Vagal afferents modulate cytokine-mediated respiratory control at the neonatal medulla oblongata
Autor: | Zana Hoxha, Catherine A. Mayer, Kannan V. Balan, Christopher G. Wilson, Richard J. Martin, Prabha Kc |
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Rok vydání: | 2011 |
Předmět: |
Lipopolysaccharides
Male Pulmonary and Respiratory Medicine medicine.medical_specialty Physiology medicine.medical_treatment Hypoxic ventilatory response Biology Article Proinflammatory cytokine Internal medicine medicine Animals Medulla Afferent Pathways Medulla Oblongata General Neuroscience Area postrema Solitary tract Vagus Nerve Vagotomy Rats Inbred F344 Rats Vagus nerve Endocrinology Animals Newborn Anesthesia Respiratory Mechanics Medulla oblongata Cytokines Female |
Zdroj: | Respiratory Physiology & Neurobiology. 178:458-464 |
ISSN: | 1569-9048 |
DOI: | 10.1016/j.resp.2011.03.003 |
Popis: | Perinatal sepsis and inflammation trigger lung and brain injury in preterm infants, and associated apnea of prematurity. We hypothesized that endotoxin exposure in the immature lung would upregulate proinflammatory cytokine mRNA expression in the medulla oblongata and be associated with impaired respiratory control. Lipopolysaccharide (LPS, 0.1 mg/kg) or saline was administered intratracheally to rat pups and medulla oblongatas were harvested for quantifying expression of mRNA for proinflammatory cytokines. LPS-exposure significantly increased medullary mRNA for IL-1β and IL-6, and vagotomy blunted this increase in IL-1β, but not IL-6. Whole-body flow plethysmography revealed that LPS-exposed pups had an attenuated ventilatory response to hypoxia both before and after carotid sinus nerve transection. Immunochemical expression of IL-1β within the nucleus of the solitary tract and area postrema was increased after LPS-exposure. In summary, intratracheal endotoxin-exposure in rat pups is associated with upregulation of proinflammatory cytokines in the medulla oblongata that is vagally-mediated for IL-1β and associated with an impaired hypoxic ventilatory response. |
Databáze: | OpenAIRE |
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