Development of ventilatory control in infants - 03/08/11

Doi : 10.1016/j.prrv.2010.06.002

John L. Carroll ^⁎ , Amit Agarwal ^{^{1
Tel.: +1 501 364 1006; Fax: +1 501 364 3930.}}
University of Arkansas for Medical Sciences, Department of Pediatrics, Division of Pulmonary Medicine, Arkansas Children’s Hospital, mail slot 512-17, 1 Children’s Way, Little Rock, Arkansas 72212

Corresponding author. Tel.: +1 501 364-1006; Fax: +1 501 364 3930.

Summary

Most abnormalities of ventilatory control in infants are due to immaturity or abnormal development of ventilatory control. This includes a broad range, from rare disorders like congenital central hypoventilation syndrome to common problems such as apnoea of prematurity. Development of the ventilatory control system, including central respiratory rhythmogenesis and central and peripheral chemoreception, begins early in gestation and continues for weeks or months after birth. Development of the neural components of central rhythmogenesis and their highly complex interconnectivity results from complex, timing-sensitive interactions between patterning and other genes, transcription factors and neurotrophic factors. At birth, nearly all aspects of ventilatory control remain immature, especially in preterm infants; and postnatal maturation can be altered by hypoxia, toxins and other stressors. Clinical care may be greatly enhanced by increased awareness of ventilatory control maturation and related disorders.

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Abbreviations : ALTE, ANS, ATP, BötC, CB, CCHS, CNS, CO₂, CPG, CSN, cVRG, DRG, E1, E2, E-aug, EGR2 (aka KROX20), e-I, FRC, H⁺, HASH-1 (aka ASCL1), HIF, Hox, HOXA1, HOXA3, HOXB2, I, I-aug, K⁺, late-I, LMX1B, MAFB, MASH-1, NDN, NTS, O₂, PET-1 (aka FEV), pFRG, PHOX2A, PHOX2B, post-I, pre-BötC, pre-I, PWS, RNX (aka TLX3), RTN, rVRG, SIDS, TASK-2 (aka KCNK5, K2P5.1), V_E

Keywords : infant, respiratory center, brainstem, chemoreceptor cells, carotid body, fetal development, hypoventilation, apnea, SIDS (sudden infant death syndrome)