RESUMO
Pressure ulcers are a major clinical problem, with a large burden on healthcare resources. This study evaluated the effects of the heparan sulfate glycosaminoglycan mimetic, OTR4120, on pressure ulceration and healing. Ischemia-reperfusion (I-R) was evoked to induce pressure ulcers by external clamping and then removal of a pair of magnet disks on rat dorsal skin for a single ischemic period of 16 hours. Immediately after magnet removal, rats received an intramuscular injection of OTR4120 weekly for up to 1 month. During the ischemic period, normal skin perfusion was reduced by at least 60% and at least 20-45% reperfused into the ischemic region after compression release. This model caused sustained skin incomplete necrosis for up to 14 days and led to grade 2-3 ulcers. OTR4120 treatment decreased the area of skin incomplete necrosis and degree of ulceration. OTR4120 treatment also reduced inflammation and increased angiogenesis. In OTR4120-treated ulcers, the contents of vascular endothelial growth factor, platelet-derived growth factor, and transforming growth factor beta-1 were increased. Moreover, OTR4120 treatment promoted early expression of alpha-smooth muscle actin and increased collagen biosynthesis. Long-term restoration of wounded tissue biomechanical strength was significantly enhanced after OTR4120 treatment. Taken together, we conclude that OTR4120 treatment reduces pressure ulcer formation and potentiates the internal healing bioavailability.
Assuntos
Glicosaminoglicanos/farmacologia , Úlcera por Pressão/terapia , Cicatrização/efeitos dos fármacos , Actinas/metabolismo , Animais , Fenômenos Biomecânicos , Colágeno/biossíntese , Modelos Animais de Doenças , Feminino , Inflamação/tratamento farmacológico , Injeções Intramusculares , Neovascularização Fisiológica/efeitos dos fármacos , Fator de Crescimento Derivado de Plaquetas/metabolismo , Ratos , Traumatismo por Reperfusão , Fator de Crescimento Transformador beta1/metabolismo , Fator A de Crescimento do Endotélio Vascular/metabolismoRESUMO
Gastrointestinal perforation due to infection, including disseminated histoplasmosis, is a rare cause of the surgical acute abdomen, especially in an apparently healthy patient. We describe a rare case of gastrointestinal histoplasmosis-induced small intestine perforation as the first manifestation of acquired immune deficiency syndrome in a healthy patient. Remarkably, the disease mimicked peritonitis carcinomatosis during explorative laparoscopy.