title: Structural alterations in adult rat carotid bodies exposed to hyperbaric oxygenation.
abstract: Inhibition of carotid body (CB) function is the main mechanism involved in the attenuation of respiratory drive observed during hyperoxia. However, only a few studies at 5.0 atmospheres absolutes (ATA) have analyzed carotid body structure or function in hyperbaric oxygenation (HBO2) situations. We hypothesized that rats will present CB structural alterations when exposed to different lower hyperbaric oxygen doses enough to alter their chemosensory response to hypoxia.
  
  
  METHODS
  Twenty-one adult male Wistar rats, divided into three groups, were maintained in room air or exposed to O2 at 2.4 or 3.0 ATA for six hours. Histological, ultrastructural and immunohistochemical analyses for neuronal nitric oxide synthase (nNOS) and F2-isoprostane were performed in the excised CBs.
  
  
  RESULTS
  Histological analyses revealed signs of intracellular edema in animals exposed to both conditions, but this was more marked in the 3.0 ATA group, which showed ultrastructural alterations at the mitochondrial level. There was a significant increase in the volume density of intraglomic-congested capillaries in the 3.0 ATA group associated with an arteriolar vasoconstriction. In the 2.4 ATA group, there was a relative increase of glomic light cells and a decrease of glomic progenitor cells. Additionally, there was a stronger immunoreactivity for F2-isoprostane in the 3.0 ATA O2-exposed carotid bodies. The glomic cells stained positive for nNOS, but no difference was observed between the groups. Our results show that high O2 exposures may induce structural alterations in glomic cells with signs of lipid peroxidation. We further suggest that deviation of blood flow toward intraglomic capillaries occurs in hyperbaric hyperoxia.
authors.affiliation: Experimental Air Pollution Laboratory, Department of Pathology, School of Medicine, University of Sao Paulo, Sao Paulo, Brazil. magnochi@bol.com.br
authors.forename: M S
authors.initials: MS
authors.lastname: Leite
authors.forename: N R
authors.initials: NR
authors.lastname: Damaceno-Rodrigues
authors.forename: M R P T
authors.initials: MR
authors.lastname: Simone
authors.forename: A B G
authors.initials: AB
authors.lastname: Santos
authors.forename: H M S
authors.initials: HM
authors.lastname: Bueno
authors.forename: C N
authors.initials: CN
authors.lastname: Battlehner
authors.forename: T
authors.initials: T
authors.lastname: Mauad
authors.forename: E G
authors.initials: EG
authors.lastname: Caldini
authors.forename: P H N
authors.initials: PH
authors.lastname: Saldiva
mesh_terms: D000818:Animals; D001160:Arterioles / Q000473:pathology; D002196:Capillaries / Q000473:pathology; D002344:Carotid Body / Q000378:metabolism / Q000503:physiopathology / Q000648:ultrastructure*; D004487:Edema / Q000209:etiology; D028441:F2-Isoprostanes / Q000378:metabolism; D006931:Hyperbaric Oxygenation / Q000009:adverse effects*; D007150:Immunohistochemistry / Q000379:methods; D015227:Lipid Peroxidation; D008297:Male; D008928:Mitochondria / Q000648:ultrastructure; D052248:Nitric Oxide Synthase Type I / Q000378:metabolism; D018384:Oxidative Stress; D051381:Rats; D017208:Rats, Wistar; D014661:Vasoconstriction
chemical_list: D028441:F2-Isoprostanes; D052248:Nitric Oxide Synthase Type I