Abstract
We used lipopolysaccharide (LPS) to induce cytokine‐mediated inflammation and preterm labor. Dams injected with LPS gave birth on G18.5, one day early. Saline injected dams either gave birth at term (G19.5) or had a c‐section (C‐S) on G18.5. Breathing and cardiac function were then assessed <10 and >60 min. after birth. C‐S preterm and term animals had high survival rates (~94%). LPS preterm animals had low survival rates (43%). Survival corresponded with a fast transition from a low frequency, high tidal volume, long duration ('large') breath pattern to a eupneic pattern. Non‐survivors failed to make the transition. Heart rate was directly related to breathing rate and correlated with survival. However, cardiac activity continued after non‐survivors took their last breath indicating that respiratory, not cardiac, failure was the primary cause of death. A subset of animals that did not transition to a eupneic pattern were administered caffeine. Caffeine improved survival outcomes, however, after an anoxic bout these animals had delayed heart and breathing rate recovery times. In conclusion, LPS‐mediated preterm birth increases mortality rates. This is due to a failure to transition from an initial 'large' respiratory pattern to a eupneic pattern and may correspond with an inability to alter network dynamics when transitioning from a low to high oxygen environment.Grant Funding Source: Supported by Seattle Children's Hospital Inter‐Center Funds
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