RESUMO
Surgical delay of skin flaps before transfer is known to improve flap viability. This study attempts to elucidate the mechanism of vasodilation by exploring the effects of nitric oxide on the microcirculation of delayed skin flaps. Using a skin flap model in 22 CD-1 white mice, the diameter of two nonterminal choke arteries was measured using in vivo videomicroscopy. Vessel flow was also measured using an optical Doppler velocimeter. Similar measurements were recorded in several animals on the same vessels in which subcutaneous dissection without elevation was performed. Average vessel diameter ranged from 21.77 to 25.55 microm before skin flap delay. Average flow ranged from 1.72 to 2.44 nl/sec before delay. Next, each animal received an intraperitoneal dose of nitro-aminomethyl-1-arginine (L-NAME), a nitric oxide synthase inhibitor delivered by means of osmotic pump at a level of 0 (n = 13 arteries), 20 (n = 10), 50 (n = 8), or 100 mg/kg/day (n = 7). Flaps were re-elevated 72 hours later and the aforementioned measurements were repeated. Vessel diameter increased to 44.92 microm in the control (0 mg/kg L-NAME) animals. Flow increased to 7.66 nl/sec in the control animals. Vessel dilation and flow did not change significantly in the nonoperative vessels. As the dose of L-NAME increased in the treated animals, there was a significant decrease in vasodilation and flow (p = 0.015 and p = 0.03, respectively). The authors' results demonstrate that nitric oxide is an important element of vasodilation and contributor to the phenomenon of skin flap delay.