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Systemic inflammation suppresses hypoxic and hypercapnic ventilatory responses in rats.
Author(s) -
Windelborn James A,
Mitchell Gordon S
Publication year - 2010
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.24.1_supplement.799.32
Subject(s) - hypercapnia , lipopolysaccharide , inflammation , hypoxia (environmental) , systemic inflammation , hypoxic ventilatory response , medicine , endocrinology , intermittent hypoxia , lung , immunology , anesthesia , respiratory system , chemistry , oxygen , organic chemistry , obstructive sleep apnea
Chemoreflex responses to hypoxia and hypercapnia are critical elements of ventilatory control. However, chemoreflexes may be undermined by factors frequently associated with lung disease, such as systemic inflammation. Here, we tested the hypothesis that systemic inflammation suppresses ventilatory responses to hypoxia and hypercapnia in rats. Ventilatory responses were assessed in unanesthetized adult rats via whole‐body plethysmography 1 day after lipopolysaccharide administration (LPS: 1 mg in saline, i.p.). In Lewis rats, LPS suppressed both hypoxic (10.5% O 2 ; vehicle: 90±19%; LPS: 37±11%; p < 0.05) and hypercapnic ventilatory responses (7% CO 2 ; vehicle: 223±22%; LPS: 66±26%; p < 0.05). Splenic iNOS mRNA increased 6.5‐fold (qPCR) in LPS‐treated Lewis rats, demonstrating systemic inflammation. In contrast, there was no evidence for suppressed hypoxic (vehicle: 127±14%; LPS: 92±21%) or hypercapnic ventilatory responses (vehicle: 216±19%; LPS: 239±27%) in LPS‐treated Sprague Dawley rats, nor were splenic iNOS mRNA levels increased. Thus, although LPS sensitivity varies among rat strains, systemic inflammation suppressed chemoreflex responses to hypoxia and hypercapnia. Suppressed chemoreflex responses may impair the ability to respond appropriately to ventilatory challenges in disease states associated with inflammation, including many lung diseases (NIH HL69064 and HL007654 ). Grant Funding Source : NIH HL69064 and HL007654