Premium
Sleep fragmentation attenuates the hypercapnic ventilatory response via adenosine A1 receptors in awake rats
Author(s) -
Liu Chun,
Cao Ying,
Ling Liming
Publication year - 2009
Publication title -
the faseb journal
Language(s) - English
Resource type - Journals
SCImago Journal Rank - 1.709
H-Index - 277
eISSN - 1530-6860
pISSN - 0892-6638
DOI - 10.1096/fasebj.23.1_supplement.784.2
Subject(s) - hypercapnia , peripheral chemoreceptors , medicine , anesthesia , hypoxic ventilatory response , ventilation (architecture) , control of respiration , adenosine receptor , adenosine , obstructive sleep apnea , antagonist , respiratory system , endocrinology , receptor , agonist , chemoreceptor , mechanical engineering , engineering
As a primary feature of obstructive sleep apnea (OSA), sleep fragmentation (SF) impairs respiratory long‐term facilitation and poikilocapnic hypoxic ventilatory responses. This study investigated the effect of SF on hypercapnic ventilatory responses (HCVR) and its underlying neurochemical mechanism in conscious adult male Sprague‐Dawley rats. SF was achieved by periodic, forced locomotion in a rotating drum (30s rotation/90s stop for 24h). Ventilation during baseline and hypercapnia (FiCO2=0.06) was measured using plethysmography. At ~1h after SF, resting ventilation (43.2±2.4 vs. 47.6±1.8 ml/100g/min) and arterial blood gases (PaCO2: 40.7±0.7 vs. 40.0±0.9; PaO2: 103.8±1.4 vs. 101.6±1.8 mmHg) were not significantly changed, but the HCVR (control: 172.8±17.5% above baseline) was attenuated (129.5±9.6%, p<0.05). This attenuated HCVR then approached spontaneously to the control level ~4h after SF (168.9±12.1%). This HCVR attenuation was also reversed (184.0±17.5%) by systemic injection of the adenosine A1 receptor antagonist 8‐CPT (2.5 mg/kg) shortly after SF, while 8‐CPT had little effect on HCVR in control rats (169.9±11.8%). These findings suggest that: 1) 24h SF causes an attenuated HCVR, which lasts only for several hours; 2) This attenuation requires activation of A1 receptors; and 3) SF of OSA may exacerbate OSA via impaired respiratory chemoreflexes. (Supported by: NIH HL64912)