Ethanol ingestion potentiates PMN migration into small intestine after ischemia

Neutrophils have been identified to play a major role in ischemia/reperfusion injury through several mechanisms. Neutrophil migration into reperfused gut may reduce bacterial translocation, but may also enhance the reperfusion injury. Ethanol ingestion impairs cutaneous chemotaxis, but its effects on neutrophil migration to postischemic small bowel are unknown. This study investigates the effects of ethanol on small bowel accumulation of neutrophils after ischemia/reperfusion. Ninety-five rats were divided into five groups; normal control, sham operation, ethanol-sham, ischemia, and ethanol-ischemia groups. Ethanol was given once acutely by gavage (3 g/kg, 20% solution) to the animals in the ethanol-sham and the ethanol-ischemia groups 4 hr before ischemic injury. Ischemia was produced for 1 hr by placing a vessel loop around the superior mesenteric vessels. After 1 hr, 87% of animals had gut ischemia and the loop was removed. Three hours later the small bowel was examined for necrosis and the reperfused viable small bowel was extirpated for measurement of neutrophil infiltration by colorimetric assay for myeloperoxidase (MPO), an enzyme restricted to neutrophils. Both ethanol and ischemia/reperfusion produced significant independent increase in the MPO activity. When ethanol was given prior to ischemia, the MPO activity was further increased by statistically significant margin. The present study demonstrated that ethanol enhanced the effects of gut ischemia/reperfusion injury on PMN accumulation into the intestinal wall. These observations suggest that ethanol may potentiate ischemic injury to the gut and lead to increased problems when gut blood flow is significantly impaired.