Cardiorespiratory effects of nicotine exposure during development

Respir Physiol Neurobiol. 2005 Nov 15;149(1-3):325-41. doi: 10.1016/j.resp.2005.05.004. Epub 2005 Jun 20.

Abstract

Exposure to tobacco smoke is a major risk factor for the sudden infant death syndrome. Nicotine is thought to be the ingredient in tobacco smoke that is responsible for a multitude of cardiorespiratory effects during development, and pre- rather than postnatal exposure is considered to be most detrimental. Nicotine interacts with endogenous acetylcholine receptors in the brain and lung, and developmental exposure produces structural changes as well as alterations in neuroregulation. Abnormalities have been described in sympathicovagal balance, arousal threshold and latency, breathing pattern at rest and apnea frequency, ventilatory response to hyperoxia or hypoxia, heart rate regulation and ability to autoresuscitate during severe hypoxia. This review discusses studies performed on infants of smoking mothers and nicotine-exposed animals yielding varying and sometimes inconsistent results that may be due to differences in experimental design, species and the dose of exposure. Taken together however, developmental nicotine exposure appears to induce vulnerability during hypoxia and a potential inability to survive severe asphyxia.

Publication types

  • Review

MeSH terms

  • Animals
  • Cardiovascular Diseases / chemically induced*
  • Cardiovascular System / drug effects
  • Female
  • Humans
  • Infant, Newborn
  • Nicotine / adverse effects*
  • Pregnancy
  • Prenatal Exposure Delayed Effects / physiopathology*
  • Respiratory Mechanics / drug effects*
  • Respiratory System / drug effects
  • Respiratory Tract Diseases / chemically induced*
  • Smoking / adverse effects

Substances

  • Nicotine