GUT IS NOT A SOURCE OF CYTOKINES IN A PORCINE MODEL OF ENDOTOXICOSIS

Background. We sought to determine whether ischemic gut is a source of endotoxin, tumor necrosis factor (TNF), and interleukin-6 (IL-6) in a porcine model of endotoxicosis. Methods. Under general anesthesia pig s underwent neck dissection and laparotomy for placement of catheters in the carotid artery and portal vein and application of an ultrasonic flow probe around the portal vein. Endotoxin, TNF, and IL-6 levels we re measured from the carotid artery and the portal vein during a 4 hou r period in animals given endotoxin (50 mg/kg; n = 6) and in animals i n the control group (n = 6). Gut fluxes of the substances of interest were calculated as the product of concentration and portal venous flow . A tonometer placed in the terminal ileum was used to monitor mucosal pH. Results. Small bowel mucosal pH was significantly depressed in en dotoxemic (6.8 +/- 0.1) when compared with baseline (7.1 +/- 0.1; p < 0.05) and control levels. In the control group portal venous levels of endotoxin, TNF, and IL-6 did not change significantly from baseline l evels (1.5 +/- 0.4 endotoxin units (EU)/ml, 24 +/- 3 pU/ml, and 1.3 +/ - 0.4 nU/ml, respectively). In the endotoxemic animals portal venous e ndotoxin and TNF levels peaked immediately after the endotoxin infusio n (2186 +/- 437 EU/ml and 293 +/- 125 pU/ml, respectively), and portal venous IL-6 levels peaked at 180 minutes (168 +/- 21 nU/ml). At no ti me did endotoxin, TNF, or IL-6 levels differ between arterial and port al venous blood, and at no time did efflux from the gut significantly exceed gut influx in either the control or endotoxemic animals. Conclu sions. Ischemic gut as indicated by decreased mucosal pH is not associ ated with gut release of endotoxin, IL-6, or TNF in this porcine model of endotoxicosis.