Abstract

Objective: To assess if endotoxin increases vulnerability to hypoxia and if resuscitation with 100% O2 increases brain damage in the presence of inflammation.Method: After anaesthesia and surgery, newborn piglets (n=31) were randomized to four interventional groups. Two groups received pretreatment with saline for 60 min followed by hypoxia and resuscitation with 21% (Group I, n=8) or 100% oxygen (Group II, n=8). The other two groups received pretreatment with endotoxin for 60 min followed by hypoxia and resuscitation with 21% (Group III, n=7) or 100% oxygen (Group IV, n=8). Hypoxia was administered until base excess (BE) reached –20 mmol/L. Reoxygen with either 21% oxygen or 100% oxygen was administered for the first 30 minutes, followed by 21% oxygen for 150 min for all groups. During the experiment, we measured extracellular brain tissue glucose, glycerol, and lactate/pyruvate by microdialysis, brain tissue oxygen tension and laser doppler flow.Results: Administration of endotoxin caused a reduction in the time to reach BE –20 by median 31.5 minutes compared with saline (p<0.05). We found no differences in biochemical markers, brain tissue microcirculation or brain tissue oxygen tension between piglets pretreated with saline or endotoxin and resuscitated with room air or 100% oxygen in the four groupsConclusion: Endotoxin and hypoxia acted synergistically in inducing arterial acidosis. In the presence of experimental inflammation, 21% seems as safe as 100% O2 in reoxygenating newborn piglets.

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