Gut ischemia/reperfusion produces lung injury independent of endotoxin.
OBJECTIVE
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.


METHODS
Prospective, randomized study.


METHODS
Animal laboratory.


METHODS
Sprague-Dawley rats weighing 300 to 350 g.


METHODS
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.


RESULTS
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.


CONCLUSIONS
Gut ischemia/reperfusion primes circulating neutrophils and produces lung injury by a mechanism independent of endotoxin.
Koike
K
K
Department of Surgery, Denver General Hospital, CO.
Moore
E E
EE
Moore
F A
FA
Read
R A
RA
Carl
V S
VS
Banerjee
A
A
D000818:Animals; D004731:Endotoxins / Q000097:blood; D007421:Intestine, Small / Q000098:blood supply*; D008168:Lung / Q000503:physiopathology*; D017538:Mesenteric Artery, Superior; D008641:Mesenteric Vascular Occlusion / Q000150:complications*; D009504:Neutrophils / Q000502:physiology; D011446:Prospective Studies; D011897:Random Allocation; D051381:Rats; D017207:Rats, Sprague-Dawley; D015427:Reperfusion Injury / Q000209:etiology / Q000503:physiopathology*
D004731:Endotoxins