Nitric oxide synthesis inhibition alters rat cutaneous wound healing

• Published in: Journal of cutaneous pathology Vol. 33; no. 7; pp. 465 - 473
• Main Authors: Amadeu, Thaís P., Costa, Andréa M. A.
• Format: Journal Article
• Language: English
• Published: Oxford, UK; Malden, USA Blackwell Publishing Ltd 01.07.2006
• Subjects: Administration, Oral; Animals; Cell Count; Collagen - metabolism; Disease Models, Animal; Enzyme Inhibitors - pharmacology; Male; Mast Cells - drug effects; Mast Cells - pathology; NG-Nitroarginine Methyl Ester - pharmacology; Nitric Oxide - metabolism; Nitric Oxide Synthase - antagonists & inhibitors; Nitric Oxide Synthase - metabolism; Rats; Rats, Wistar; Skin - drug effects; Skin - enzymology; Water Supply; Wound Healing - drug effects; Wound Healing - physiology
• ISSN: 0303-6987; 1600-0560
• DOI: 10.1111/j.1600-0560.2006.00472.x

Background:  Nitric oxide (NO) is an important molecule that participates in wound repair, but its effects on cutaneous wound healing are not well understood. The aim of this study was to investigate the effects of NO synthesis blockade on rat cutaneous wound healing by the administration of NG‐nitro‐l‐arginine methyl ester (l‐NAME), a non‐selective inhibitor of NO synthases. Methods:  NO synthesis was inhibited by administration of l‐NAME (20 mg/kg/day) in drinking water. An excisional wound was done, and the animals were killed 7, 14, and 21 days later. Wound contraction and blood pressure were evaluated. The lesion and adjacent skin were formalin fixed and paraffin embedded. Mast cells were quantified, and vessels were evaluated using stereological methods. Results:  l‐NAME‐treated animals presented delayed wound contraction, alterations in collagen organization, and neoepidermis thickness. The inhibition of NO synthesis increased mast cell migration 7 days after wounding, but decreased 21 days after wounding. Volume density of vessels was decreased in l‐NAME‐treated animals, 21 days after lesion. Surface density of vessels was frequently smaller in l‐NAME‐treated animals than in controls. Conclusion:  The blockade of NO synthesis impaired cutaneous wound healing, acting in early and late phases of wound repair.