apnea, swallowing, and obstructed inspiratory efforts. Intermittently, this response pattern was more extensive and resulted in prolonged apnea. We compared the frequency of prolonged apnea immediately after saline boluses with spontaneously occurring prolonged apnea and found that apnea frequency after saline was greater than spontaneous apnea frequency in all 10 infants (p less than 0.0025). Also, the incidence of prolonged apnea occurring immediately after saline stimuli was significantly greater than that after randomly delivered control stimuli (p less than 0.005). These observations indicate that saline can induce prolonged apnea. Swallowing, a distinctive feature of the chemoreflex, occurred during 76% of spontaneous prolonged apnea spells. Spontaneous and postsaline prolonged apnea were nearly identical with respect to general features and frequency of specific airway protective responses. We conclude that the majority of spontaneous prolonged apneic spells in preterm infants have multiple features that are characteristic of an exaggerated airway protective response to an upper airway fluid stimulus. Circumstantial evidence suggests that endogenous upper airway secretions may be an important source of stimuli-inducing apneic spells in preterm infants.
我们检验了这样一种假设，即早产儿中大多数特发性长时间呼吸暂停发作起源于一种上呼吸道保护性反射形式。我们通过向10名患有早产呼吸暂停的睡眠中的早产儿口咽部滴注生理盐水并记录呼吸、心率和吞咽情况，诱发了一种先前描述的上呼吸道反射。在一小团温热盐水进入咽部后，大多数刺激试验立即出现了几种特征性气道反射反应中的一种或多种。这些反应包括短暂的中枢性呼吸暂停、吞咽和吸气受阻。间歇性地，这种反应模式更为广泛，导致呼吸暂停延长。我们将生理盐水推注后立即出现的长时间呼吸暂停频率与自发出现的长时间呼吸暂停频率进行了比较，发现所有10名婴儿在推注生理盐水后的呼吸暂停频率均高于自发呼吸暂停频率（p小于0.0025）。此外，生理盐水刺激后立即出现的长时间呼吸暂停发生率显著高于随机给予的对照刺激后（p小于0.005）。这些观察结果表明生理盐水可诱发长时间呼吸暂停。吞咽是化学反射的一个显著特征，在76%的自发长时间呼吸暂停发作期间出现。自发和推注生理盐水后的长时间呼吸暂停在一般特征和特定气道保护反应频率方面几乎相同。我们得出结论，早产儿中大多数自发的长时间呼吸暂停发作具有多种特征，这些特征是对上呼吸道液体刺激的过度气道保护反应所特有的。间接证据表明，内源性上呼吸道分泌物可能是诱发早产儿呼吸暂停发作的重要刺激源。
