Gasping and autoresuscitation in the developing rat:  effect of antecedent intermittent hypoxia

Gozal, David; Gozal, Evelyne; Reeves, Stephen R.; Lipton, Andrew J.

doi:10.1152/japplphysiol.00972.2001

Cited by 51 publications

(55 citation statements)

References 29 publications

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“…Hypoxia causes a transient tachycardia followed by a parasympathetically mediated bradycardia in vivo (Guntheroth and Kawabori, 1975;Taylor and Butler, 1982;Loewy and Spyer, 1990;Schuen et al, 1997;Slotkin et al, 1997;Deshpande et al, 1999;Gozal et al, 2002). It is important to note that the time course of the changes in spontaneous glycinergic and GABAergic IPSC frequencies in CVNs is strikingly similar to the time course of hypoxiainduced heart rate changes in neonatal rats (Slotkin et al, 1997).…”

mentioning

confidence: 91%

“…Hypoxia initially elicits an increase, followed by a decrease, in respiratory frequency. In addition, hypoxia transforms eupnic respiratory activity to gasping activity, which is characterized by infrequent, robust breaths of short duration (Guntheroth and Kawabori, 1975;Gozal et al, 2002). Prolonged hypoxia eventually produces a terminal apnea.…”

Section: Introductionmentioning

confidence: 99%

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Prenatal Nicotine Exposure Alters Central Cardiorespiratory Responses to Hypoxia in Rats: Implications for Sudden Infant Death Syndrome

Neff

Simmens²,

Evans³

et al. 2004

J. Neurosci.

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Maternal cigarette smoking and prenatal nicotine exposure are the highest risk factors for sudden infant death syndrome (SIDS). During hypoxia, respiratory frequency and heart rate transiently increase and subsequently decrease. These biphasic cardiorespiratory responses normally serve to prolong survival during hypoxia by reducing the metabolic demands of cardiac and respiratory muscles. However, exaggerated responses to hypoxia may be life threatening and have been implicated in SIDS. Heart rate is primarily determined by the activity of brainstem preganglionic cardioinhibitory vagal neurons (CVNs) in the nucleus ambiguus. We developed an in vitro rat brainstem slice preparation that maintains rhythmic inspiratory-related activity and contains fluorescently labeled CVNs. Synaptic inputs to CVNs were examined using patch-clamp electrophysiological techniques. Hypoxia evoked a biphasic change in the frequency of both GABAergic and glycinergic IPSCs in CVNs, comprised of an initial increase followed by a decrease in IPSC frequency. Prenatal exposure to nicotine changed the GABAergic response to hypoxia from a biphasic response to a precipitous decrease in spontaneous GABAergic IPSC frequency. This study establishes a likely neurochemical mechanism for the heart rate response to hypoxia and a link between prenatal nicotine exposure and an exaggerated bradycardia during hypoxia that may contribute to SIDS.

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mentioning

confidence: 91%

Section: Introductionmentioning

confidence: 99%

Prenatal Nicotine Exposure Alters Central Cardiorespiratory Responses to Hypoxia in Rats: Implications for Sudden Infant Death Syndrome

Neff

Simmens²,

Evans³

et al. 2004

J. Neurosci.

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“…In addition, respiratory challenges, such as hypoxia or hypercapnia, evoke strong coordinated cardiorespiratory responses. Hypoxia transforms respiration from eupnea to gasping, characterized by a transient increase, followed by a subsequent decrease in respiratory frequency (Guntheroth and Kawabori, 1975;Gozal et al, 2002). In addition, hypoxia and hypercapnia evoke an initial tachycardia, followed by a bradycardia mediated primarily by increases in parasympathetic activity (Taylor and Butler, 1982;Schuen et al, 1997).…”

Section: Introductionmentioning

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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“…Treatment guidelines for pregnant women with OSA are similar to that of the general population because data in pregnant women are limited. Data from animal studies demonstrated fetal growth retardation with maternal hypoxia; [61][62][63] an important goal in pregnant women is to avoid maternal hypoxemia 51 (strength of recommendation, C). CPAP is the standard treatment for OSA among general population 64 (strength of recommendation, A).…”

Section: Treatment Of Osa During Pregnancymentioning

confidence: 99%

Sleep-Disordered Breathing During Pregnancy

Venkata

Venkateshiah

2009

The Journal of the American Board of Family Medicine

101

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Pregnancy is associated with many physiologic and hormonal changes along with changes in sleep architecture, placing pregnant women at risk for the development of sleep-disordered breathing or worsening of preexisting sleep apnea. Snoring, the most common symptom of sleep-disordered breathing, is markedly increased during pregnancy. The exact prevalence of obstructive sleep apnea in pregnant women is unknown. Because the apneic episodes are commonly associated with oxyhemoglobin desaturations, the combination of obstructive sleep apnea and pregnancy can be potentially harmful to the fetus given the low oxygen reserves during pregnancy. Obstructive sleep apnea has been associated with an increased risk of hypertension among the general population, and this raises the possibility of its association with gestational hypertension and preeclampsia. In this clinical review, we discuss the physiologic changes of pregnancy that predispose pregnant women to the development of obstructive sleep apnea and the effects of sleep-disordered breathing on pregnancy outcomes. We also review the recom- Sleep-disordered breathing (SDB) includes snoring, upper airway resistance syndrome, and obstructive sleep apnea (OSA)-hypopnea syndrome. OSA-hypopnea syndrome is characterized by recurrent episodes of upper airway collapse and obstruction during sleep and is associated with recurrent oxygen desaturations and arousals from sleep. These disorders represent a continuum of SDB, with snoring at one end of the spectrum and OSAhypopnea syndrome at the other end. The exact prevalence of OSA among pregnant women is unknown. The prevalence of OSA is estimated to be 5% to 6% among women of reproductive age.

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Gasping and autoresuscitation in the developing rat: effect of antecedent intermittent hypoxia

Cited by 51 publications

References 29 publications

Prenatal Nicotine Exposure Alters Central Cardiorespiratory Responses to Hypoxia in Rats: Implications for Sudden Infant Death Syndrome

Prenatal Nicotine Exposure Alters Central Cardiorespiratory Responses to Hypoxia in Rats: Implications for Sudden Infant Death Syndrome

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

Sleep-Disordered Breathing During Pregnancy

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