THERMOTOLERANCE INDUCES HEAT-SHOCK-PROTEIN-72 EXPRESSION AND PROTECTSAGAINST ISCHEMIA-REPERFUSION-INDUCED LUNG INJURY

Background Ischaemia-reperfusion injury is mediated by neutrophil-endo thelial interaction. Induction of heat shock proteins attenuates neutr ophil-endothelial interactions. The aim of this study was to determine whether thermal preconditioning could have a protective effect on neu trophil-mediated lung injury in an animal model of lower torso ischaem ia-reperfusion. Methods Sprague-Dawley rats were randomized into: cont rol, ischaemia-reperfusion, and ischaemia-reperfusion preconditioned w ith hyperthermia groups. Ischaemia-reperfusion injury was induced by i nfrarenal aortic clamping for 30 min and reperfusion for 120 min. Ther motolerance was induced by raising the core body temperature to 40.5-4 1.5 degrees C for 15 min, 18 h before ischaemia-reperfusion. Wet:dry l ung (W:D) weight ratio, bronchoalveolar lavage protein (BAL(prot)) con centration, tissue myeloperoxidase (MPO) activity and bronchoalveolar lavage polymorphonuclear neutrophil (BAL PMN) count were measured. Hea t shock protein 72 (hsp72) expression in lung, intestine and mesentery was measured using Western immunoblotting. Results Ischaemia-reperfus ion resulted in a significant increase in tissue oedema (W:D weight ra tio) and BAL,,,, concentration. In addition there was a marked increas e in tissue neutrophil infiltration (MPO activity, BAL PMN concentrati on). Preconditioning with hyperthemia resulted in increased expression of hsp72 and significantly reduced tissue oedema and neutrophil infil tration. Conclusion Thermal preconditioning protects against neutrophi l-mediated ischaemia-reperfusion-induced lung injury, possibly by incr easing the expression of heat shock proteins.