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Highlights: [•] Mice deficient in stress peptide PACAP have a SIDS-like phenotype. [•] We examined effects of PACAP on neonatal breathing in rats using the neonatal working heart brainstem preparation. [•] We found that exogenous PACAP stimulates and stabilizes neonatal breathing. [•] The stimulatory effect of PACAP required intact carotid bodies; the stabilizing effect persisted after carotid body denervation. [Copyright &y& Elsevier]

Abstract: Infection in infancy may dramatically aggravate an underlying cardiorespiratory dysfunction during a susceptible postnatal period. Children with immature brainstem respiratory control, as well as infants, may have periodic irregular breathing with potential detrimental apneas that are increased during sleep as well as during infectious episodes. Data now indicate that the proinflammatory cytokine interleukin (IL)-1β impairs respiration during infection via prostaglandin E2 (PGE2) and that infection, with associated eicosanoid release, is one of the main causes of respiratory disorders in preterm infants. Moreover, brainstem microsomal prostaglandin E synthase-1 (mPGES-1) is rapidly activated during transient hypoxia. An inflammatory mediated activation of the mPGES-1 pathway, e.g., by viral or bacterial infection, rapidly induces release of PGE2 in the vicinity of brainstem cardio-respiratory-related centers. This will depress the autonomic control networks, including the central drive to breathe. Hypoxia may then further reduce the activity of vital brainstem centers and the ability to autoresuscitate. This might have fatal consequences in vulnerable infants during a susceptible time frame. Here the evidence from human, animal and molecular studies to support this hypothesis is reviewed and how the pathogenesis of apnea and the response to hypoxia is associated with inflammatory pathways is discussed. [Copyright &y& Elsevier]

Abstract: Respiratory function of the cricothyroid muscle (CT) is virtually unknown in the neonatal period. This study was aimed at assessing CT electrical activity (EMG) during respiration and central apneas in non-sedated lambs. Seven full-term and four preterm lambs were instrumented for polysomnographic recording, including EMG of the diaphragm, thyroarytenoid (TA, a glottal constrictor), posterior cricoarytenoid (PCA, the primary glottal dilator) and CT. Phasic CT EMG was usually observed during inspiration and late expiration, whereas phasic TA EMG was observed during early expiration. While TA EMG virtually disappeared in REM sleep, both inspiratory and expiratory CT EMG increased. Overall, while CT EMG was not frequently observed during central apneas in either full-term (10% of apneas, but never simultaneously with TA EMG) or preterm lambs (30% of apneas), it was associated with decreased lung volume and subglottal pressure when present alone or with PCA EMG. Our results concur with the assumption that CT behaves as a laryngeal dilator in the neonatal period. [Copyright &y& Elsevier]