Postprandial Gastrointestinal Blood Flow and Oxygen Consumption: Effects of Hypoxemia in Neonatal Piglets

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Abstract
The effects of feeding on gastrointestinal (GI) perfusion and oxygen transport in hypoxemic neonates is unknown. We evaluated these effects in unanesthetized, spontaneously breathing newborn piglets by comparing three experimental groups: nine hypoxemic piglets (mean PaO2 26 torr) which were fed with formula, six hypoxemic piglets (mean PaO2 27 torr) which were not fed, and four normoxemic piglets (mean PaO2 79 torr) which were fed and served as controls. The control-fed group exhibited an increase in stomach and small intestinal mucosal-submucosal blood flow within 30 min following feeding which was significantly greater than that observed in the hypoxemic fed piglets. GI O2 delivery and O2 uptake rose significantly (p2 content led to significant decreases in GI O2 delivery. Gastrointestinal oxygen uptake remained stable with a compensatory increase in GI O2 extraction. In the hypoxemic-fed piglets, hypoxia significantly decreased stomach blood flow and led to unchanged blood flow in the remainder of the GI tract. Significant reductions in arterial O2 content and GI O2 delivery were observed, accompanied by significant increases in O2 extraction. Hypoxemic fed animals did not exhibit the expected increase in O2 uptake to meet postprandial metabolic demands. When the hypoxemic insult was terminated, fed piglets demonstrated significant total and regional GI hyperemia leading to increased GI O2 uptake when compared with hypoxemic nonfed piglets. We conclude that in the presence of hypoxemia, the newborn piglet's GI tract is subject to decreased oxygen availability. In contrast to the fasted GI tract, the fed GI tract exhibits a significant hyperemia following a limited period of severe hypoxemia and an ability to increase oxygen uptake in an attempt to meet the demands of nutrient absorption. Oxygen uptake is not increased to the same extent as in normoxemic fed animals, thus the efficiency of these mechanisms in satisfying the postprandial O2 demand remains to be determined.

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