Gut ischemia/reperfusion produces lung injury independent of endotoxin

• Published in: Critical care medicine Vol. 22; no. 9; p. 1438
• Main Authors: Koike, K, Moore, E E, Moore, F A, Read, R A, Carl, V S, Banerjee, A
• Format: Journal Article
• Language: English
• Published: United States 01.09.1994
• Subjects: Animals; Endotoxins - blood; Intestine, Small - blood supply; Lung - physiopathology; Mesenteric Artery, Superior; Mesenteric Vascular Occlusion - complications; Neutrophils - physiology; Prospective Studies; Random Allocation; Rats; Rats, Sprague-Dawley; Reperfusion Injury - etiology; Reperfusion Injury - physiopathology
• ISSN: 0090-3493
• DOI: 10.1097/00003246-199409000-00014

Bacterial translocation from the gut has been invoked as a common inciting event for postinjury multiple organ failure. We previously showed that gut ischemia/reperfusion induces remote organ injury. The purpose of this study was to ascertain if endotoxin has a pivotal mechanistic role in this process. Prospective, randomized study. Animal laboratory. Sprague-Dawley rats weighing 300 to 350 g. Anesthetized animals underwent 45 mins of superior mesenteric artery occlusion and 2 hrs of reperfusion; sham laparotomy served as controls. Endotoxin was eliminated with the murine immunoglobulin (Ig) M antibody E5, 3 mg/kg i.v. before the study. Plasma endotoxin was measured by the limulus amebocyte lysate assay. At 2 hrs of reperfusion, circulating neutrophil priming was determined by the difference in superoxide generation with and without the activating stimulus, N-formyl-Met-Leu-Phe. Neutrophil sequestration in the lung was quantitated by myeloperoxidase activity, and by lung endothelial permeability by 125I albumin lung/blood ratio. Endotoxin concentrations were not significantly (significance determined as p < .05) different between the gut ischemia/reperfusion and laparotomy groups (n = > or = 5) during ischemia or reperfusion. Circulating neutrophil priming, neutrophil accumulation in the lung, and lung injury were provoked by gut ischemia/reperfusion, but not altered by endotoxin elimination. Gut ischemia/reperfusion primes circulating neutrophils and produces lung injury by a mechanism independent of endotoxin.