ABSTRACT
The aim of the present study was to compare healing obtained with biomembranes with the natural healing process (sham) using biochemical and immunohistological assays. C57BL/6 mice were divided into 4 groups of 15 mice each and received different subcutaneous implants: natural latex biomembrane (NLB), denatured latex (DL), expanded polytetrafluorethylene (ePTFE), or sham. On the 2nd, 7th, and 14th days post-treatment, 5 mice per group were sacrificed and biopsied for the following measurements: oxidative stress based on malondialdehyde (MDA), myeloperoxidase (MPO) and hydrogen peroxide by the method of ferrous oxidation-xylenol orange (FOX), as well as glutathione and total proteins; histological evaluation to enumerate inflammatory cells, fibroblasts, blood vessels, and collagen, and immunohistochemical staining for inducible nitric oxide synthase, interleukin-1β, vascular endothelial growth factor (VEGF), and transforming growth factor-β1 (TGF-β1). On day 2 post-treatment, NLB stimulated a dense inflammatory infiltrate mainly consisting of polymorphonuclear cells, as indicated by increased MPO (P < 0.05), but oxidative stress due to MDA was not observed until the 7th day (P < 0.05). The number of blood vessels was greater in NLB (P < 0.05) and DL (P < 0.05) mice compared to sham animals on day 14. NLB induced fibroplasia by day 14 (P < 0.05) with low expression of TGF-β1 and collagenesis. Thus, NLB significantly induced the inflammatory phase of healing mediated by oxidative stress, which appeared to influence the subsequent phases such as angiogenesis (with low expression of VEGF) and fibroplasia (independent of TGF-β1) without influencing collagenesis.
Subject(s)
Animals , Male , Mice , Biocompatible Materials/therapeutic use , Latex/therapeutic use , Membranes, Artificial , Oxidative Stress/physiology , Polytetrafluoroethylene/therapeutic use , Wound Healing/physiology , Immunohistochemistry , Inflammation/physiopathology , Oxidative Stress/drug effects , Wound Healing/drug effectsABSTRACT
Isolated superfused rat atria release [3H]-acetylcholine when depolarized with 57 mM potassium. The depolarization-induced [3H]-acetylcholine overflow was significantly reduced in atria from chronically T. cruzi-infected rats with electrocardiographically characterized cardiopathy. This fact suggests the occurrence of functional alterations of cardiac parasympathetic control in these animals, probably related to cardiac ganglioma cell destruction