Clinically, ischemic necrosis is one of the most common complications in skin flap surgery, but the etiology is still unclear. The objective of the present experiments was to study the important role of the locally released noradrenaline in the pathogenesis of ischemic necrosis in acute and delayed random pattern skin flaps (4 × 10 cm) raised on both flanks of the pig. In Experiment 1, it was observed that 93, 96, and 94% of the skin contents of noradrenaline were depleted in skin flaps delayed for 2, 4, and 14 days, respectively, compared to the acute skin flaps ( n = 8) raised in the same pig. Although the maximum depletion of noradrenaline in the delayed flaps occurred within 2 days of delay, significant ( P < 0.001) increase in the length of dye penetration in the delayed skin flaps was seen after 2 days of delay, compared to the acute skin flaps ( n = 12). In Experiments 2 and 3, 5 days of intravenous phenoxybenzamine treatment, starting 2 days preoperatively and at the doses of 0.25, 0.5, 1.0, or 1.5 mg/kg/day, did not have any significant effect on the skin blood flow ( n = 24) or viability (1 mg/kg/day; n = 32) in the acute skin flaps compared with the saline-treated control. Similarly, 5 days of intravenous phentolamine treatment (5 mg/kg/day) also did not have any significant effect on the skin blood flow ( n = 24) or viability ( n = 32) of acute skin flaps compared with the control. These results indicate that the hyperadrenergic state of the skin per se is unlikely a direct principal cause of skin flap ischemic necrosis in the pig.
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