Augmentation of skeletal muscle flap survival using acute ischaemic preconditioning

Abstract

Large skeletal muscle flaps when elevated in their entirety are complicated by distal ischaemia and necrosis. Flap necrosis is determined by the proximal vascular pedicle’s ability to reperfuse the distal segments and the time taken for that reperfusion. Therefore prolonging the myocytes capacity to withstand ischaemia until reperfusion occurs could increase flap survival. Research in cardiology has shown that ischaemic preconditioning (IPC), i.e. repeated brief periods of ischaemia and reperfusion, prolongs the ability of the myocardium to withstand subsequent extended ischaemia with reduced infarct size.1 Following IPC, two ‘windows of opportunity’ (early and late) exist during which prolonged ischaemia can occur with reduced myocardial infarction. We investigated if IPC of skeletal muscle, prior to flap creation, improved subsequent flap survival and perfusion in either early or late windows. The animal model used was the latissimus dorsi muscle (LDM) of Sprague-Dawley rats: 1. Group 1: (control, n = 12). The LDM was acutely elevated, without IPC, as a thoracodorsally based island flap. 2. Group 2: (early IPC, n = 8). The LDM was preconditioned with two 30-min episodes of normothermic global ischaemia each followed by a 10-min episode of reperfusion and elevated 15 min after IPC. 3. Group 3: (late IPC, n = 8). The LDM was elevated 24 h after IPC. In all groups, muscle perfusion was assessed before and after flap elevation by a laser Doppler perfusion imager; percentage muscle flap necrosis was measured 7 days after flap elevation using computer-assisted digital planimetry. Results: (Table 1) IPC significantly reduced muscle flap necrosis in both early and late windows. Muscle flap perfusion was similar in all groups. We have shown for the first time that (1) IPC of skeletal muscle prior to flap elevation significantly reduces subsequent muscle flap necrosis in both the early and late windows; (2) our results suggest that the protective effects of IPC are not conferred through changes in muscle perfusion; (3) further elaboration of the mechanisms of IPC may allow pharmacological preconditioning in the clinical setting.