Nitric oxide in flow-through venous flaps and effects of L-arginine and nitro-L-arginine methyl ester (L-NAME) on nitric oxide and flap survival in rabbits.

Object: Venous flaps are relatively recent practices in plastic surgery, and their life mechanisms are not known exactly. Partial necroses frequently occur in these flaps; therefore, their survival should be enhanced. Nitric oxide (NO) is an endogenous compound which has recently been dwelt upon frequently in flap pathophysiology, and its effect on viability in conventional flaps has been demonstrated. However, its role in venous flaps is unknown. The purpose of this study is to determine possible changes in the NO level in venous flaps and to investigate the possible effects of NO synthesis precursor and inhibitor on the venous flap NO level and flap survival. Material and Methods: Thirty white male rabbits of New Zealand type, aged 6 months, were divided into 3 groups as control (n = 10), L-arginine (n = 10), and nitro-L-arginine methyl ester (L-NAME) (n = 10). Blood and tissue samples were taken from one ear of 10 rabbits in the control group for the determination of NO basal levels 2 weeks before flap practice. The 3-X-5-cm flow-through venous flaps, which are sitting on the anterior branch of the central vein, were elevated on each ear of 10 rabbits in all groups. After flaps were sutured to their beds, 2 mL/d saline, 1 g/kg/d L-arginine (NO synthesis precursor), and 50 mg/kg/d L-NAME (NO synthesis inhibitor) were administered intraperitoneally in control, L-arginine, and L-NAME groups, respectively, for 3 days. At the 24th postoperative hour, blood and tissue samples were taken from all animals for biochemical analyses. At day 7, flap survivals were assessed. Results: Mean NO levels in the blood following the flap elevation (129 ± 76 μmol/mg protein) increased in comparison with basal levels (59 ± 44 μmol/mg protein) (P < 0.06); however, the tissue level remained unchanged. NO levels in the blood in the L-arginine and L-NAME groups were alike compared with the control group. The tissue NO level in L-NAME group (0.08 ± 0.03 μmol/mg protein) decreased significantly compared to the control group (0.46 ± 0.36 μmol/mg protein) (P < 0.001). Mean flap survival in the L-arginine group (95% ± 6) increased according to the control group (61% ± 14) (P < 0.001), whereas it did not change in the L-NAME group (55% ± 13). Conclusion: In our model of venous flap, NO level in the blood increased, while it did not change in the tissue; L-arginine significantly enhanced flap viability without affecting NO level. Additionally, L-NAME decreased NO level, but it did not affect flap survival. In light of these findings, NO increases in venous flaps; the change in its level does not affect flap survival, though. However, L-arginine enhances venous flap survival if not by virtue of NO.