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Published ahead of print on February 28, 2008, doi:10.1164/rccm.200711-1739OC
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American Journal of Respiratory and Critical Care Medicine Vol 177. pp. 1255-1261, (2008)
© 2008 American Thoracic Society
doi: 10.1164/rccm.200711-1739OC


Original Article

Respiratory Control in Neonatal Rats Exposed to Prenatal Cigarette Smoke

Jonathan D. Pendlebury1, Richard J. A. Wilson2, Shehr Bano1, Kathleen J. Lumb1, Jennifer M. Schneider1 and Shabih U. Hasan1

1 Department of Pediatrics and 2 Department of Physiology and Biophysics, Institute of Maternal and Child Health, Faculty of Medicine, University of Calgary, Calgary, Alberta, Canada

Correspondence and requests for reprints should be addressed to Shabih U. Hasan, M.D., Health Sciences Center, 3330 Hospital Drive NW, Calgary, AB, T2N 4N1, Canada. E-mail: hasans{at}ucalgary.ca

Rationale: Prenatal cigarette smoke (CS) exposure, increased environmental temperature, and hypoxic episodes have been postulated as major risk factors for sudden infant death syndrome.

Objectives: To test the hypothesis that maternal CS exposure disrupts eupneic breathing and depresses breathing responses of neonatal rats to thermal and hypoxic challenges.

Methods: Experiments were performed on 1-week-old rat pups exposed prenatally to CS (n = 39) or room air (sham; n = 30). Breathing patterns were recorded by whole-body plethysmography during thermoneutral or hyperthermic states under normoxic and hypoxic conditions.

Measurements and Main Results: Mean pup weight, breaths per minute, and gasping respiratory patterns were measured for both smoke- and sham-exposed groups during thermoneutral and hyperthermic states under normoxic and hypoxic conditions. Under thermoneutral conditions, hypoxia caused gasping in CS-exposed animals but not in sham-exposed animals. Furthermore, under hyperthermic conditions, whereas hypoxia induced gasping in both groups, only CS-exposed animals exhibited a pronounced and longer lasting respiratory depression after the termination of hypoxia.

Conclusions: We show that prenatal CS exposure increases the likelihood of gasplike respiration and provide the first experimental evidence that the combined effects of prenatal CS exposure and hyperthermia dramatically prolong the time required for neonates to return to eupneic breathing after hypoxia. These observations provide important evidence of how prenatal CS exposure, hypoxic episodes, and hyperthermia might place infants at higher risk for sudden infant death syndrome.

Key Words: apnea • hyperthermia • hypoxia • nicotine • sudden infant death syndrome


AT A GLANCE COMMENTARY

Scientific Knowledge on the Subject
Hypoxic episodes and increased body temperature have been proposed as possible triggers for sudden infant death syndrome (SIDS). How prenatal cigarette smoke exposure, the leading risk factor for SIDS, affects respiratory responses to these triggers is unknown.

What This Study Adds to the Field
Increased ambient temperature and hypoxia adversely affect breathing patterns in neonates exposed prenatally to cigarette smoke. Addressing these risk factors through tobacco reduction programs and better infant care practices could potentially decrease the incidence of SIDS.

 



This article has been cited by other articles:


Home page
Am. J. Respir. Crit. Care Med.Home page
J. Schneider, I. Mitchell, N. Singhal, V. Kirk, and S. U. Hasan
Prenatal Cigarette Smoke Exposure Attenuates Recovery from Hypoxemic Challenge in Preterm Infants
Am. J. Respir. Crit. Care Med., September 1, 2008; 178(5): 520 - 526.
[Abstract] [Full Text] [PDF]




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