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本文引用的文献

1
CD109, a novel TGF-β antagonist, decreases fibrotic responses in a hypoxic wound model.CD109是一种新型转化生长因子-β拮抗剂,可降低缺氧伤口模型中的纤维化反应。
Exp Dermatol. 2014 Jul;23(7):475-9. doi: 10.1111/exd.12439.
2
Consequences of age on ischemic wound healing in rats: altered antioxidant activity and delayed wound closure.年龄对大鼠缺血性伤口愈合的影响:抗氧化活性改变与伤口愈合延迟。
Age (Dordr). 2014 Apr;36(2):733-48. doi: 10.1007/s11357-014-9617-4. Epub 2014 Jan 21.
3
Hyperbaric oxygen reduces matrix metalloproteinases in ischemic wounds through a redox-dependent mechanism.高压氧通过氧化还原依赖机制减少缺血性伤口中的基质金属蛋白酶。
J Invest Dermatol. 2014 Jan;134(1):237-246. doi: 10.1038/jid.2013.301. Epub 2013 Jul 18.
4
Animal models of wound repair: Are they cutting it?动物创伤修复模型:它们是否可行?
Exp Dermatol. 2012 Aug;21(8):581-5. doi: 10.1111/j.1600-0625.2012.01540.x.
5
Hypoxia inducible microRNA 210 attenuates keratinocyte proliferation and impairs closure in a murine model of ischemic wounds.缺氧诱导 microRNA 210 可减弱角质形成细胞增殖并损害缺血性创面小鼠模型的闭合。
Proc Natl Acad Sci U S A. 2010 Apr 13;107(15):6976-81. doi: 10.1073/pnas.1001653107. Epub 2010 Mar 22.
6
Characterization of a preclinical model of chronic ischemic wound.慢性缺血性伤口临床前模型的特征描述
Physiol Genomics. 2009 May 13;37(3):211-24. doi: 10.1152/physiolgenomics.90362.2008. Epub 2009 Mar 17.
7
Hyperbaric oxygen attenuates apoptosis and decreases inflammation in an ischemic wound model.高压氧可减轻缺血性伤口模型中的细胞凋亡并减轻炎症。
J Invest Dermatol. 2008 Aug;128(8):2102-12. doi: 10.1038/jid.2008.53. Epub 2008 Mar 13.
8
Altered collagen metabolism and delayed healing in a novel model of ischemic wounds.缺血性伤口新模型中胶原蛋白代谢改变与愈合延迟
Wound Repair Regen. 1995 Apr-Jun;3(2):204-12. doi: 10.1046/j.1524-475X.1995.30212.x.
9
Optimization and validation of an ischemic wound model.缺血性伤口模型的优化与验证
Wound Repair Regen. 2005 Nov-Dec;13(6):576-82. doi: 10.1111/j.1524-475X.2005.00080.x.
10
Rat models of skin wound healing: a review.皮肤伤口愈合的大鼠模型:综述
Wound Repair Regen. 2004 Nov-Dec;12(6):591-9. doi: 10.1111/j.1067-1927.2004.12601.x.

大鼠缺血性皮肤伤口模型的演示。

Demonstration of the rat ischemic skin wound model.

作者信息

Trujillo Andrea N, Kesl Shannon L, Sherwood Jacob, Wu Mack, Gould Lisa J

机构信息

Department of Molecular Pharmacology and Physiology, University of South Florida.

Department of Molecular Pharmacology and Physiology, University of South Florida; Department of Surgery, University of South Florida.

出版信息

J Vis Exp. 2015 Apr 1(98):e52637. doi: 10.3791/52637.

DOI:10.3791/52637
PMID:25866964
原文链接:https://pmc.ncbi.nlm.nih.gov/articles/PMC4401402/
Abstract

The propensity for chronic wounds in humans increases with ageing, disease conditions such as diabetes and impaired cardiovascular function, and unrelieved pressure due to immobility. Animal models have been developed that attempt to mimic these conditions for the purpose of furthering our understanding of the complexity of chronic wounds. The model described herein is a rat ischemic skin flap model that permits a prolonged reduction of blood flow resulting in wounds that become ischemic and resemble a chronic wound phenotype (reduced vascularization, increased inflammation and delayed wound closure). It consists of a bipedicled dorsal flap with 2 ischemic wounds placed centrally and 2 non-ischemic wounds lateral to the flap as controls. A novel addition to this ischemic skin flap model is the placement of a silicone sheet beneath the flap that functions as a barrier and a splint to prevent revascularization and reduce contraction as the wounds heal. Despite the debate of using rats for wound healing studies due to their quite distinct anatomic and physiologic differences compared to humans (i.e., the presence of a panniculus carnosus muscle, short life-span, increased number of hair follicles, and their ability to heal infected wounds) the modifications employed in this model make it a valuable alternative to previously developed ischemic skin flap models.

摘要

人类慢性伤口的易发性会随着年龄增长、糖尿病等疾病状况以及心血管功能受损,还有因行动不便导致的长期压力而增加。为了进一步了解慢性伤口的复杂性,人们已经开发出了试图模拟这些状况的动物模型。本文所述的模型是一种大鼠缺血性皮瓣模型,它能使血流量长期减少,从而导致伤口缺血,并呈现出类似慢性伤口的表型(血管化减少、炎症增加和伤口愈合延迟)。它由一个双蒂背侧皮瓣组成,在皮瓣中央有2个缺血性伤口,在皮瓣外侧有2个非缺血性伤口作为对照。这个缺血性皮瓣模型的一个新特点是在皮瓣下方放置了一块硅胶片,其作用是作为屏障和夹板,在伤口愈合时防止血管再生并减少收缩。尽管由于大鼠与人类在解剖学和生理学上存在明显差异(即存在肉膜肌、寿命短、毛囊数量增加以及它们愈合感染伤口的能力),在伤口愈合研究中使用大鼠存在争议,但该模型所采用的改进使其成为先前开发的缺血性皮瓣模型的一个有价值的替代方案。