Hypoxia-induced bacterial translocation in the puppy

Abstract

Because hypoxia is one of the most common major stresses to which a neonate is exposed, we postulated that it alone might be the cause of intestinal bacterial translocation, which could be the underlying etiology of neonatal sepsis. An animal model, in which hypoxia is the sole stress, was developed in our laboratory and tested in 18 puppies to determine the effect of hypoxia and reoxygenation on intestinal bacterial translocation. In group I (n = 8), following laparotomy and cannulation of the superior mesenteric vein (SMV), the FIO 2 was decreased from 21% to 9% for 90 minutes followed by reoxygenation at 21% for 120 minutes. The abdomen was closed and the animals were allowed to recover. After 24 hours the mesenteric lymph nodes (MLNs), spleen, and liver were harvested for bacterial determination and the ileum and jejunum for histological evaluation. Group II (n = 7) was treated the same as group I with the FIO 2 maintained at 21%. Group III (n = 3) animals were killed, without intervention, for bacterial analysis. In group I, the systemic PO 2 decreased by 75%, SMV PO 2 decreased by 64%, and oxygen delivery to the small bowel decreased by 80% in comparison with group II. The mean arterial pressure and cardiac output were not significantly different between group I and group II; however, the mucosal blood flow was decreased by 60% ( P < .001) in group I. Arterial and SMV blood lactic acid levels were unchanged in group I in comparison with group II, suggesting that anerobic metabolism was not initiated in the splanchnic circulation during hypoxia. In group I, products of lipid peroxidation, leukotrienes, thromboxane, and prostaglandins were not significantly changed in comparison with group II. Minimal histological injury was demonstrated in both group I and group II animals; however, the incidence of bacterial translocation to the MLNs in group I (50%, P < .001) was significantly higher than in groups II and III (0%, P < .001). This study demonstrates that severe systemic hypoxia and subsequent reoxygenation does not initiate oxidant-mediated, lipid peroxidation injury to the small bowel mucosa, but does allow bacterial translocation to the MLNs. Thus, hypoxia-induced bacterial translocation could serve as a model for neonatal sepsis without apparent bowel injury.