The effect of chemical hemodynamic regulation on the survival of arterialized venous flaps.

The role of nitric oxide (NO) on the microcirculation of arterialized venous flaps (AVFs) remains controversial. We aimed to investigate the effect of hemodynamic regulation using nitric oxide synthase (NOS) inhibitor and its agonist as a chemical intervention on the survival of AVF. A 10 x 8 cm arterialized venous flap was designed symmetrically on the rabbit abdomen. Thirty-six rabbits were used and randomly divided into three groups: control group, L-arg group and L-NAME group, respectively. The L-arg group and the L-NAME group received intraperitoneal injections of L-arginine (a NOS agonist, 1 g/kg/d) and L-NAME (nitro-L-arginine-methyl ester, a NOS inhibitor, 50 mg/kg/d) respectively, whereas the control group received intraperitoneal injections of the same amount of saline. Flap viability, water content, status of vascular perfusion and gene expression of eNOS and HIF-1 alpha in each group were observed and analyzed. The average value of water content (venous congestion) in the L-arg group was the highest in comparison with the control group and the L-NAME group with a statistically significant difference (all p < .001). Similar results regarding blood perfusion state, gene expression of eNOS and HIF-1 alpha and flap survival status were found among the three groups. The early application of L- NAME as a chemical hemodynamic intervention could stop the cascade of flap swelling, congestion and necrosis due to overexpression of NO and be beneficial to the AVF survival. Our findings may develop a new strategy as a solution for the inconsistent survival of AVFs.