title: Ischemic preconditioning protects against gut dysfunction and mucosal injury after ischemia/reperfusion injury.
abstract: Mesenteric ischemia/reperfusion (IR) damages the gastrointestinal epithelia and impairs gut function. Ischemic preconditioning (IPC) has been shown to protect organs against IR injury. We hypothesized that IPC protects the gut from IR injury. Rats were randomized to a sham group, a sham early IPC + IR group (sham IPC + SMA occlusion for 30 min and 6 h of reperfusion), an early IPC + IR group (IPC, three cycles of SMA occlusion for 4 min and reperfusion for 10 min) followed immediately by SMA occlusion for 30 min and 6 h of reperfusion), a sham 24-h group, a sham late IPC + IR group (sham IPC followed by additional reperfusion for 24 h + SMA occlusion for 30 min and 6 h of reperfusion), and a late IPC + IR group (IPC protocol followed by additional reperfusion for 24 h, and then SMA occlusion for 30 min followed by 6 h of reperfusion). At 6 h, transit was determined and expressed as the mean geometric center. Ileum was harvested for assessment of mucosal injury and myeloperoxidase (MPO) activity. Tissue water was determined using the wet-to-dry weight ratio to assess gut edema. Early IPC + IR significantly improved transit (3.9 +/- 0.2), decreased MPO levels (3 +/- 2), and lessened mucosal injury (1.2 +/- 0.3) compared with animals subjected to sham early IPC + IR (transit, 2.9 +/- 0.2; MPO levels, 9 +/- 1; mucosal injury, 3.0 +/- 0.6). Late IPC + IR also improved transit (6.0 +/- 0.4) and decreased MPO levels (1 +/- 1) compared with sham late IPC + IR (transit, 4.4 +/- 0.2; MPO levels, 8 +/- 1), however, there was no difference in the mucosal protection between late IPC + IR (1 +/- 0.3) and sham late IPC + IR (1 +/- 1). Our results suggest that early and late IPC improves intestinal dysfunction, decreases inflammation, and provides mucosal protection in the intestine after IR. Our results show that IR-induced gut dysfunction can be improved by IPC. Both phases of IPC can potentially be useful in the clinical setting of surgical patient care.
authors.affiliation: Department of Surgery, University of Texas Medical School, Houston, TX 77030, USA.
authors.forename: Stacey D
authors.initials: SD
authors.lastname: Moore-Olufemi
authors.forename: Rosemary A
authors.initials: RA
authors.lastname: Kozar
authors.forename: Frederick A
authors.initials: FA
authors.lastname: Moore
authors.forename: Norio
authors.initials: N
authors.lastname: Sato
authors.forename: Heitham T
authors.initials: HT
authors.lastname: Hassoun
authors.forename: Charles S
authors.initials: CS
authors.lastname: Cox
authors.forename: Bruce C
authors.initials: BC
authors.lastname: Kone
mesh_terms: D000818:Animals; D004064:Digestive System / Q000098:blood supply* / Q000293:injuries* / Q000503:physiopathology; D004487:Edema / Q000209:etiology; D005772:Gastrointestinal Transit; D019194:Ischemic Preconditioning / Q000009:adverse effects / Q000379:methods; D008297:Male; D017538:Mesenteric Artery, Superior / Q000293:injuries; D009195:Peroxidase / Q000037:antagonists & inhibitors; D051381:Rats; D017207:Rats, Sprague-Dawley; D015427:Reperfusion Injury / Q000473:pathology / Q000503:physiopathology / Q000517:prevention & control*; D013152:Splanchnic Circulation
chemical_list: D009195:Peroxidase