Effect of nicotine exposure on postnatal ventilatory responses to hypoxia and hypercapnia

Bamford, Owen S.; Schuen, John; Carroll, John L.

doi:10.1016/0034-5687(96)00051-5

Cited by 96 publications

(66 citation statements)

References 20 publications

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“…Maternal cigarette smoking has been reported to have no effect on ventilatory responses to hypoxia or hypercapnia (Lewis and Bosque, 1995) and diminish the hypoxic ventilatory responses and respiratory drive (Ueda et al, 1999). Similarly, it is reported that prenatal nicotine exposure both does not alter (Bamford et al, 1996) and attenuates the ventilatory response to hypoxia or hypercapnia in rats (Simakajornboon et al, 2004). The results from this study indicate that prenatal nicotine exposure does not alter central respiratory responses to hypercapnia and suggests any potential changes in the ventilatory responses to prenatal nicotine in vivo may depend on changes in the activity of peripheral chemoreceptors rather than within the medulla.…”

Section: Discussionmentioning

confidence: 99%

Differential Control of Central Cardiorespiratory Interactions by Hypercapnia and the Effect of Prenatal Nicotine

Huang

Griffioen²,

Wang³

et al. 2006

J. Neurosci.

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Hypercapnia evokes a strong cardiorespiratory response including gasping and a pronounced bradycardia; however, the mechanism responsible for these survival responses initiated in the brainstem is unknown. To examine the effects of hypercapnia on the central cardiorespiratory network, we used an in vitro medullary slice that allows simultaneous examination of rhythmic respiratory-related activity and inhibitory synaptic neurotransmission to cardioinhibitory vagal neurons (CVNs). Hypercapnia differentially modulated inhibitory neurotransmission to CVNs; whereas hypercapnia selectively depressed spontaneous glycinergic IPSCs in CVNs without altering respiratory-related increases in glycinergic neurotransmission, it decreased both spontaneous and inspiratory-associated GABAergic IPSCs. Because maternal smoking is the highest risk factor for sudden infant death syndrome (SIDS) and prenatal nicotine exposure is proposed to be the link between maternal smoking and SIDS, we examined the cardiorespiratory responses to hypercapnia in animals exposed to nicotine in the prenatal and perinatal period. In animals exposed to prenatal nicotine, hypercapnia evoked an exaggerated depression of GABAergic IPSCs in CVNs with no significant change in glycinergic neurotransmission. Hypercapnia altered inhibitory neurotransmission to CVNs at both presynaptic and postsynaptic sites. Although the results obtained in this study in vitro cannot be extrapolated with certainty to in vivo responses, the results of this study provide a likely neurochemical mechanism for hypercapnia-evoked bradycardia and the dysregulation of this response with exposure to prenatal nicotine, creating a higher risk for SIDS.

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Section: Discussionmentioning

confidence: 99%

Differential Control of Central Cardiorespiratory Interactions by Hypercapnia and the Effect of Prenatal Nicotine

Huang

Griffioen²,

Wang³

et al. 2006

J. Neurosci.

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“…24,25 Neonatal rats exposed prenatally to nicotine had increased mortality during hypoxic challenge. 26 Nonetheless, subsequent experimental studies in the neonatal rat subjected to hypoxia, 27 anoxia, 28 or hypercapnia, 29 showed unaffected respiratory response after maternal nicotine exposure during gestation. In contrast, lambs subjected to acute infusion of nicotine had decreased ventilation during hypoxia.…”

Section: Discussionmentioning

confidence: 99%

“…NIC ϩ IL-1␤ had significantly more spontaneous apneas the last 5 minutes before induction of apnea (2 [.3-3] vs 0 [0 -0]; P Ͻ .03; Fig 2). Apneas were prolonged (46 seconds [39 -51] vs 26 seconds [22][23][24][25][26][27][28][29][30][31]; P Ͻ .01; Fig 2) with greater fall in Sao 2 (Fig 3), and followed by far more spontaneous apneas the following 5 minutes (6.6 [4.0 -7.9 Fig 3). These prolonged adverse effects on ventilation were reflected in lowered Pao 2 , elevated Paco 2 and lowered pH 2, and even 5, minutes after induction of apnea (all P Ͻ .04; Table 2).…”

mentioning

confidence: 99%

Adverse Effects of Nicotine and Interleukin-1β on Autoresuscitation After Apnea in Piglets: Implications for Sudden Infant Death Syndrome

et al. 2000

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ABSTRACT. Objectives. Maternal cigarette smoking is established as a major dose-dependent risk factor for sudden infant death syndrome (SIDS). Both prenatal and postnatal exposures to constituents of tobacco smoke are associated with SIDS, but no mechanism of death attributable to nicotine has been found. Breastfeeding gives a substantial increase in absorbed nicotine compared with only environmental tobacco smoke when the mother smokes, because the milk:plasma concentration ratio of nicotine is 2.9 in smoking mothers. Furthermore, many SIDS victims have a slight infection and a triggered immune system before their death, thus experiencing a release of cytokines like interleukin-1␤ (IL-1␤) that may depress respiration. Because apneas in infancy are associated with SIDS, we have tested the hypothesis that postnatal exposure to tobacco constituents and infections might adversely affect an infant's ability to cope with an apneic episode. This is performed by investigating the acute effects of nicotine and IL-1␤ on apnea by laryngeal reflex stimulation and on the subsequent autoresuscitation.Design. Thirty 1-week-old piglets (؎1 day) were sedated with azaperone. A tracheal and an arterial catheter were inserted during a short halothane anesthesia. The piglets were allowed a 30-minute stabilization period before baseline values were recorded and they were randomized to 4 pretreatment groups (avoiding siblings in the same group): 1) immediate infusion of 10 pmol IL-1␤ intravenously/kg (IL-1␤ group; n ‫؍‬ 8); 2) slow infusion of 5 g nicotine intravenously/kg 5 minutes later (NIC group; n ‫؍‬ 8); 3) both IL-1␤ and NIC combined (NIC ؉ IL-1␤ group; n ‫؍‬ 6); or 4) placebo by infusion of 1 ml .9% NaCl (CTR group; n ‫؍‬ 8). Fifteen minutes later, apnea was induced by insufflation of .1 ml of acidified saline (pH ‫؍‬ 2) in the subglottic space 5 times with 5-minute intervals, and variables of respiration, heart rate, blood pressure, and blood gasses were recorded.Results. Stimulation of the laryngeal chemoreflex by insufflation of acidified saline in the subglottic space produced apneas, primarily of central origin. This was followed by a decrease in heart rate, a fall in blood pressure, swallowing, occasional coughs, and finally autoresuscitation with gasping followed by rapid increase in heart rate, rise in blood pressure, and (in the CTR group) an increase of respiratory rate. Piglets pretreated with nicotine had more spontaneous apneas, and repeated spontaneous apneas caused an inability to perform a compensatory increase of the respiratory rate after induced apnea. This resulted in a lower SaO 2 than did CTR at 2 minutes after apnea (data shown as median ABBREVIATIONS. SIDS, sudden infant death syndrome; IL-1␤, interleukin-1␤; CRP, C-reactive protein; IL-6, interleukin-6; IL-1␤ group, 10 pmol IL-1␤ intravenously/kg; NIC group, 5 g nicotine intravenously/kg; NIC ϩ IL-1␤ group, both IL-1␤ and NIC combined; CTR group, placebo. M aternal cigarette smoking is established as a major dose-dependent risk factor for sudden infan...

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“…Other examples of developmental plasticity include altered adult chemoreflexes caused by maternal separation stress (118) and prenatal nicotine exposures (12,51,70,87,207). In the pond snail Lymnaea stagnalis, preventing lung ventilation from hatching through adulthood alters mechanisms of ventilatory control in adults (92).…”

Section: Developmental Plasticitymentioning

confidence: 99%

Invited Review: Neuroplasticity in respiratory motor control

Mitchell

Johnson

2003

Journal of Applied Physiology

354

313

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Although recent evidence demonstrates considerable neuroplasticity in the respiratory control system, a comprehensive conceptual framework is lacking. Our goals in this review are to define plasticity (and related neural properties) as it pertains to respiratory control and to discuss potential sites, mechanisms, and known categories of respiratory plasticity. Respiratory plasticity is defined as a persistent change in the neural control system based on prior experience. Plasticity may involve structural and/or functional alterations (most commonly both) and can arise from multiple cellular/synaptic mechanisms at different sites in the respiratory control system. Respiratory neuroplasticity is critically dependent on the establishment of necessary preconditions, the stimulus paradigm, the balance between opposing modulatory systems, age, gender, and genetics. Respiratory plasticity can be induced by hypoxia, hypercapnia, exercise, injury, stress, and pharmacological interventions or conditioning and occurs during development as well as in adults. Developmental plasticity is induced by experiences (e.g., altered respiratory gases) during sensitive developmental periods, thereby altering mature respiratory control. The same experience later in life has little or no effect. In adults, neuromodulation plays a prominent role in several forms of respiratory plasticity. For example, serotonergic modulation is thought to initiate and/or maintain respiratory plasticity following intermittent hypoxia, repeated hypercapnic exercise, spinal sensory denervation, spinal cord injury, and at least some conditioned reflexes. Considerable work is necessary before we fully appreciate the biological significance of respiratory plasticity, its underlying cellular/molecular and network mechanisms, and the potential to harness respiratory plasticity as a therapeutic tool.

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Effect of nicotine exposure on postnatal ventilatory responses to hypoxia and hypercapnia

Cited by 96 publications

References 20 publications

Differential Control of Central Cardiorespiratory Interactions by Hypercapnia and the Effect of Prenatal Nicotine

Differential Control of Central Cardiorespiratory Interactions by Hypercapnia and the Effect of Prenatal Nicotine

Adverse Effects of Nicotine and Interleukin-1β on Autoresuscitation After Apnea in Piglets: Implications for Sudden Infant Death Syndrome

Invited Review: Neuroplasticity in respiratory motor control

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