Department of Hand Surgery, The Second Affiliated Hospital and Yuying Children's Hospital of Wenzhou Medical University, Wenzhou, China; The Second School of Medicine, Wenzhou Medical University, Wenzhou, China.
Department of Hand Surgery, The Second Affiliated Hospital and Yuying Children's Hospital of Wenzhou Medical University, Wenzhou, China; The Second School of Medicine, Wenzhou Medical University, Wenzhou, China.
Biomed Pharmacother. 2020 Aug;128:110261. doi: 10.1016/j.biopha.2020.110261. Epub 2020 May 20.
Random flaps can be used to repair wounds and improve shape and functional reconstruction, but inflammation and necrosis limit their application. Modified McFarlane flap models were constructed on the backs of rats. We hypothesized that dexmedetomidine (DEX) could improve the survival rate of ischemic random flaps.
Sixty rats were randomly divided into three groups: a low-dose DEX group (DEX-L group, 10 μg/kg/D), a high-dose DEX group (DEX-H group, 20 μg/kg/D) and a control group (0.9 % saline equivalent). On day 7 after flap construction, the survival percentage of the flap model was calculated. Hematoxylin and eosin staining (H&E) was used to evaluate the histopathological status of the flaps and microvessel density (MVD). Lead oxide/gelatin angiography was used to detect angiogenesis, and laser Doppler flow imaging (LDF) was used to detect blood perfusion. The levels of superoxide dismutase (SOD) and malondialdehyde (MDA) in the middle areas of the flaps were measured to show the level of oxidative stress. The expressions of Toll-like receptor (TLR4), nuclear factor-kappa B (NF-κB), interleukin (IL)-1β, IL-6, tumor necrosis factor-α (TNF-α) and vascular endothelial growth factor (VEGF) were detected by immunohistochemistry.
DEX significantly increased the average survival percentage of the flaps and reduced ischemia and necrosis of the distal end of the flaps. SOD activity significantly increased, while MDA significantly decreased, indicating that DEX reduces oxidative damage. The expression of inflammatory immunoregulatory proteins (TLR4, NF-κB) was downregulated, and the levels of inflammatory factors (IL-1β, IL-6 and TNF-α) were lower. In addition, DEX upregulated VEGF expression, promoted angiogenesis, and increased blood perfusion.
In random flap transplantation, a high dose of DEX is beneficial to flap survival.
随意皮瓣可用于修复创伤，改善形状和功能重建，但炎症和坏死限制了其应用。我们构建了大鼠背部改良 McFarlane 皮瓣模型，并假设右美托咪定（DEX）可提高缺血性随意皮瓣的成活率。
60 只大鼠随机分为三组：低剂量 DEX 组（DEX-L 组，10μg/kg/d）、高剂量 DEX 组（DEX-H 组，20μg/kg/d）和对照组（0.9%生理盐水）。在皮瓣构建后第 7 天，计算皮瓣模型的成活率。苏木精-伊红（H&E）染色评估皮瓣的组织病理学状态和微血管密度（MVD）。采用硝酸铅/明胶血管造影检测血管生成，激光多普勒血流成像（LDF）检测血流灌注。测量皮瓣中部超氧化物歧化酶（SOD）和丙二醛（MDA）的水平，以显示氧化应激水平。采用免疫组化法检测 Toll 样受体（TLR4）、核因子-κB（NF-κB）、白细胞介素（IL）-1β、IL-6、肿瘤坏死因子-α（TNF-α）和血管内皮生长因子（VEGF）的表达。
DEX 显著提高了皮瓣的平均成活率，减少了皮瓣远端的缺血和坏死。SOD 活性显著增加，MDA 显著降低，表明 DEX 减轻了氧化损伤。炎症免疫调节蛋白（TLR4、NF-κB）的表达下调，炎症因子（IL-1β、IL-6 和 TNF-α）水平降低。此外，DEX 上调 VEGF 表达，促进血管生成，增加血流灌注。
在随意皮瓣移植中，高剂量 DEX 有利于皮瓣存活。
Zotero 插件