Abstract
Preischemic perfusion washout with an acellular physiologic solution delays the no-reflow phenomenon and improves tissue survival in rat epigastric free flaps following 18 and 24 hours of normothermic ischemia. This implies that stagnating blood may be a causative agent in the no-reflow phenomenon. A possible mechanism for this is capillary endothelial damage secondary to the presence of formed blood cells or their products of hemolysis. Perfusion washout may improve ischemic tolerance by preventing this blood cell-induced endothelial damage and by the prevention of sludge and thrombus. Whether any of the metabolic components of the perfusate actively enhance ischemic tolerance cannot be definitively stated.
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