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In-utero exposure to nicotine alters the development of the rabbit cardiac conduction system and provides a potential mechanism for sudden infant death syndrome

  • Reproductive Toxicology
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Abstract

In-utero exposure to tobacco smoke remains the highest risk factor for sudden infant death syndrome (SIDS). To alleviate the risks, nicotine replacement therapies are often prescribed to women who wish to quit smoking during their pregnancy. Cardiac arrhythmias is considered the final outcome leading to sudden death. Our goal in this study was to determine if exposing rabbit fetus to nicotine altered the cardiac conduction system of newborn kittens in a manner susceptible to cause SIDS. Using neuronal markers and a series of immunohistological and electrophysiological techniques we found that nicotine delayed the development of the cardiac pacemaker center (sinoatrial node) and decreased its innervation. At the molecular level, nicotine favored the expression of cardiac sodium channels with biophysical properties that will tend to slow heart rate and diminish electrical conduction. Our results show that alterations of the cardiac sodium current may contribute to the bradycardia, conduction disturbances and other cardiac arrhythmias often associated to SIDS and raise awareness on the use of replacement therapy during pregnancy.

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Acknowledgements

This work was supported by grants from the Canadian Heart and Stroke foundation and the Canadian Institutes of Health of Canada to RD.

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Correspondence to Robert Dumaine.

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204_2017_2006_MOESM1_ESM.docx

Table 2 (PCR primers to supplemental mat.) All PCR results were obtained with 35 cycles of amplification. Numbers under start-end correspond to the primer sequence position in the gene sequence as published in PubMed (DOCX 19 kb)

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Ton, A.T., Biet, M., Delabre, JF. et al. In-utero exposure to nicotine alters the development of the rabbit cardiac conduction system and provides a potential mechanism for sudden infant death syndrome. Arch Toxicol 91, 3947–3960 (2017). https://doi.org/10.1007/s00204-017-2006-x

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