Abstract 224

Background: IL-1β, a cytokine released in the acute phase reaction to injury, has been shown to induce a local release of prostaglandin E2 (PGE2) in the brainstem. We have shown that PGE2 inhibit brainstem respiratory neurons and hypothesized that IL-1β via PGE2 can impair the ability to autorescucitate and survive an anoxic challenge.

Methods: 7 day old Bkl:SD rats were placed in a barometric plethysmographic chamber, continuous measurement of respiration and skin temperature was performed. IL-1β or Lipopolysaccharides (LPS) (induces release of IL-1β), Indomethacin (a cyclooxygenase inhibitor) and NaCl was injected with 30 min interval i.p. 90 and 60 min before the rats were exposed to 100% N2. 100% oxygen was applied to the chamber when autorescuscitation through gasping had ceased for 60 seconds.

Results: LPS (n=10) and IL-1β (n=8) significantly(p<0.05) decreased the ability to autorescucitate and survive an anoxic challenge. Indomethacin (n=20), 30 min before LPS or IL-1β, could stop this decrease in survival. NaCl (n=15) or Indomethacin (n=10) by themselves did not change survival rate (80%).

Conclusions: These findings indicate that infection and IL-1β via PG have an inhibitory effect on the possibility to autorescucicate after an anoxic challenge. We propose that this is caused by a PGE2 induced depression of brainstem respiratory neurons.