Abstract

Increasing evidence recognizes the harm of excess oxygen to lungs, eyes, and brain of preterm infants, but not yet to the intestine. We assessed changes in splanchnic oxygenation during reoxygenation with 21% compared to 100% O2 in a newborn piglet model of perinatal asphyxia. We randomized 25 piglets to control or intervention. Intervention groups underwent global hypoxia until acidosis and hypotension occurred. Piglets were reoxygenated for 30 min with 21% or 100% O2 and observed for 9 h. We continuously measured regional splanchnic oxygen saturation (rsSO2) using near-infrared spectroscopy (NIRS). We calculated mean rsSO2 and rsCoVar (as SD/mean). We measured PaO2 and SaO2, sampled from the right carotid artery. Reoxygenation after global hypoxia restored rsSO2. Reoxygenation with 100% O2 increased rsSO2 to values significantly higher than baseline. In intervention groups, rsCoVar decreased during observation compared to baseline. We found a correlation between rsSO2 and PaO2 (r = 0.420, P < 0.001) and between rsSO2 and SaO2 (r = 0.648, P < 0.001) in pooled data from the entire experiment. Reoxygenation after global hypoxia improves splanchnic oxygenation, but is associated with reduced variability of rsSO2. Reoxygenation with 100% O2 exposes the intestine to hyperoxia. Splanchnic NIRS is able to detect intestinal hypoxia and hyperoxia. Splanchnic oxygenation improves during reoxygenation after global hypoxia, though reoxygenation with 100% O2 exposes the intestine to hyperoxia. Decreased variability of splanchnic oxygenation several hours after hypoxia and reoxygenation seems to be independent of the resuscitation strategy, and may indicate intestinal injury. Splanchnic NIRS monitoring was able to detect intestinal hypoxia and exposure to hyperoxia, as evidenced by a strong correlation between splanchnic oxygenation and arterial oxygen content.

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