Inhibition of inducible nitric oxide synthase results in reductions in wound vascular endothelial growth factor expression, granulation tissue formation, and local perfusion

Surgery
T R HowdieshellPaul L McNeil

Abstract

Wound repair results from a series of highly orchestrated cellular and biochemical events, including increased synthesis of the bioregulatory molecule nitric oxide (NO). The goal of this work was to test the functional role of NO in promotion of vascular endothelial growth factor (VEGF) production and the vigorous granulation tissue formation characteristic of this wound model. A ventral hernia, surgically created in the abdominal walls of 12 swine, was repaired with silicone sheeting and skin closure. An osmotic infusion pump, inserted in a remote subcutaneous pocket, delivered saline solution (n = 6) or the selective inducible NO synthase inhibitor N(6) (iminoethyl)-L-lysine (L-NIL; n = 6) into the wound environment. Granulation tissue thickness was determined with ultrasonography, and local wound perfusion was measured with laser Doppler analysis for 2 weeks. Fluid was aspirated serially from the wound compartment for measurement of nitrite/nitrate, VEGF, and transforming growth factor-beta(1)concentrations. On day 14, the animals were killed and the abdominal wall was harvested for immunohistochemical and molecular analysis. In animals that received saline solution, a nearly linear 4-fold increase in granulation tissue thic...Continue Reading

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