Octreotide does not prevent bacterial translocation in an infant piglet model of intestinal ischemia-reperfusion.

The process of bacterial translocation (BT) after ischemia/reperfusion (I/R) injury is reported to be mediated by local mucosal factors, the effects of pancreatic enzymes, epithelial disruption, and by dysfunctional intestinal motility. Octreotide (OCT), a somatostatin analog, has been postulated to protect against BT by influencing one or more of these factors. Twenty-two formula-fed piglets (weight, 3.5 +/- 0.5 kg; age, 20 +/- 5 days) were divided into four groups: control (no drug given; no I/R; n = 6), I/R (no drug given; n = 5), I/R plus low-dose OCT (LD OCT, 0.08 microgram/kg; n = 6), and I/R plus high-dose OCT (HD OCT, 8 micrograms/kg; n = 5). All experimental subjects had nonocclusive mesenteric ischemia induced by reversible pericardial tamponade with mesenteric flow decreased to 25 +/- 5% of baseline for 5 hours followed by 15 +/- 5 hours of reperfusion. Mesenteric lymph nodes (MLN), liver, spleen, blood, and peritoneum were harvested for blind microbial analysis. None of the animals in the control group experienced translocation to the tissues tested. All of the animals in the I/R group experienced BT to the MLN. The subjects in the LD OCT and HD OCT groups experienced BT to the MLN 66% and 80% of the time, respectively. Despite the reported clinical evidence that OCT can protect the intestinal mucosa from injury and increase the clearance of bacteria from the gastrointestinal tract, in this study in which variables other than I/R known to promote bacterial translocation were eliminated, OCT failed to modify or prevent the occurrence of translocation to the MLN after I/R injury.