Respiratory plasticity after perinatal hyperoxia is not prevented by antioxidant supplementation
Autor: | Elizabeth F. Dmitrieff, E. Burt Olson, Julie M. Wenninger, Gerald E. Bisgard, Ryan W. Bavis, Gordon S. Mitchell, Brooke M. Miller |
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Jazyk: | angličtina |
Rok vydání: | 2007 |
Předmět: |
Pulmonary and Respiratory Medicine
medicine.medical_specialty Physiology Metalloporphyrins medicine.medical_treatment Hypoxic ventilatory response Biology Hyperoxia medicine.disease_cause Article Antioxidants Protein Carbonylation Rats Sprague-Dawley Asphyxia Internal medicine Sodium Cyanide medicine Animals Vitamin E Drug Interactions Oxygen toxicity Analysis of Variance Dose-Response Relationship Drug General Neuroscience Carotid sinus Hypoxia (medical) medicine.disease Anorexia Rats Phrenic Nerve medicine.anatomical_structure Endocrinology Carotid Sinus Animals Newborn Anesthesia Carotid body medicine.symptom Oxidative stress |
Popis: | 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 maladaptive plasticity through the increased production of reactive oxygen species (ROS). Rats were born and raised in 60% O2 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 |
Databáze: | OpenAIRE |
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