Maturation of peripheral arterial chemoreceptors in relation to neonatal apnoea

Gauda, Estelle B.; McLemore, Gabrielle L.; Tolosa, José Nieto; Marston-Nelson, Jannette; Kwak, D. J.

doi:10.1016/j.siny.2003.11.002

Cited by 80 publications

(43 citation statements)

References 133 publications

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“…The cause of this depressive phase is not well understood, but this type of response can persist for various weeks of post-natal life. 16 Various neurotransmitters are involved in the hypoxic depressive response, including adenosine, endorphins, and gamma-aminobutyric acid. Neurotransmitter blockers (methylxanthines for adenosine, naloxone for endorphins) act before the late depressive ventilation phase.…”

Section: Control Of Breathing and Responses To Hypercapnia And Hypoxiamentioning

confidence: 99%

Apnea of prematurity: challenges and solutions

Picone¹,

Aufieri²,

Paolillo³

2014

RRN

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Apnea of prematurity is a developmental disorder that frequently affects preterm infants, especially those with lower gestational age. Even if apnea of prematurity is by definition a self-limiting condition, it can cause serious problems during the hospital stay and can potentially have long-term neurological and cognitive consequences depending on the severity and intensity of the episodes. The diagnosis of apnea of prematurity can be made only after excluding a number of diseases of the preterm infant in which apnea may be an epiphenomenon. Etiological diagnosis is essential for selection of appropriate treatment, which may be nonpharmacological or involve use of drugs.

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Section: Control Of Breathing and Responses To Hypercapnia And Hypoxiamentioning

confidence: 99%

Apnea of prematurity: challenges and solutions

Picone¹,

Aufieri²,

Paolillo³

2014

RRN

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“…It is believed that some respiratory disorders of the newborn, such as the sudden infant death syndrome (SIDS) could be due to primary alterations of the CB chemoreceptors [80,81]. Abnormalities in CB size or transmitter content have been reported in victims of SIDS.…”

Section: Carotid Body Function and Mechanisms Of Diseasementioning

confidence: 99%

Carotid body oxygen sensing

López‐Barneo¹,

Ortega-Sáenz²,

Pardal³

et al. 2008

European Respiratory Journal

122

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The carotid body (CB) is a neural crest-derived organ whose major function is to sense changes in arterial oxygen tension to elicit hyperventilation in hypoxia. The CB is composed of clusters of neuron-like glomus, or type-I, cells enveloped by glia-like sustentacular, or type-II, cells. Responsiveness of CB to acute hypoxia relies on the inhibition of O 2 -sensitive K + channels in glomus cells, which leads to cell depolarisation, Ca 2+ entry and release of transmitters that activate afferent nerve fibres. Although this model of O 2 sensing is generally accepted, the molecular mechanisms underlying K + channel modulation by O 2 tension are unknown. Among the putative hypoxia-sensing mechanisms there are: the production of oxygen radicals, either in mitochondria or reduced nicotinamide adenine dinucleotide phosphate oxidases; metabolic mitochondrial inhibition and decrease of intracellular ATP; disruption of the prolylhydroxylase/ hypoxia inducible factor pathway; or decrease of carbon monoxide production by haemoxygenase-2. In chronic hypoxia, the CB grows with increasing glomus cell number. The current authors have identified, in the CB, neural stem cells, which can differentiate into glomus cells. Cell fate experiments suggest that the CB progenitors are the glia-like sustentacular cells. The CB appears to be involved in the pathophysiology of several prevalent human diseases.

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“…N umerous studies in mammalian species support a role for peripheral arterial chemoreceptors in stabilizing ventilation at a critical period during early postnatal development, which establishes rhythmogenesis that is sustained throughout life (1,2). The components of the peripheral arterial chemoreceptors are found within the carotid body that is located in the bifurcation of the carotid artery and consists of three major neuronal components that include: 1) type I chemosensory cells, also known as glomus cells, which contain neurotransmitters and autoreceptors; 2) type II cells, which are similar to supportive glial cells; and 3) chemoafferent nerve fibers from the carotid sinus nerve, a branch of the IX cranial nerve, with cell bodies in the petrosal ganglion (PG) (3,4).…”

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confidence: 99%

The Effect of Hyperoxia on Reactive Oxygen Species (ROS) in Rat Petrosal Ganglion Neurons During Development Using Organotypic Slices

Kwak

Gauda

2006

Pediatr Res

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Hyperoxia, during development in rats, results in hypoxic chemosensitivity ablation, carotid body hypoplasia, and reduced chemoafferents. We hypothesized that hyperoxia increases reactive oxygen species (ROS) in cell bodies of chemoafferents. Organotypic slices of petrosal-nodose ganglia from rats at day of life (DOL) 5-6 and 17-18 were exposed to 8%, 21%, or 95% O 2 for 4 h in the presence or absence of the ROS-sensitive fluorescent indicator, CM-H 2 DCFDA, and propidium iodide was used to determine the relationship between cell death and oxygen tension. In tissue slices from DOL 5-6 rats, fluorescence intensity was 182.5 Ϯ 2.9 for hypoxia, 217.5 Ϯ 3.3 for normoxia, and 336.6 Ϯ 3.8 for hyperoxia, (mean Ϯ SEM, p Ͻ 0.001, ANOVA). Normoxia increased ROS levels by 19.2% from hypoxia (p Ͻ 0.01) with a further increase of 54.8% from normoxia to hyperoxia (p Ͻ 0.001). In tissue slices from DOL 17-18 rats, ROS levels increased with increasing oxygen tension but were less than in younger animals (p Ͻ 0.01, ANOVA). The antioxidants, NAC and TEMPO-9-AC, attenuated ROS levels and cell death. Electron microscopy demonstrated that hyperoxia damages the ultrastructure within petrosal ganglion neurons. Hyperoxic-induced increased levels of ROS in petrosal ganglion neurons may contribute to loss of hypoxic chemosensitivity during early postnatal development. N umerous studies in mammalian species support a role for peripheral arterial chemoreceptors in stabilizing ventilation at a critical period during early postnatal development, which establishes rhythmogenesis that is sustained throughout life (1,2). The components of the peripheral arterial chemoreceptors are found within the carotid body that is located in the bifurcation of the carotid artery and consists of three major neuronal components that include: 1) type I chemosensory cells, also known as glomus cells, which contain neurotransmitters and autoreceptors; 2) type II cells, which are similar to supportive glial cells; and 3) chemoafferent nerve fibers from the carotid sinus nerve, a branch of the IX cranial nerve, with cell bodies in the petrosal ganglion (PG) (3,4).Exposure to chronic hyperoxia, during the first weeks of postnatal development, depresses ventilatory responses to subsequent acute hypoxia in newborn animals and in premature infants (5-7). Hyperoxic exposure in newborn rat pups is cytotoxic to peripheral arterial chemoreceptors as evidenced by hypoplasia of the carotid body and a 41% reduction in the number of chemoafferent neurons (8). The mechanisms leading to cytotoxic changes in the carotid body and the reduction in chemoreflexes after hyperoxicexposure during early postnatal development are unknown. In other model systems, hyperoxia is associated with increased production of ROS, including superoxide, hydroxyl radical, and hydrogen peroxide, which can contribute to cellular damage via lipid peroxidation, enzyme inactivation, and protein and nucleic acid oxidation, resulting in apoptosis or necrosis (9). Using a novel ex vivo organotypic s...

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Maturation of peripheral arterial chemoreceptors in relation to neonatal apnoea

Cited by 80 publications

References 133 publications

Apnea of prematurity: challenges and solutions

Apnea of prematurity: challenges and solutions

Carotid body oxygen sensing

The Effect of Hyperoxia on Reactive Oxygen Species (ROS) in Rat Petrosal Ganglion Neurons During Development Using Organotypic Slices

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