LOWER-LIMB ISCHEMIA-REPERFUSION INJURY CAUSES ENDOTOXEMIA AND ENDOGENOUS ANTIENDOTOXIN ANTIBODY CONSUMPTION BUT NOT BACTERIAL TRANSLOCATION

Background It has been suggested that reperfusion of the acutely ischa emic lower limb alters gut permeability. The effect of lower limb isch aemia-reperfusion on systemic endotoxin and antiendotoxin antibody con centrations and the incidence of bacterial translocation was investiga ted. Methods Systemic endotoxin and antiendotoxin antibody concentrati ons were measured in five groups of male Wistar rats: control, after 3 h of bilateral hind limb ischaemia alone, and after 3 h of bilateral hind limb ischaemia followed by 1, 2 or 3 h of reperfusion. A second e xperiment examined translocation of indigenous bacteria following 2 h of reperfusion in a similar model. Results Ischaemia followed by reper fusion for 1, 2 or 3 h caused a significant increase in plasma endotox in concentration to mean(s.e.m.) 10.0(3.0), 44.8(19.2) and 20.2(6.2) p g/ml compared with that in control animals (2.58(0.91) pg/ml) or anima ls in the ischaemia alone group (1.2(0.9)pg/ml) (P < 0.05). This was a ssociated with a significant reduction in endogenous antiendotoxin ant ibody (immunoglobulin (Ig) G and IgM) concentration. No significant ba cterial translocation was detected in any of the groups studied. Concl usion These results demonstrate that a remote and isolated ischaemia-r eperfusion injury to the lower limb, in the absence of infection or ba cterial translocation, causes endotoxaemia. Further studies are needed to evaluate the role of endogenous antiendotoxin antibodies in this s ituation.