Influence of Maternal Smoking on Autonomic Nervous System in Healthy Infants

Franco, Patricia; Chabanski, Sophie; Szliwowski, Henri; Dramaix, M.; Kahn, André

doi:10.1203/00006450-200002000-00011

Cited by 99 publications

(59 citation statements)

References 49 publications

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“…Still, the effects were dose-dependent and consistent across type of chemoreceptor stimulus and direction of ventilatory change during a 3-month age span. Our findings are in accordance with previous work indicating that cigarette smoke exposure may influence autonomic nervous function even in apparently healthy individuals, both before birth (39), in infants (40), and in adults (23)(24)(25)(26). In a situation with heavy exposure, individual high susceptibility, a vulnerable developmental period, or the presence of disease, it is possible that cigarette smoke exposure could affect infant HR control critically.…”

supporting

confidence: 82%

Heart Rate Response to Transient Chemoreceptor Stimulation in Term Infants Is Modified by Exposure to Maternal Smoking

2001

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Modulation of heart rate (HR) during transient hyperoxia, hypoxia, and hypercapnia was studied in 46 healthy term infants on 103 occasions (postnatal d 2 to 82). Twenty-three infants had smoking mothers (median, 11 cigarettes/d). Transient chemoreceptor stimuli (100% O 2 , 15% O 2 , or 3% CO 2 ) were presented repeatedly during quiet sleep. Beat-by-beat HR and breath-bybreath ventilation were recorded continuously. The coherently averaged HR and ventilation responses to each stimulus were calculated for each infant at each age. Outcome variables (HR change from baseline to end of stimulation, maximum HR change, and time to half-maximum) were analyzed by ANOVA. Overall, HR declined during hyperoxia (median change, 4.2 beats/min) and rose during hypoxia (median change, 4.2 beats/ min) and hypercapnia (median change, 4.6 beats/min). The percentage change in HR was positively correlated with the percentage change in ventilation (p Ͻ 0.001). Increasing number of cigarettes smoked by the mother was correlated with deeper HR declines and smaller HR rises (p ϭ 0.02). For the population as a whole, the HR response lagged 3.8 s behind the ventilatory response during hyperoxia and hypoxia (p Ͻ 0.001), whereas during hypercapnia there was no significant lag. The lag in HR response in the smoke-exposed group was 2.5 s greater than that in the control group for all three stimuli (p ϭ 0.001), and the difference increased with the number of cigarettes smoked by the mother (p Ͻ 0.01). Both pulmonary reflexes and the type of the chemoreceptor stimulus seemed to influence HR. In fetal life, peripheral chemoreceptor stimulation by hypoxia or hypercapnia produces bradycardia and peripheral vasoconstriction (1, 2). After birth, however, the same stimuli cause hyperventilation, tachycardia, and peripheral vasodilation (3-5). These responses are thought to result from an interaction of reflexes. The primary cardiac effect of chemoreceptor stimulation is bradycardia, mediated via the vagal innervation of the heart. However, a concomitant increase in V E will increase lung stretch receptor activity, give slight hypocapnia, and affect central respiratory neurons, and these responses together cause an overriding tachycardia. This interaction has been described in a number of species, including primates (4 -8).In anesthetized animals, elaborate experiments can be performed in which marked changes in arterial O 2 and CO 2 content are introduced or the peripheral chemoreceptors are stimulated chemically or electrically. Cardiovascular effects may then be assessed while V E is kept constant, the degree of lung inflation is controlled, or pulmonary afferent nerves are cut or pharmacologically blocked. It is not possible to achieve a similar level of control in noninvasive studies in humans. However, trained subjects can voluntarily keep their V E constant, and in some pathologic conditions breathing movements are temporarily absent. Experiments making use of these phenomena have given more indirect indications of an interaction between the effe...

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confidence: 82%

Heart Rate Response to Transient Chemoreceptor Stimulation in Term Infants Is Modified by Exposure to Maternal Smoking

2001

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“…In addition, a growing body of research has documented an association between prenatal exposure to cigarettes and deficits in affective behaviors and regulation. Exposed infants have been found to show deficits in arousal and attention throughout the first year of life (Franco et al, 1999;Franco et al, 2000;Fried & Makin, 1987;Jacobson, Fein, Jacobson, Schwartz & Dowler, 1984;Picone, Allen, Olsen, & Ferris, 1982;Saxton, 1978;Schuetze & Eiden, 2006;Schuetze & Zeskind, 2001;Streissguth, Barr, & Martin, 1983). Studies have also found differences in affective behaviors among exposed infants as compared to nonexposed infants as early as the neonatal period and persisting into childhood.…”

mentioning

confidence: 99%

The association between prenatal exposure to cigarettes and infant and maternal negative affect

Schuetze

Eiden

2007

Infant Behavior and Development

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This study examined the association between prenatal exposure to cigarettes and infant and maternal negative affect. Participants were 115 mother-infant dyads (69 prenatally exposed to cigarettes and 46 nonexposed). Infant and maternal negative affect were both assessed during the neonatal period (2-4 weeks of age) and again at 7 months of infant age. Results indicated that only prenatal exposure to cigarettes predicted infant negative affect. Infants who were prenatally exposed to more cigarettes had higher levels of negative affect at both time points. Furthermore, regression analyses indicated that both infant and maternal negative affect during the neonatal period predicted maternal negative affect at 7 months of age. These results highlight the importance of considering the reciprocal relationship between infant and maternal behavior when examining developmental outcomes among infants prenatally exposed to cigarettes.Keywords prenatal exposure to cigarettes; infant negative affect; maternal negative affect; cross-lagged panel design Prenatal exposure to cigarettes has consistently been associated with adverse perinatal outcomes (Abel, 1980;Fried & O'Connell, 1987;Fried & Oxorn, 1980;Olsen, Pereira, & Olsen, 1991). In addition, a growing body of research has documented an association between prenatal exposure to cigarettes and deficits in affective behaviors and regulation. Exposed infants have been found to show deficits in arousal and attention throughout the first year of life (Franco et al., 1999;Franco et al., 2000;Fried & Makin, 1987;Jacobson, Fein, Jacobson, Schwartz & Dowler, 1984;Picone, Allen, Olsen, & Ferris, 1982;Saxton, 1978;Schuetze & Eiden, 2006;Schuetze & Zeskind, 2001;Streissguth, Barr, & Martin, 1983). Studies have also found differences in affective behaviors among exposed infants as compared to nonexposed infants as early as the neonatal period and persisting into childhood. Specifically, studies with infants and toddlers who were prenatally exposed to cigarettes have found evidence of increased irritability (Brook, Brook & Whiteman, 2000;Jacobson et al., 1984 Publisher's Disclaimer: This is a PDF file of an unedited manuscript that has been accepted for publication. As a service to our customers we are providing this early version of the manuscript. The manuscript will undergo copyediting, typesetting, and review of the resulting proof before it is published in its final citable form. Please note that during the production process errors may be discovered which could affect the content, and all legal disclaimers that apply to the journal pertain. Corneal, 2001;Ramsay, Bendersky, & Lewis, 1996;Schuetze & Zeskind, 2001). The extent to which these effects are due to the direct, teratological impact of prenatal exposure to cigarettes or are mediated by other maternal factors that are associated with maternal smoking is not clear. NIH Public AccessPrevious studies highlight the importance of examining both direct and indirect pathways to the development of affect among cigarette-expo...

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“…1 Because sympathetic overreactivity and autonomic dysfunction more generally are involved in the initiation and progression of disease, [2][3][4][5] we undertook a 1-year follow-up study to track the natural history and to assess the likely impact of the incipient hyperreactivity seen in a smoker's newborn infant.…”

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confidence: 99%

Long-Term Reprogramming of Cardiovascular Function in Infants of Active Smokers

et al. 2010

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Abstract-Newborn infants of smokers show symptoms of cardiovascular stress hyperreactivity. Persistent hyperreactivity could increase the risk of short-and/or long-term complications, such as hypertension. Here we determined whether incipient dysfunction in a smoker's infant persists or worsens with age, by comparing cardiovascular reflex function of control and tobacco-exposed infants longitudinally from birth to 1 year. We compared infants born at term to nonsmoking couples (controls; nϭ19) and mothers who smoked moderately (average consumptionϭ15 cigarettes per day; nϭ17). All were tested at 1 to 3 weeks, 3 months, and 1 year during sleep. We recorded blood pressure and heart rate noninvasively during passive repositioning (60°head-up tilt). Tilting control infants raised blood pressure slightly above baseline at 1 week (ϩ2%) and much more at 1 year (ϩ10%). This trend was reversed in the tobacco-exposed cohort (ϩ10% at 1 week but only ϩ4% at 1 year). At 3 months and 1 year, the heart rate response of tobacco-exposed infants to tilt was also abnormal (highly exaggerated). Our study reveals that maternal smoking leads to long-lasting "reprogramming" of infant blood pressure control mechanisms. The underlying dysfunction in a smoker's infant could plausibly be a precursor or early marker of long-term susceptibility to complications, such as raised blood pressure. (Hypertension. 2010;55:722-728.)

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Influence of Maternal Smoking on Autonomic Nervous System in Healthy Infants

Cited by 99 publications

References 49 publications

Heart Rate Response to Transient Chemoreceptor Stimulation in Term Infants Is Modified by Exposure to Maternal Smoking

Heart Rate Response to Transient Chemoreceptor Stimulation in Term Infants Is Modified by Exposure to Maternal Smoking

The association between prenatal exposure to cigarettes and infant and maternal negative affect

Long-Term Reprogramming of Cardiovascular Function in Infants of Active Smokers

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