BACTERIAL TRANSLOCATION IN MESENTERIC ISCHEMIA-REPERFUSION INJURY - IS DYSFUNCTIONAL MOTILITY THE LINK

The authors previously reported that mesenteric ischemia and reperfusion ( I R) in a chronic newborn piglet model creates dysfunctional intestinal motility. Whether this leads to inadequate bacterial clearance and translocation (BT) through the gastrointestinal tract remains unclear. To test this hypothesis the authors used their chronic piglet model (weight, 3.5 ± 0.3 kg; age, 18 ± 4 days; on formula feeding); nonocclusive mesenteric ischemia was induced via reversible pericardial tamponade. Mesenteric flow (SMA Doppler measurement via the retroperitoneal approach) was decreased to 25% ± 5% of baseline for 300 minutes in the ischemia group (n = 7) and followed by 14 hours of reperfusion in the I R group (n = 6). Control subjects had a sham operation (n = 7). Mesenteric lymph nodes (MLN), liver (L), spleen (S), ileum, peritoneum, and blood were harvested for blind quantitative microbial analysis. Subjects in the control group had no cultures positive for growth. Eighty-five percent of animals in the ischemia group had positive MLN cultures only (P < .05 v control). All piglets in the I R group had positive MLN cultures (P < .05 v control), and one third of them manifested bacteremia. Histological examination did not show mucosal disruption in any group. The validity of this model is confirmed by the negative cultures in the control group and by the presence of normal ileal flora in all animals. In the ischemia and I R groups, MLN cultures were consistently positive with gram-negative bacilli (Escherichia coli and/or Klebsiella pneumoniae). When subjects of the I R group had more than 1,000 colonies in the MLN, bacteremia with the translocating organisms was also identified. The overall solid organ (L&S) translocation rate was 17% in the I R group but absent in the ischemia-only group. Variables known to contribute to BT were eliminated in our model. The peritoneal cavity was not violated, subjects were studied without the influence of any drugs or anesthesia, and mesenteric ischemia was accomplished without mechanical manipulation of the SMA or hypovolemic shock. To our knowledge, this is the first report of an infant animal model that demonstrates the occurrence of enteric BT following ischemia and I R injury. We suggest that BT is mediated by the dysfunctional motility induced by I R, an abnormality that may be operant in many critically ill infants. © 1994.