Prenatal nicotine exposure blunts the cardiorespiratory response to hypoxia in lambs
Abstract
Because smoking during pregnancy is a major risk factor for late fetal death and the sudden infant death syndrome, we investigated cardiorespiratory defense mechanisms to hypoxia in 7 prenatally nicotine-exposed (N) lambs (approximate maternal dose: 0.5 mg/kg/day) and 11 control (C) lambs all at an average age of 5 days. The ventilatory response to 10% oxygen (hyperpnea) was significantly attenuated during quiet sleep in N lambs compared with C lambs and in N lambs aroused from sleep later compared with C lambs (161 +/- 90 versus 75 +/- 66 seconds, p < 0.05). The ventilatory response to hypoxia was similar in the two groups during wakefulness (W), whereas the heart rate response (tachycardia) was significantly lower in N lambs compared with C lambs during both activity states. The ventilatory response to hyperoxia was significantly lower in N lambs compared with C lambs during both activity states. Transition from W to quiet sleep was associated with a significant decrease in ventilation in C lambs but not in N lambs. In conclusion, prenatal nicotine exposure, at a dose comparable with moderate smoking, blunts major elements of the cardiorespiratory defense to hypoxia, i.e., the heart rate and ventilatory and arousal responses, and abolishes the normal decrease in ventilation during sleep compared with W.
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Giving nicotine to pregnant ewes can produce the same deficit in newborn lambs.
“The administration of nicotine to pregnant ewes can evoke the same deficit in newborn lambs.”
From Developmental toxicity of nicotine: A transdisciplinary synthesis and implications for emerging tobacco products (2017) · cites this paper as [119]
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- Authors
- Hafström, O., Milerad, J., & Sundell, H. W.
- Affiliations
- Vanderbilt University (US)
- Department of Pediatrics, Vanderbilt University School of Medicine, Nashville, Tennessee
- ORCID
- Milerad, Joseph
- Venue
- American Journal of Respiratory and Critical Care Medicine
- Publisher
- Oxford University Press (OUP)
- Published
- 2002-12
- Volume
- 166
- Issue
- 12
- Pages
- 1544-1549
- ISSN
- 1073-449X (ISSN-L)
- 1535-4970
- OpenAlex
- W2108907303
- Cited by
- 102
- References
- 52
- Citations by year
- 2025: 1 · 2023: 2 · 2022: 2 · 2021: 1 · 2020: 2 · 2019: 1 · 2018: 4 · 2017: 4 · 2016: 6 · 2015: 6 · 2014: 3 · 2013: 2 · 2012: 6
- FWCI
- 2.21
- Type
- journal article
- Language
- en
- Open access
- closed
- Locations
- American Journal of Respiratory and Critical Care Medicine (publishedVersion)
- PubMed (publishedVersion)
- Funders
- National Institutes of Health (5r01hd028916-04, 5p50hl014214-25)
- National Heart, Lung, and Blood Institute (HL14214)
- Eunice Kennedy Shriver National Institute of Child Health and Human Development (HD28916)
- Topics
- Life Sciences › Neuroscience › Endocrine and Autonomic Systems › Neuroscience of respiration and sleep
- Health Sciences › Medicine › Pediatrics, Perinatology and Child Health › Prenatal Substance Exposure Effects
- Health Sciences › Medicine › Pulmonary and Respiratory Medicine › Neonatal Respiratory Health Research
- Keywords
- prenatal nicotine exposure, maternal smoking, hypoxia, ventilatory response, heart rate, hyperoxia, sleep arousal, lambs, sudden infant death syndrome, fetal death
- MeSH terms
- Animals, Hypoxia, Blood Pressure, Chemoreceptor Cells, Female, Heart Rate, Nicotine, Pregnancy, Prenatal Exposure Delayed Effects, Respiration, Sheep
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