title: The effect of lower limb ischaemia-reperfusion on intestinal permeability and the systemic inflammatory response.
abstract: OBJECTIVE
  a relationship has been demonstrated between increased intestinal permeability, endotoxaemia and the development of the systemic inflammatory response syndrome (SIRS) after aortic surgery. The aim of this study was to evaluate whether isolated lower limb ischaemia-reperfusion (I/R) injury affects intestinal mucosal barrier function and cytokine release.
  
  
  METHODS
  four groups of patients were investigated, group I, patients with critical limb ischaemia (CLI) undergoing infra-inguinal bypass surgery (n=18); group II, patients with intermittent claudication (IC) undergoing infra-inguinal bypass surgery (n=14); group III, patients with CLI unsuitable for arterial reconstruction, undergoing major amputation (n=12); and group IV, patients undergoing carotid endarterectomy for symptomatic carotid stenosis (n=13). Intestinal permeability, endotoxaemia and urinary soluble tumour necrosis factor receptors were assessed (p55TNF-R).
  
  
  RESULTS
  an increase in intestinal permeability was observed on the 3rd postoperative day only in CLI group. This was found to correlate with arterial clamp time. Patients who had a femoro-distal bypass had significantly higher intestinal permeability compared to those who had femoro-popliteal bypass. Endotoxaemia was not detected in any of the groups. Postoperative urinary p55TNF-R concentrations were significantly higher in CLI group compared to the other groups. These did not correlate with the increased intestinal permeability.
  
  
  CONCLUSIONS
  our results support the hypothesis that revascularisation of critically ischaemia limbs leads to intestinal mucosal barrier dysfunction and cytokine release. They also suggest that the magnitude of the inflammatory response following I/R injury is related to the degree of initial ischaemia.
authors.affiliation: Vascular Surgery Unit, Belfast City Hospital, Lisburn Road, Belfast, BT9 7AB, Northern Ireland.
authors.forename: W K
authors.initials: WK
authors.lastname: Edrees
authors.forename: L L
authors.initials: LL
authors.lastname: Lau
authors.forename: I S
authors.initials: IS
authors.lastname: Young
authors.forename: M G
authors.initials: MG
authors.lastname: Smye
authors.forename: K R
authors.initials: KR
authors.lastname: Gardiner
authors.forename: B
authors.initials: B
authors.lastname: Lee
authors.forename: R J
authors.initials: RJ
authors.lastname: Hannon
authors.forename: C V
authors.initials: CV
authors.lastname: Soong
mesh_terms: D000368:Aged; D000369:Aged, 80 and over; D016893:Carotid Stenosis / Q000150:complications* / Q000503:physiopathology* / Q000601:surgery; D016207:Cytokines / Q000032:analysis; D005260:Female; D006801:Humans; D007383:Intermittent Claudication / Q000150:complications* / Q000503:physiopathology* / Q000601:surgery; D007413:Intestinal Mucosa / Q000503:physiopathology*; D007511:Ischemia / Q000150:complications* / Q000503:physiopathology* / Q000601:surgery; D007866:Leg / Q000098:blood supply* / Q000503:physiopathology* / Q000601:surgery; D008297:Male; D008875:Middle Aged; D010539:Permeability; D015427:Reperfusion Injury / Q000150:complications* / Q000503:physiopathology*; D012720:Severity of Illness Index; D018746:Systemic Inflammatory Response Syndrome / Q000209:etiology* / Q000503:physiopathology*
chemical_list: D016207:Cytokines