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缺氧参与大鼠模型深部组织损伤的形成

Hypoxia is Involved in Deep Tissue Injury Formation in a Rat Model .

作者信息

Sari Yunita, Nagase Takashi, Minematsu Takeo, Akase Tomoko, Nakagami Gojiro, Sanada Hiromi, Sugama Junko

机构信息



Department of Gerontological Nursing/Wound Care Management, Graduate School of Medicine, The University of Tokyo, Tokyo, Japan; Email:

出版信息

Wounds. 2010 Feb;22(2):44-51.

Abstract

Abstract: Pressure ulcers that develop from deep tissue are known as deep tissue injuries (DTI). Although several mechanisms, including ischemic hypoxia, are attributed to pressure ulcer formation, the mechanisms involved in DTI formation are still unclear. Previous studies have suggested that hypoxia is involved in DTI in vitro, but it has yet to be determined whether hypoxia is also involved in DTI in vivo. Therefore, this study aimed to investigate whether hypoxia is involved in DTI using a newly established DTI model. Rats were divided into control, low pressure DTI, and high pressure DTI groups. Results of wound healing tests indicated that more severe DTI resulted in prolonged healing time, more severe inflammation and muscle damage, higher levels of exudate creatine phosphokinase, and greater muscle edema. Increased hypoxia was observed in severe DTI-nuclear localization of hypoxia-inducible factor-1α was markedly increased in the high pressure DTI group, while the low pressure group showed more increased cytoplasm localization compared to the control group on day 3. Study results revealed that hypoxia is involved in DTI in vivo.

摘要

摘要

由深部组织形成的压疮被称为深部组织损伤(DTI)。尽管包括缺血缺氧在内的多种机制被认为与压疮形成有关,但DTI形成所涉及的机制仍不清楚。先前的研究表明缺氧在体外与DTI有关,但缺氧在体内是否也与DTI有关尚待确定。因此,本研究旨在使用新建立的DTI模型来研究缺氧是否与DTI有关。将大鼠分为对照组、低压DTI组和高压DTI组。伤口愈合测试结果表明,更严重的DTI导致愈合时间延长、炎症和肌肉损伤更严重、渗出液肌酸磷酸激酶水平更高以及肌肉水肿更严重。在严重DTI中观察到缺氧增加——缺氧诱导因子-1α的核定位在高压DTI组中明显增加,而在第3天,低压组与对照组相比显示出更多的细胞质定位增加。研究结果表明缺氧在体内与DTI有关。

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