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Ventilatory instability persists 1 week after lipopolysaccharide (LPS) exposure in newborn rat pups.
Author(s) -
Mason Ariel Vanessa,
Kostuk Eric,
Shirahata Machiko,
Gauda Estelle B
Publication year - 2013
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.27.1_supplement.1135.9
Subject(s) - hyperoxia , medicine , hypoxia (environmental) , lipopolysaccharide , ventilation (architecture) , respiratory rate , apnea , plethysmograph , respiratory system , anesthesia , endocrinology , lung , heart rate , chemistry , blood pressure , oxygen , mechanical engineering , organic chemistry , engineering
Premature infants are frequently exposed to prenatal and postnatal infections, and have persistent and intractable apnea. Since pro‐inflammatory cytokines affect neural mechanisms that control breathing, we hypothesized that LPS given to rat pups at postnatal day 2 (P2 ) would induce unstable breathing that would persist beyond the acute inflammatory episode. Sprague Dawley littermates (n=8, each group) were given either LPS (50–100mcg/kg) or saline, intraperitoneally at P2, and at P9 ventilation was measured with plethysmography and the inter breath interval (IBI) was calculated at baseline and in response to hypoxia and hyperoxia. At baseline, LPS animals had a 3 fold greater number of breaths with an IBI >;0.6 secs in comparison to control animals (6±2 vs 2%, p<0. 01), which persisted during hyperoxia (16±3%vs6±1%, p<0.02). Hypoxia shortened the IBI in both groups with <2% of breaths with a IBI >;0.6 secs. From hypoxia to hyperoxia there was an 14±3% increase in breaths with IBI >;0.6 secs in LPS animals vs a 5±2% increase in control animals (p<0.03). 70±6% and 53±11% of the breaths had IBI <0.35 secs in control and LPS animals, respectively. These data suggest that LPS exposure in newborn rat pups reconfigures the respiratory network leading to breathing instability at baseline and in response to hyperoxia that persist for at least 1 week after the acute inflammatory event. Support: HL81345, R25DA021630