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1.
J Reconstr Microsurg ; 33(4): 292-297, 2017 May.
Artigo em Inglês | MEDLINE | ID: mdl-28099976

RESUMO

Background Tip necrosis in the perforator flap is a significant problem in clinical practice. This study aimed to characterize the vasculature of a multiterritory perforator flap using a rat model and to investigate the impact of the vasculature on flap survival. Methods In total, 105 Sprague Dawley rats were divided into seven groups, including the control, 3 hours postoperative (PO), 12 hours PO, 1 day PO, 3 days PO, 5 days PO, and 7 days PO. A perforator flap with three territories based on the deep iliac circumflex artery was performed. Flaps with only skin incisions and vessel exposure were performed in the control group. The first choke zone (FCZ) was located between the anatomical and dynamic territories, and the second choke zone (SCZ) was located between the dynamic and potential territories. Sodium fluorescein and lead oxide-gelatin angiography and histological examination were performed in each group. Results Sodium fluorescein angiography revealed delayed staining in the perforator flap PO, particularly in the FCZ and SCZ. The delay phenomenon disappeared after 12 hours PO in the FCZ and after 1 day PO in the SCZ. Nonfluorescein-stained areas were found distal to the potential territory. In the FCZ PO, the choke vessels were dilated, while the number of microvessels was increased in the SCZ without choke vessel dilation. Conclusions The remodeling of choke vessels and increase in microvessel number represent arteriogenesis and angiogenesis, respectively. This neovascularization was responsible for flap survival in the entire dynamic territory and part of the potential territory.


Assuntos
Retalho Perfurante/irrigação sanguínea , Angiografia , Animais , Modelos Animais de Doenças , Sobrevivência de Enxerto , Artéria Ilíaca/patologia , Masculino , Necrose/patologia , Neovascularização Patológica , Neovascularização Fisiológica , Retalho Perfurante/patologia , Ratos , Ratos Sprague-Dawley , Fluxo Sanguíneo Regional
2.
J Reconstr Microsurg ; 32(9): 643-649, 2016 Nov.
Artigo em Inglês | MEDLINE | ID: mdl-27367807

RESUMO

Background Inducible nitric oxide synthase (iNOS) plays an important role in vasodilation, angiogenesis, and ischemia-reperfusion injury. We investigated the effects of iNOS on the survival and choke vessels of multiterritory perforator flaps in rats. Methods In this study, 84 rats were divided into two groups of 42 rats each and subjected to multiterritory perforator flap operations. Rats in group A received daily intraperitoneal doses of 100 mg per kg of aminoguanidine (AG) and rats in group B received daily intraperitoneal injections of the same volume of saline solution. On postoperative day 7, the surviving flap area was calculated as a percentage of the total flap dimensions using DP2-BSW software. The diameter and density of microvessels in the second choke zone of the flap were calculated from histology studies. The nitric oxide (NO) content was measured using NO concentration assay kits, and the levels of vascular endothelial growth factor (VEGF) and iNOS were assessed using western blotting. Superoxide dismutase (SOD) activity and malondialdehyde (MDA) content were measured using test kits. Laser Doppler imaging was used to evaluate flap perfusion in the second choke zone for 7 days after surgery. Results The flap survival area, diameter and density of microvessels, iNOS and VEGF levels, NO content, blood perfusion, and MDA content were significantly higher in the control group compared with the AG group, whereas SOD activity was significantly lower in the control group. Conclusions iNOS has a beneficial effect on the survival of multiterritory perforator flaps.


Assuntos
Inibidores Enzimáticos/farmacologia , Guanidinas/farmacologia , Óxido Nítrico Sintase/metabolismo , Retalho Perfurante/fisiologia , Retalho Perfurante/cirurgia , Ferimentos e Lesões/cirurgia , Animais , Velocidade do Fluxo Sanguíneo , Western Blotting , Modelos Animais de Doenças , Sobrevivência de Enxerto , Injeções Intraperitoneais , Masculino , Malondialdeído/metabolismo , Microvasos/metabolismo , Retalho Perfurante/irrigação sanguínea , Ratos , Ratos Sprague-Dawley , Fator A de Crescimento do Endotélio Vascular/metabolismo , Vasodilatação , Ferimentos e Lesões/patologia
3.
Sci Rep ; 6: 18945, 2016 Jan 06.
Artigo em Inglês | MEDLINE | ID: mdl-26732750

RESUMO

Calcitriol, a metabolite of vitamin D, is often used in osteoporosis clinics. However, the material has other bioactivities; for example, it accelerates angiogenesis, has anti-inflammatory properties, and inhibits oxidative stress. We investigated the effects of calcitriol in a random skin flap rat model. "McFarlane flap" models were established in 84 male Sprague Dawley rats, divided into two groups. One group received intraperitoneal injections of calcitriol (2 µg/kg/day) whereas control rats received intraperitoneal injections of saline. The percentage flap survival area and tissue water content were measured 7 days later, which showed that calcitriol improved flap survival area and reduced tissue edema. It also increased the mean vessel density and upregulated levels of VEGF mRNA/protein, both of which promote flap angiogenesis. Moreover, it decreased leukocyte and macrophage infiltration, reduced the inflammatory proteins IL1ß and IL6, increased SOD activity, decreased MDA content, and upregulated the level of autophagy. Overall, our results suggest that calcitriol promotes skin flap survival by accelerating angiogenesis, having anti-inflammatory effects, reducing oxidative stress, and promoting autophagy.


Assuntos
Calcitriol/farmacologia , Sobrevivência de Enxerto/efeitos dos fármacos , Retalhos Cirúrgicos , Animais , Anti-Inflamatórios/farmacologia , Autofagia/efeitos dos fármacos , Edema/tratamento farmacológico , Edema/patologia , Masculino , Neovascularização Fisiológica/efeitos dos fármacos , Estresse Oxidativo/efeitos dos fármacos , RNA Mensageiro/genética , RNA Mensageiro/metabolismo , Ratos , Transplante de Pele , Retalhos Cirúrgicos/patologia , Retalhos Cirúrgicos/transplante , Fator A de Crescimento do Endotélio Vascular/genética , Fator A de Crescimento do Endotélio Vascular/metabolismo
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