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Developmental plasticity of the hypoxic ventilatory response1 Paper presented at the conference on Neural Control of Breathing: Molecular to Organismal Perspectives, Madison, WI, 21–25 July, 19961

Authors
Journal
Respiration Physiology
0034-5687
Publisher
Elsevier
Publication Date
Volume
110
Identifiers
DOI: 10.1016/s0034-5687(97)00091-1
Keywords
  • Carotid Body
  • Hypoxia
  • Control Of Breathing
  • Hypoxia
  • Development
  • Hypoxic Control
  • Hypoxia
  • Development
  • Mammals
  • Rat
Disciplines
  • Medicine
  • Physics

Abstract

Abstract This paper will describe recent studies concerning the existence of developmental plasticity in the hypoxic ventilatory control system and the locus of the functional impairment following perinatal sensory suppression. Suppression of peripheral arterial chemoreceptor activity was achieved by exposing rats to hyperoxia (60% O 2) for the first month of life; all measurements were conducted 2–5 months after the exposure (perinatal treated rats). Hypoxic (but not hypercapnic) ventilatory responses were severely attenuated in awake perinatal treated rats, but not in rats exposed to hyperoxia as adults, indicating that the persistent effect is unique to development and is not the nonspecific result of O 2 toxicity. Impairments of the hypoxic ventilatory response due to changes in pulmonary mechanics, gas exchange or central integration of carotid chemoafferent inputs were all ruled out as primary causal factors. However, a persistent impairment of carotid chemotransduction in perinatal treated rats was apparent. These studies suggest that the hypoxic ventilatory response is susceptible to developmental plasticity, and that a carotid chemoreceptor deficit is the primary cause. These findings may have important clinical implications for patients subjected to excessive O 2 therapy during neonatal intensive care.

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