Pathophysiology of Sudden Upper Airway Obstruction in Sleeping Infants and Its Relevance for SIDS<sup>a</sup>

Thach, Bradley T.; Davies, Alison; Koenig, Joel

doi:10.1111/j.1749-6632.1988.tb37261.x

Cited by 25 publications

(12 citation statements)

References 32 publications

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“…This may increase the risk for SIDS-e.g., by interference with other chemoreflexes such as vagal laryngeal chemoreflexes (49,50), a situation that, in fact, has been suggested to relate to SIDS (49,(51)(52)(53)(54). Corroborating this idea is the finding that some infants who have suffered from chronic lung disease, a group of children that are at high risk of dying of SIDS, show a depressed hyperoxic response (55).…”

Section: Discussionmentioning

confidence: 99%

“…The present data also suggest that nicotine may interfere with the postnatal resetting of these receptors. Thus, two possible mechanisms are proposed by which nicotine from smoking may interfere with the first line of defense against hypoxia (9-11) and may lead to SIDS, either alone or by interference with other reflexes (49,(51)(52)(53)(54).…”

Section: Discussionmentioning

confidence: 99%

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Functional and developmental studies of the peripheral arterial chemoreceptors in rat: effects of nicotine and possible relation to sudden infant death syndrome.

Holgert

Hökfelt

Hertzberg

et al. 1995

Proc. Natl. Acad. Sci. U.S.A.

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The drive on respiration mediated by the peripheral arterial chemoreceptors was assessed by the hyperoxic test in 3-day-old rat pups. They accounted for 22.5 ± 8.8% during control conditions, but only for 6.9 + 10.0% after nicotine exposure, an effect counteracted by blockade of peripheral dopamine type 2 receptors (DA2Rs). Furthermore, nicotine reduced dopamine (DA) content and increased the expression of tyrosine hydroxylase (TH) in the carotid bodies, further suggesting that DA mediates the acute effect of nicotine on arterial chemoreceptor function. During postnatal development TH and DA2R mRNA levels in the carotid bodies decreased. Thus, nicotine from smoking may also interfere with the postnatal resetting of the oxygen sensitivity of the peripheral arterial chemoreceptors by increasing carotid body TH mRNA, as well as DA release in this period. Collectively these effects of nicotine on the peripheral arterial chemoreceptors may increase the vulnerability to hypoxic episodes and attenuate the protective chemoreflex response. These mechanisms may underlie the well-known relation between maternal smoking and sudden infant death syndrome.Epidemiological studies have shown a dose-dependent relationship between maternal smoking and sudden infant death syndrome (SIDS) (1-6). However, no clear mechanism(s) explaining this relation has been identified. Among numerous compounds present in cigarette smoke, nicotine is of particular interest, since it acts on the peripheral arterial chemoreceptors (7, 8), the most important organs in the defense against hypoxia (9-11). A deficient function of these chemoreceptors has been suggested to be one factor contributing to . This suggestion is supported by the findings that carotid body denervation caused unexpected death not only in lambs at 4-5 weeks of age (15, 16) but also in some children with asthma who were "treated" with bilateral carotid body resection (17). Moreover, denervation impaired survival of infant rats (18) and piglets (19). Nicotine is readily transferred in high concentrations to the fetus via the placenta and to the infant by the breast milk (20-23). In fact, a majority (-75%) of infants who succumbed by SIDS in Stockholm were exposed to nicotine shortly prior to death (24); this should be compared with the fact that only 18% of the mothers in Sweden smoke (25).High levels of dopamine (DA) have been found in carotid bodies of SIDS victims (13). This may be of relevance, since DA modulates peripheral arterial chemoreceptor activity in most species, including rats (26) and humans (27,28), and since DA is probably involved in the postnatal resetting of the peripheral arterial chemoreceptors from the low fetal to the high adult sensitivity (29-31). Furthermore, nicotine induces synthesis and release of carotid body DA in vitro (8). In vivo this effect of nicotine may interfere with the dopaminergic modulation of the hypoxic defense and with the postnatal development of the peripheral arterial chemoreceptors and thus relate smoking to SIDS.The present...

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Section: Discussionmentioning

confidence: 99%

Section: Discussionmentioning

confidence: 99%

Functional and developmental studies of the peripheral arterial chemoreceptors in rat: effects of nicotine and possible relation to sudden infant death syndrome.

Holgert

Hökfelt

Hertzberg

et al. 1995

Proc. Natl. Acad. Sci. U.S.A.

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“…In infancy, babies with recurrent and prolonged sleep apnoeas were more lethargic [5], more exhausted at feeding [23], had abnormal spontaneous movements [9], and sometimes were even developmentally delayed [30]. Obstructive sleep apnoeas in infants were implicated in the mechanisms of sudden infant death (SID) [21,37,38], and it was shown that some SID victims had certain behavioural peculiarities including less activity [26], less intense reactions to environmental stimuli, and more abnormal cries [9,33]. Partial or complete repetitive obstructions of the upper airway during sleep in infants give rise to clinical symptoms associated with chronic snoring.…”

Section: Introductionmentioning

confidence: 99%

Snoring, noisy breathing in sleep and daytime behaviour in 2–4-month-old infants

Kelmanson

2000

Eur J Pediatr

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“…Inefficient breathing efforts induce drops in heart rates, cardiac output, and transcuta neous oxygen saturation values [23,27,34], Occasional reports in children indicate that repeated obstructive apneas may lead to pul monary edema, hypertension, and congestive heart failure. Pulmonary or systemic hyper tension, and polycythemia may also develop [2,21,26], Repeated obstructive apneas have also been associated with the occurrence of sudden deaths in infants [9,[35][36][37],…”

Section: Clinical Consequences Of Obstructive Apneasmentioning

confidence: 99%

“…Both its sympathetic and para sympathetic components could be involved [22][23][24]. Obstructed sleep apneas were re ported in children suffering from various au tonomic nervous system disorders, including familial dysautonomia, diabetes, ganglioneu roma, Shy-Drager syndrome, and breath holding spells [25][26][27][28] …”

Section: Factors Associated With Sleep Apneasmentioning

confidence: 99%

Mechanisms of Obstructive Sleep Apneas in Infants

et al. 1994

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During sleep, infants with obstructive sleep apneas are characterised by snoring, laborious breathing, and profuse sweating. During wakefulness, they may have breath-holding spells, and during feeding, difficult breathing and swallowing coordination. Abnormal weight, difficult growth, and recurring ear infections may also develop. During sleep apneas, cinefiuoroscopy shows approximation of tongue and hypopharyngeal tissues, with an obliteration of the air space. The obstructed breaths occur mainly in REM, and light NREM sleep, associated with total short sleep time, and frequent arousals. Preterm infants, and term neonates are more prone to obstructive apneas than older healthy infants. Apneas are more frequently seen in boys and in case of excess in body weight. Obstructive apneas are frequently associated with upper airway anatomic abnormalities: malformations, soft tissue infiltration, and neurologic lesions impairing muscle contractions. Alterations of the autonomic nervous control may induce airways obstructions. Contributing factors include mucopolysaccharide storage disease, hypothyroidism, or Down’s syndrome. Superimposed factors may occur, such as nasal obstruction, secretions in the airways, or tissue edema. Pressure- and chemo-sensitive reflexes may also favor obstruction. Environmental factors also contribute to the development of sleep apneas: body position, neck flexion, sleep deprivation, or the effects of sedative drugs.

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Pathophysiology of Sudden Upper Airway Obstruction in Sleeping Infants and Its Relevance for SIDS^a

Cited by 25 publications

References 32 publications

Functional and developmental studies of the peripheral arterial chemoreceptors in rat: effects of nicotine and possible relation to sudden infant death syndrome.

Functional and developmental studies of the peripheral arterial chemoreceptors in rat: effects of nicotine and possible relation to sudden infant death syndrome.

Snoring, noisy breathing in sleep and daytime behaviour in 2–4-month-old infants

Mechanisms of Obstructive Sleep Apneas in Infants

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Pathophysiology of Sudden Upper Airway Obstruction in Sleeping Infants and Its Relevance for SIDSa

Cited by 25 publications

References 32 publications

Functional and developmental studies of the peripheral arterial chemoreceptors in rat: effects of nicotine and possible relation to sudden infant death syndrome.

Functional and developmental studies of the peripheral arterial chemoreceptors in rat: effects of nicotine and possible relation to sudden infant death syndrome.

Snoring, noisy breathing in sleep and daytime behaviour in 2–4-month-old infants

Mechanisms of Obstructive Sleep Apneas in Infants

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Pathophysiology of Sudden Upper Airway Obstruction in Sleeping Infants and Its Relevance for SIDS^a