Arousal and ventilatory responses to mild hypoxia in sleeping preterm infants

Verbeek, Marjan M A; Richardson, Heidi L.; Parslow, Peter M; Walker, Adrian M.; Harding, Richard; Horne, Rosemary Sylvia Claire

doi:10.1111/j.1365-2869.2008.00653.x

Cited by 30 publications

(16 citation statements)

References 38 publications

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“…Arousals and increased ventilatory response characterized by changes in respiratory rate and rhythm have been seen in hypoxia and hypercarbia in both animal and human adult and infant studies (8,30,31,36,37). In our study, separately as well as in parallel, upon spontaneous and induced esophageal stimulation, arousal responses have been noted in both quiet and active sleep states.…”

Section: Discussionmentioning

confidence: 51%

Esophageal sensation in premature human neonates: temporal relationships and implications of aerodigestive reflexes and electrocortical arousals

Jadcherla

Parks

Peng

et al. 2012

American Journal of Physiology-Gastrointestinal and Liver Physi

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Jadcherla SR, Parks VN, Peng J, Dzodzomenyo S, Fernandez S, Shaker R, Splaingard M. Esophageal sensation in premature human neonates: temporal relationships and implications of aerodigestive reflexes and electrocortical arousals. Am J Physiol Gastrointest Liver Physiol 302: G134 -G144, 2012. First published August 18, 2011 doi:10.1152/ajpgi.00067.2011 as an effect of visceral provocation or of its temporal relationships with aerodigestive reflexes in premature neonates is not known. We tested the hypothesis that esophageal provocation results in both esophageal reflex responses and ECAs during sleep and that ECAs are dependent on the frequency characteristics of esophageal neuromotor responses. We defined the spatiotemporal relationship of ECAs in relation to 1) spontaneous pharyngoesophageal swallow sequences and gastroesophageal reflux (GER) events and 2) sensory-motor characteristics of esophageal reflexes. Sixteen healthy premature neonates born at 27.9 Ϯ 3.4 wk were tested at 36.8 Ϯ 1.9 wk postmenstrual age. Ninety-five midesophageal and 31 sham stimuli were given in sleep during concurrent manometry and videopolysomnography. With stimulus onset as reference point, we scored the response latency, frequency occurrence and duration of arousals, peristaltic reflex, and upper esophageal sphincter contractile reflex (UESCR). Changes in polysomnography-respiratory patterns and esophageal sensory-motor parameters were scored by blinded observers. Significantly (for each characteristic listed, P Ͻ 0.05), swallow sequences were associated with arousals and sleep state changes, and arousals were associated with incomplete peristalsis, response delays to lower esophageal sphincter relaxation, and prolonged esophageal clearance. GER events (73.5%) provoked arousals, and arousals were associated with response delays to peristaltic reflexes or clearance, sleep state modification, and prolonged respiratory arousal. Midesophageal stimuli (54%) provoked arousals and were associated with increased frequency, prolonged latency, prolonged response duration of peristaltic reflexes and UESCR, and increased frequency of sleep state changes and respiratory arousals. In human neonates, ECAs are provoked upon esophageal stimulation; the sensory-motor characteristics of esophageal reflexes are distinct when accompanied by arousals. Aerodigestive homeostasis is defended by multiple tiers of aerodigestive safety mechanisms, and when esophageal reflexes are delayed, cortical hypervigilance (ECAs) occurs.

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Section: Discussionmentioning

confidence: 51%

Esophageal sensation in premature human neonates: temporal relationships and implications of aerodigestive reflexes and electrocortical arousals

Jadcherla

Parks

Peng

et al. 2012

American Journal of Physiology-Gastrointestinal and Liver Physi

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“…Research in this area has focused on physiological responses to air challenges. In term infants, normal biphasic responses to hypoxia were present at 2–5 weeks, 2–3 months, and 5–6 months postnatal (Richardson et al, 2007; Verbeek et al, 2008). In preterm infants, the ventilatory response to hypoxia appears to transition from a monophasic depressive response at 31.5 weeks post-conception (Alvaro et al, 1992) to a biphasic response by 35.5 weeks post-conception (Martin et al, 1998) and is still present at 45 weeks post-conception (Verbeek et al, 2008).…”

Section: Prematurity and Sidsmentioning

confidence: 99%

“…In term infants, normal biphasic responses to hypoxia were present at 2–5 weeks, 2–3 months, and 5–6 months postnatal (Richardson et al, 2007; Verbeek et al, 2008). In preterm infants, the ventilatory response to hypoxia appears to transition from a monophasic depressive response at 31.5 weeks post-conception (Alvaro et al, 1992) to a biphasic response by 35.5 weeks post-conception (Martin et al, 1998) and is still present at 45 weeks post-conception (Verbeek et al, 2008). The early monophasic depressive response may reflect the transition from fetal-like to neonatal respiratory and autonomic function in preterm infants (Boddy et al, 1974; Alvarez et al, 1992) and is similar in some ways to the attenuated ventilatory augmentation seen in anesthetized infants and animal models after prenatal nicotine exposure (Ueda et al, 1999; Hafstrom et al, 2002; Sawnani et al, 2004; Eugenin et al, 2008).…”

Section: Prematurity and Sidsmentioning

confidence: 99%

The physiological determinants of Sudden Infant Death Syndrome

Garcia¹,

Koschnitzky²,

Ramirez

2013

Respiratory Physiology & Neurobiology

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It is well-established that environmental and biological risk factors contribute to Sudden Infant Death Syndrome (SIDS). There is also growing consensus that SIDS requires the intersection of multiple risk factors that result in the failure of an infant to overcome cardio-respiratory challenges. Thus, the critical next steps in understanding SIDS are to unravel the physiological determinants that actually cause the sudden death, to synthesize how these determinants are affected by the known risk factors, and to develop novel ideas for SIDS prevention. In this review, we will examine current and emerging perspectives related to cardio-respiratory dysfunctions in SIDS. Specifically, we will review: (1) the role of the preBötzinger complex (preBötC) as a multi-functional network that is critically involved in the failure to adequately respond to hypoxic and hypercapnic challenges; (2) the potential involvement of the pre-BötC in the gender and age distributions that are characteristic for SIDS; (3) the link between SIDS and prematurity; and (4) the potential relationship between SIDS, auditory function, and central chemosensitivity. Each section underscores the importance of marrying the epidemiological and pathological data to experimental data in order to understand the physiological determinants of this syndrome. We hope that a better understanding will lead to novel ways to reduce the risk to succumb to SIDS.

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“…Moreover, preterm infants (26-32 weeks of gestation) with a history of apnoea and bradycardia of prematurity showed decreased responses in both active sleep and quiet sleep at term, and in quiet sleep at 2-3 months post-term (Horne et al, 2001). After a mild hypoxia challenge (15% oxygen), preterm infants had a longer arousal latency in active sleep at 2-3 weeks of age and reached significantly lower SpO 2 levels at 2-5 weeks in both active sleep and quiet sleep and at 2-3 months in quiet sleep (Verbeek et al, 2008). The greater desaturation during the hypoxic challenge combined with the longer arousal latency suggested that in preterm infants there was an impairment or inadequate response to hypoxia during sleep, which may explain the enhanced risk for SIDS in this group.…”

Section: Sids Risk Factors and Preterm Birthmentioning

confidence: 94%