Kinetics of endotoxin concentration and tumor necrosis factor-alpha, interleukin-1beta, and interleukin-6 activities in the systemic and portal circulation during small intestinal ischemia and reperfusion in dogs.
OBJECTIVE
To determine whether small intestinal ischemia and reperfusion induces bacterial translocation and proinflammatory cytokine response in either the systemic or portal circulation in dogs.


METHODS
17 healthy adult Beagles.


METHODS
The superior mesenteric artery (SMA) was occluded for 0 (group-3 dogs), 30 (group-1 dogs), or 60 (group-2 dogs) minutes, followed by reperfusion for 180 minutes; serum lactate and endotoxin concentrations and tumor necrosis factor-alpha (TNF-alpha), interleukin-1beta (IL-1beta), and IL-6 activities in the systemic and portal circulation and intramucosal pH were measured at various time points.


RESULTS
In group-2 dogs, TNFalpha activity was found to be significantly increased in the portal circulation, peaking at 60 minutes of reperfusion; TNF-alpha activity, in the systemic circulation, gradually increased from 60 minutes of reperfusion to the end of the experiment; however, the increase was not significant. In group-1 and -2 dogs, IL-6 activities significantly and gradually increased in the systemic and portal circulation during the reperfusion phase, and the magnitude of these increases was dependent on the duration of the ischemic phase. There were no significant changes in IL-1beta activity or endotoxin concentration in any dog group.


CONCLUSIONS
Results of the our study indicate that intestinal ischemia and reperfusion leads to significant increases of the circulating TNF-alpha and IL-6 activities, depending on the duration of the ischemia phase, in the absence of detectable endotoxin in the circulation. This finding suggests that intestinal ischemia and reperfusion induces a systemic proinflammatory cytokine response in dogs.
Nezu
Yoshinori
Y
Department of Veterinary Science, Division of Veterinary Surgery, Nippon Veterinary and Animal Science University, 1-7-1 Kyonan-cho, Musashino-shi, Tokyo 18048602, Japan.
Tagawa
Masahiro
M
Sakaue
Yoko
Y
Hara
Yasushi
Y
Tsuchida
Shuichi
S
Ogawa
Ryo
R
D000818:Animals; D001681:Biological Assay / Q000662:veterinary; D003601:Cytotoxicity Tests, Immunologic / Q000662:veterinary; D004283:Dog Diseases / Q000097:blood* / Q000276:immunology; D004285:Dogs; D004731:Endotoxins / Q000096:biosynthesis / Q000097:blood*; D005260:Female; D006801:Humans; D007378:Interleukins / Q000096:biosynthesis / Q000097:blood*; D007421:Intestine, Small / Q000098:blood supply* / Q000276:immunology; D007511:Ischemia / Q000097:blood / Q000276:immunology; D019344:Lactic Acid / Q000097:blood; D008297:Male; D008638:Mesenteric Arteries; D051379:Mice; D011168:Portal System; D015427:Reperfusion Injury / Q000097:blood / Q000276:immunology / Q000662:veterinary*; D014065:Tonometry, Ocular / Q000662:veterinary; D014407:Tumor Cells, Cultured; D014409:Tumor Necrosis Factor-alpha / Q000096:biosynthesis / Q000378:metabolism*
D004731:Endotoxins; D007378:Interleukins; D014409:Tumor Necrosis Factor-alpha; D019344:Lactic Acid