Endotoxin and transient hypoxia cause severe acidosis in the piglet.

PURPOSE

Both hypoxia and gram-negative sepsis are thought to play a role in the development of necrotizing enterocolitis (NEC). Endotoxin, a lipopolysaccharide (LPS), is a potent mediator of gram-negative sepsis. The author investigated the effect of LPS and hypoxia on arterial and mesenteric venous blood gas values in a piglet model.

METHODS

16 piglets (mean age, 9 days; mean weight, 3.2 kg) were anesthetized and mechanically ventilated. Catheters were placed in the aorta and the superior mesenteric vein (SMV). After a 30-minute stabilization period, piglets were randomly assigned to four experimental groups: normoxic ventilation (FIO2, 0.21), normoxic ventilation and LPS infusion (200 microg/kg, intravenously), hypoxic ventilation (FIO2, 0.10 for 20 minutes), or hypoxic ventilation and LPS infusion. All subjects were then monitored for an additional 30 minutes (recovery period). Multiple, paired blood gas samples were obtained from the aorta and SMV during the stabilization, experimental, and recovery periods.

RESULTS

Piglets subjected to both hypoxia and LPS experienced a much more severe acidosis in both the aorta (pH, 7.10 +/- 0.08) and SMV (pH, 7.03 +/- 0.09) than piglets subjected to either hypoxia or LPS alone (P < .05). In addition, LPS lowered the arterial oxygen saturation in piglets exposed to acute, transient hypoxia (36 +/- 4% v 59 +/- 12%, P < .05).

CONCLUSION

This study suggests that the combination of transient hypoxia and gram-negative sepsis may act synergistically to produce both a severe acidosis and decreased tissue oxygenation.