Abstract
Wound healing is a complex process that necessitates organization of different cell types and several signalling molecules. The aim of this study is to evaluate the effect of different concentrations of sildenafil citrate, which decreases cGMP degradation, on wound healing by secondary intention.This study was performed using 25 Sprague Dawley rats weighing 200-250 grams. 4 dorsal defects were created. Four different treatment modalities which were 1% and 5% sildenafil citrate gel prepared with carbopol, pure carbopol gel without any drug in it and 0,9% NaCl solution; were applied to each lesion of the same rat. Randomly selected five rats (25 rats in total) were sacrificed on 3rd, 5th, 7th, 10th, and 14th days; and the effect of each modality was evaluated by means of defect area measurement, histopathological examination and measurement of tissue hydroxyproline levels.Sildenafil citrate gel application decreased the defect areas in a dose independent manner starting from 3rd day and dose dependent manner after 7th day. By means of vascularization, sildenafil citrate increased vascularity starting from 3rd day. The strength of acute inflammation was superior in sildenafil groups starting from 5th day; and the amount and maturation of granulation in the wound bed, as well as the strength of chronic inflammation were superior in defects treated with sildenafil citrate as early as 7th day.
Highlights
Wound healing is a complex, organized process that includes nitric oxide (NO) and many messenger molecules
Sildenafil increases NO release by stimulating inducible nitric oxide synthase [2] and endothelial derived nitric oxide synthase at the mRNA and protein level [9,10]
Since increased collagen deposition seen in arginine supplementation studies [24] was not obtained in our study, we suggest this effect not to be through cyclic guanosine monophosphate (cGMP) pathway but through arginase pathway or through other effects of NO
Summary
Wound healing is a complex, organized process that includes nitric oxide (NO) and many messenger molecules. There are several studies that prove the functional and critical role of NO on wound healing [1,2,3,4,5,6]. NO is shown to have many regulatory roles in cellular proliferation, collagen synthesis and epithelization [4]. Inhibition of iNOS by competitive inhibitors reduces collagen deposition and decrease wound tension strength in incisional wounds [5]. Use of NO donors increases incisional and excisional wound healing in rats [11]. NOS activity was shown to have a peak within 24 hours after injury, and followed with a constant decrease line and a plateau line between 14 and 35 days [6]
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