Experimental cooling-induced preconditioning attenuates skin flap failure

Background: 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. Methods: Ears of hairless mice were subjected to local hypothermia (30 min, 4°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. Results: 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). Conclusion: In this experimental study preoperative cooling was associated with the expression of HO‐1 and was an effective conditioning procedure. Copyright © 2005 British Journal of Surgery Society Ltd. Published by John Wiley & Sons, Ltd. May help in free flap transfer