ArticleRespiratory physiology & neurobiology2008
Respiratory plasticity after perinatal hyperoxia is not prevented by antioxidant supplementation.
Article in Respiratory physiology & neurobiology, 2008. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 14 papers.
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Who cites it
14 citing papers in PubMed, 26 citations in OpenAlex.
- Acute and chronic changes in the control of breathing in a rat model of bronchopulmonary dysplasia.American journal of physiology. Lung cellular and molecular physiology · 2019Article
- Combined effects of intermittent hyperoxia and intermittent hypercapnic hypoxia on respiratory control in neonatal rats.Respiratory physiology & neurobiology · 2019Article
- Central and peripheral chemoreceptors in sudden infant death syndrome.The Journal of physiology · 2018Review
- Chronic intermittent hyperoxia alters the development of the hypoxic ventilatory response in neonatal rats.Respiratory physiology & neurobiology · 2016Article
- Hypoxic pulmonary vasoconstriction, carotid body function and erythropoietin production in adult rats perinatally exposed to hyperoxia.The Journal of physiology · 2015Article
- Changes in carotid body and nTS neuronal excitability following neonatal sustained and chronic intermittent hypoxia exposure.Respiratory physiology & neurobiology · 2015Article
- Postnatal development of eupneic ventilation and metabolism in rats chronically exposed to moderate hyperoxia.Respiratory physiology & neurobiology · 2014Article
- Chronic hyperoxia and the development of the carotid body.Respiratory physiology & neurobiology · 2013Review
- Effect of hyperoxic exposure during early development on neurotrophin expression in the carotid body and nucleus tractus solitarii.Journal of applied physiology (Bethesda, Md. : 1985) · 2012Article
- Carotid body growth during chronic postnatal hyperoxia.Respiratory physiology & neurobiology · 2012Article
- Peripheral chemoreceptors: function and plasticity of the carotid body.Comprehensive Physiology · 2012Review
- Chronic hyperoxia alters the early and late phases of the hypoxic ventilatory response in neonatal rats.Journal of applied physiology (Bethesda, Md. : 1985) · 2010Article
- Time course of alterations in pre- and post-synaptic chemoreceptor function during developmental hyperoxia.Respiratory physiology & neurobiology · 2009Article
- Developmental hyperoxia attenuates the hypoxic ventilatory response in Japanese quail (Coturnix japonica).Respiratory physiology & neurobiology · 2008Article
Corrections and comments
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Authors and funding
7 authors at 2 institutions in 1 country.
Funding
Abstract
Perinatal hyperoxia attenuates the hypoxic ventilatory response in rats by altering development of the carotid body and its chemoafferent neurons. In this study, we tested the hypothesis that hyperoxia elicits this plasticity through the increased production of reactive oxygen species (ROS). Rats were born and raised in 60% O(2) for the first two postnatal weeks while treated with one of two antioxidants: vitamin E (via milk from mothers whose diet was enriched with 1000 IU vitamin E kg(-1)) or a superoxide dismutase mimetic, manganese(III) tetrakis (1-methyl-4-pyridyl) porphyrin pentachloride (MnTMPyP; via daily intraperitoneal injection of 5-10 mg kg(-1)); rats were subsequently raised in room air until studied as adults. Peripheral chemoreflexes, assessed by carotid sinus nerve responses to cyanide, asphyxia, anoxia and isocapnic hypoxia (vitamin E experiments) or by hypoxic ventilatory responses (MnTMPyP experiments), were reduced after perinatal hyperoxia compared to those of normoxia-reared controls (all P<0.01); antioxidant treatment had no effect on these responses. Similarly, the carotid bodies of hyperoxia-reared rats were only one-third the volume of carotid bodies from normoxia-reared controls (P <0.001), regardless of antioxidant treatment. Protein carbonyl concentrations in the blood plasma, measured as an indicator of oxidative stress, were not increased in neonatal rats (2 and 8 days of age) exposed to 60% O(2) from birth. Collectively, these data do not support the hypothesis that perinatal hyperoxia impairs peripheral chemoreceptor development through ROS-mediated oxygen toxicity.
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