HOME HELP FEEDBACK SUBSCRIPTIONS ARCHIVE SEARCH TABLE OF CONTENTS		QUICK SEARCH:   [advanced] Author: Keyword(s): Year:  Vol:  Page:

This Article Full Text Full Text (PDF) All Versions of this Article: 287/2/R369    most recent 00128.2004v1 Alert me when this article is cited Alert me if a correction is posted Citation Map Services Email this article to a friend Similar articles in this journal Similar articles in Web of Science Similar articles in PubMed Alert me to new issues of the journal Download to citation manager Citing Articles Citing Articles via Web of Science (2) Citing Articles via Google Scholar Google Scholar Articles by Reeves, S. R. Articles by Gozal, D. Search for Related Content PubMed PubMed Citation Articles by Reeves, S. R. Articles by Gozal, D.

ENVIRONMENTAL, EXERCISE AND RESPIRATORY PHYSIOLOGY

Platelet-activating factor receptor modulates respiratory adaptation to long-term intermittent hypoxia in mice

Departments of Pediatrics and Pharmacology and Toxicology, Kosair Children's Hospital Research Institute, University of Louisville School of Medicine, Louisville, Kentucky 40202

Submitted 24 February 2004 ; accepted in final form 14 April 2004

During hypoxia, release of platelet-activating factor (PAF) and activation of its cognate receptor (PAFR) regulate neural transmission and are required for full expression of peak hypoxic ventilatory response (pHVR) but not hypercapnic ventilatory response. However, it is unclear whether PAFR underlie components of long-term ventilatory adaptations to hypoxia. To examine this issue, adult male PAFR(+/+) and PAFR(–/–) mice were exposed to intermittent hypoxia (IH) consisting of 90 s 21% O₂ and 90 s 10% O₂ for 30 days, and normoxic and hypoxic ventilatory patterns were assessed using whole body plethysmography. Starting at day 14 of IH, normoxic ventilation in PAFR(–/–) was reduced significantly compared with PAFR(+/+) mice (P < 0.001), the latter exhibiting a prominent long-term ventilatory facilitation (LTVF). However, IH-exposed PAFR(–/–) mice had markedly enhanced pHVR and hypoxic ventilatory decline that became similar to those of IH-exposed PAFR(+/+) mice. Thus we postulate that PAFR expression and/or function underlies critical components of IH-induced LTVF but does not play a role in the potentiation of the hypoxic ventilatory response after IH exposures.

respiratory control; hypoxia; synaptic plasticity; central chemosensitivity; ventilatory adaptation; long-term facilitation