VISUALIZATION OF NUTRITIVE PERFUSION FOLLOWING TOURNIQUET ISCHEMIA INARTERIAL PATTERN SKIN FLAPS - EFFECT OF VASOACTIVE MEDICATION

We present an experimental model that makes it possible to investigate the effects of global ischemia and reperfusion on microvascular perfu sion and viability of ill-proportioned (poorly designed) arterial patt ern skin flaps in hairless mice. Skin flaps were created on the ears o f hairless mice by dissecting two of three nutritional vessel bundles at the ear base. Under these nonischemic conditions, 19 percent of the total flap area went on to necrose (as a result of poor flap design). Global ischemia was induced to the flap tissue for 6 hours with a tou rniquet clamp directly after flap incision. The extension of perfused tissue area and flap viability were assessed at the microcirculatory l evel by intravital video microscopy at 1, 3, 6, and 18 hours and 7 day s after reperfusion in animals treated with either normal saline (cont rol) or the vasoactive drug buflomedil hydrochloride (3 mg/kg of body weight per day, IV, starting 4 hours prior to flap creation and contin ued at daily intervals until the end of the experiments). In untreated animals (n = 18), 1 hour after clamp release we observed reperfusion of 39.55 percent (38.5/44.9) of total flap area. Reperfusion remained unchanged within the following 5 hours. Within the next 12 hours, repe rfused flap area was dramatically reduced to 21.9 percent (15.1/58.4). Seven days thereafter, only 18.8 percent (10.9/42.2) of total flap ar ea remained viable. In contrast, we found in buflomedil-treated animal s (n = 18) that 57.3 percent (53.5/62.9) of the total flap tissue was reperfused within the first hour after clamp release (p < 0.01). As in control experiments, reperfusion remained unchanged during the follow ing measurements 3 and 6 hours after reperfusion and then started to d ecline slowly to 54.7 percent (46.9/63.3) of total flap area 18 hours after reperfusion. In buflomedil-treated animals, we observed a more h omogeneous perfusion of capillaries and reduced macromolecular leakage . At the end of the experiments, preoperative treatment with the vasoa ctive drug significantly increased skin-flap viability from 18.8 perce nt (10.2/42.2) in control animals to 53.2 percent (41.8/68.7) (p < 0.0 01). This study provides evidence that formation of skin-flap necrosis in ischemic flaps in our model is caused by the combination of poor f lap design and tissue damage induced by ischemia as well as by reperfu sion and reoxygenation of the flaps.