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Aerosolized capsaicin (CAP) pretreatment prevents lipopolysaccharide (LPS)‐induced inhibition of ventilatory responses to hypoxia and hypercapnia in rats
Author(s) -
Zhuang Jianguo,
Zhang Cancan,
Xu Fadi
Publication year - 2008
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.22.1_supplement.1172.14
Subject(s) - hypercapnia , lipopolysaccharide , hypoxic ventilatory response , bronchoalveolar lavage , capsaicin , medicine , hypoxia (environmental) , anesthesia , inflammation , respiratory system , pharmacology , lung , endocrinology , chemistry , receptor , organic chemistry , oxygen
LPS causes pulmonary inflammation and blunted hypoxic (HVR) and hypercapnic ventilatory responses (HCVR) in anesthetized rats. Because CAP is a potent stimulant of bronchopulmonary C‐fibers (PCFs) and it promotes pulmonary inflammation, we hypothesized that the LPS‐induced inhibition of HCVR and HVR was aggravated by CAP pretreatment. Rats were exposed to either aerosolized CAP (0.4 mg/ml) or vehicle for 5 days for two 5‐min episodes daily that were 4 hr apart. After the pretreatment, the rats were intratracheally instilled with LPS (0.5 mg/0.5 ml) or saline, and anesthetized and tracheotomized 2 days later. Animals’ ventilatory responses to 10% O 2 and 10% CO 2 for 1 min and apneic response to right atrial bolus‐injections of CAP (1 and 4 μg/0.1 ml) were measured, and the bronchoalveolar lavage fluid (BALF) collected at the end of the experiments. We found that: 1) CAP and/or LPS pretreatment did not affect baseline ventilation; 2) LPS rather than CAP pretreatment alone inhibited HCVR (↓ 63%, P < 0.01) and HVR (↓47%, P < 0.05); 3) these LPS‐induced inhibitions disappeared in CAP‐pretreated rats; and 4) BALF total cell count was significantly increased by LPS, and this increase was not affected by coupling it with CAP pretreatment. We conclude that CAP pretreatment eliminates the LPS‐induced inhibitory effects on HVR and HCVR with little impact on LPS‐induced pulmonary inflammation. (Supported by NIH 74183).