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Exposure to chronic intermittent hypoxia does not elicit aberrant respiratory plasticity in adult guinea pig
Author(s) -
O'Connor Karen M.,
Lucking Eric F.,
Burns David P.,
O'Halloran Ken D.
Publication year - 2017
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.31.1_supplement.1055.16
Subject(s) - hypercapnia , hypoxic ventilatory response , hypoxia (environmental) , medicine , tidal volume , ventilation (architecture) , carotid body , anesthesia , respiratory system , respiratory minute volume , basal metabolic rate , respiratory rate , plethysmograph , endocrinology , cardiology , heart rate , blood pressure , oxygen , chemistry , stimulation , mechanical engineering , organic chemistry , engineering
Chronic intermittent hypoxia (CIH), a major pathological feature of obstructive sleep apnoea, enhances carotid body (CB) chemosensory responses to hypoxia producing enhanced basal breathing and ventilatory responsiveness to hypoxia, increased respiratory instability, autonomic dysfunction, cardiac arrhythmias, and hypertension. CIH may also affect metabolic rate. We sought to explore if CIH induces ventilatory and/or metabolic changes in guinea‐pigs, a species that presents with hypoxia insensitive carotid bodies. Duncan Hartley adult male guinea pigs were exposed to repeated 5 minute cycles consisting of 90s hypoxia (FiO 2 =0.05 nadir) and 210s normoxia (FiO 2 = 0.21) for 8 hours per day for 2 weeks (CIH, n=8). Sham animals (n=8) were subjected to the same environmental cues but were constantly exposed to room air. Guinea pigs had free access to food and water throughout the exposure. Using whole‐body plethysmography, ventilation and metabolism were measured during air breathing (FiO 2 = 0.21), hypoxia (FiO 2 = 0.10) and hypercapnia (FiCO 2 = 0.05) in unanesthetised, unrestrained animals at quiet rest. Data are presented as mean±SD and were analysed using unpaired Student t tests or Mann‐Whitney U tests. Baseline ventilation and metabolism in normoxia were unaffected by exposure to CIH. As such, the ventilatory equivalent (V E /VCO 2 ) was similar in CIH exposed and sham animals: 41.2±10.7 versus 35.6±5.2 (p=0.201; sham versus CIH). Exposure to acute hypoxia (FiO 2 = 0.10 for 10 mins) did not alter V E , tidal volume (V T ) or respiratory frequency ( f ), both in sham (47±4ml/min/100g; 0.5±0.04ml/100g and 103±9bpm, respectively) and CIH exposed animals (45±5ml/min/100g; 0.5±0.006ml/100g and 98±5bpm, respectively) compared with respective baseline values. Metabolism (VCO 2 ) during acute hypoxia was not significantly different between the two groups (1.01±0.09 versus 1.16±0.2ml/min/100g). Nonetheless, V E /VCO 2 was significantly decreased in CIH exposed animals compared with sham (46.6±2.9 versus 39.5±2.5; p=0.0001). In response to hypercapnia, CIH exposed animals had a significantly blunted tidal volume response compared with sham animals (1.1±0.01ml/100g versus 0.84±0.01ml/100g; sham versus CIH). However, V E /VCO 2 during acute hypercapnia was not different between the two groups. Our data reveals that CIH exposure does not affect basal breathing, nor does it enhance hypoxic ventilatory responsiveness, which has been described in rats and mice with hypoxia sensitive carotid bodies. Our study employing a species with hypoxia insensitive carotid bodies suggests a critical role for CIH‐induced plasticity in peripheral oxygen sensing mechanisms within the carotid body in the manifestation of aberrant respiratory control. Support or Funding Information Department of Physiology, School of Medicine, University College Cork