Loss of neonatal hypoxia tolerance after prenatal nicotine exposure: implications for sudden infant death syndrome.

Published

Journal Article

Maternal cigarette smoking has a high correlation with sudden Infant Death Syndrome, a condition in which cardiorespiratory failure occurs during an hypoxic episode, as in sleep apnea. Pregnant rats were given nicotine infusions of 2 or 6 mg/kg/day throughout gestation, regimens that produce plasma nicotine levels spanning the range in smokers. The day after birth, animals in the high dose group displayed excessive mortality during hypoxic challenge. These animals were found to be deficient in an essential response component, namely adrenomedullary catecholamine release that is required to maintain neonatal cardiac rhythm during hypoxia; the defect was in adrenal cell function rather than in altered innervation or nicotinic receptor desensitization. We also examined brainstem and forebrain noradrenergic mechanisms that are involved in neonatal respiratory control. The nicotine group showed suppressed spontaneous neuronal activity, but were hyperresponsive to hypoxia. As these projections are inhibitory for respiration, the nicotine-induced sensitization would be expected to contribute to respiratory arrest during hypoxia. Prenatal nicotine exposure may thus provide a useful animal model with which to study the physiological mechanisms that underlie Sudden Infant Death Syndrome, while at the same time providing a biological explanation for the association of the syndrome with smoking.

Full Text

Duke Authors

Cited Authors

  • Slotkin, TA; Lappi, SE; McCook, EC; Lorber, BA; Seidler, FJ

Published Date

  • 1995

Published In

Volume / Issue

  • 38 / 1

Start / End Page

  • 69 - 75

PubMed ID

  • 7552377

Pubmed Central ID

  • 7552377

International Standard Serial Number (ISSN)

  • 0361-9230

Digital Object Identifier (DOI)

  • 10.1016/0361-9230(95)00073-n

Language

  • eng

Conference Location

  • United States