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无论缺血预适应的诱导方式如何,缺血预适应均可抑制糖尿病大鼠模型中皮瓣的坏死。

Ischaemic Preconditioning Suppresses Necrosis of Adipocutaneous Flaps in a Diabetic Rat Model Regardless of the Manner of Preischaemia Induction.

作者信息

Ottomann Christian, Küntscher Markus, Hartmann Bernd, Antonic Vlado

机构信息

Unfallkrankenhaus Berlin, Center for Severe Burn Injuries with Plastic Surgery, Berlin, Germany.

Evangelical Elisabeth Clinic, Berlin, Germany.

出版信息

Dermatol Res Pract. 2017;2017:4137597. doi: 10.1155/2017/4137597. Epub 2017 Oct 18.

DOI:10.1155/2017/4137597
PMID:29201044
原文链接:https://pmc.ncbi.nlm.nih.gov/articles/PMC5671712/
Abstract

Ischaemic insult in the skin flaps is a major problem in reconstructive surgery particularly in patients with diabetes mellitus. Here, we sought to investigate the effectiveness of ischaemic preconditioning (IP) on diabetic skin flaps in rat animal model. Hundred Wistar rats (90 streptozotocin treated animals and 10 nondiabetic controls) were used. Diabetes mellitus was confirmed by measuring glucose level in blood, HbA1c, and ketonuria. We used blood vessel clamping, hind limb tourniquet, and NO donors (Spermine/NO complex) to induce short-term ischaemia of tissues that will be excised for skin flaps. Animals were followed for 5 days. Flaps were photographed at day 5 and percent of necrosis was determined using planimetry. Significant decrease in percent of necrotic tissue in all groups that received preconditioning was observed. Results show that ischaemic preconditioning suppresses flap necrosis in diabetic rats irrespective of direct or remote tissue IP and irrespective of chemically or physically induced preischaemia. Spermine/NO complex treatment 10 minutes after the flap ischaemia suppressed tissue necrosis. Treatment with NO synthase inhibitor L-NAME reversed effects of IP showing importance of NO for this process. We show that IP is a promising approach for suppression of tissue necrosis in diabetic flaps and potential of NO pathway as therapeutic target in diabetic flaps.

摘要

皮瓣缺血损伤是整形手术中的一个主要问题,在糖尿病患者中尤为如此。在此,我们试图在大鼠动物模型中研究缺血预处理(IP)对糖尿病皮瓣的有效性。使用了100只Wistar大鼠(90只经链脲佐菌素处理的动物和10只非糖尿病对照)。通过测量血糖水平、糖化血红蛋白和尿酮体来确诊糖尿病。我们使用血管夹闭、后肢止血带和一氧化氮供体(精胺/一氧化氮复合物)来诱导即将切除用于制作皮瓣的组织的短期缺血。对动物进行了5天的随访。在第5天拍摄皮瓣照片,并使用面积测量法确定坏死百分比。观察到所有接受预处理的组中坏死组织百分比均显著降低。结果表明,无论直接或远程组织IP,也无论化学或物理诱导的缺血前状态如何,缺血预处理均能抑制糖尿病大鼠皮瓣坏死。皮瓣缺血10分钟后用精胺/一氧化氮复合物治疗可抑制组织坏死。用一氧化氮合酶抑制剂L-NAME治疗可逆转IP的作用,表明一氧化氮在此过程中的重要性。我们表明,IP是抑制糖尿病皮瓣组织坏死的一种有前景的方法,并且一氧化氮途径作为糖尿病皮瓣治疗靶点具有潜力。

https://cdn.ncbi.nlm.nih.gov/pmc/blobs/3646/5671712/ee0a49283232/DRP2017-4137597.003.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/3646/5671712/3e573914a803/DRP2017-4137597.001.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/3646/5671712/48e9a773c22b/DRP2017-4137597.002.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/3646/5671712/ee0a49283232/DRP2017-4137597.003.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/3646/5671712/3e573914a803/DRP2017-4137597.001.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/3646/5671712/48e9a773c22b/DRP2017-4137597.002.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/3646/5671712/ee0a49283232/DRP2017-4137597.003.jpg

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Remote Liver Ischemic Preconditioning Protects against Sudden Cardiac Death via an ERK/GSK-3β-Dependent Mechanism.远程肝脏缺血预处理通过一种依赖于细胞外信号调节激酶/糖原合成酶激酶-3β的机制预防心脏性猝死。
PLoS One. 2016 Oct 21;11(10):e0165123. doi: 10.1371/journal.pone.0165123. eCollection 2016.
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Cellular and molecular mechanisms of endothelial ischemia/reperfusion injury: perspectives and implications for postischemic myocardial protection.
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Am J Transl Res. 2016 Feb 15;8(2):765-77. eCollection 2016.
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Combination of ischemic preconditioning and postconditioning can minimise skin flap loss: experimental study.缺血预处理与后处理相结合可使皮瓣损失最小化:实验研究。
J Plast Surg Hand Surg. 2016 Aug;50(4):233-8. doi: 10.3109/2000656X.2016.1154468. Epub 2016 Apr 13.
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