Experimental cooling-induced preconditioning attenuates skin flap failure.

Abstract

Microvascular perfusion failure is a leading cause of tissue necrosis in reconstructive surgery. In the present experimental study the effect of local hypothermia was investigated as a possible preconditioning procedure that could induce stress proteins such as heat-shock protein (HSP) 70 and HSP-32 (haem oxygenase (HO) 1). The effect on flap microcirculation and survival was also studied. Ears of hairless mice were subjected to local hypothermia (30 min, 4 degrees C) 24 h before flap creation. A pedicled flap was elevated by incision of four-fifths of the base of the ear. Microcirculatory dysfunction and tissue necrosis were analysed quantitatively over 5 days by means of intravital fluorescence microscopy. HO-1 and HSP-70 protein expression were determined by western blot analysis. HO-1 distribution within the flap tissue was also analysed by immunohistochemistry. Animals with unconditioned flaps served as controls. Cooling induced a marked expression of HO-1 without induction of HSP-70 protein. This was paralleled by a significant improvement in microvascular perfusion (P < 0.050) that was predominantly regulated by the dilatation of nutritive capillaries. The cooling-mediated improvement in microcirculation resulted in a significant reduction in final flap necrosis (P < 0.050). In this experimental study preoperative cooling was associated with the expression of HO-1 and was an effective conditioning procedure.