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通过结扎左冠状动脉前降支对急性心肌梗死模型进行改良:一项使用易得材料的大鼠实验研究()

Modification on acute myocardial infarction model through left anterior descending coronary artery ligation: An experimental study on rats () using readily available materials.

作者信息

Nugroho Johanes, Yuniarti Wiwik Misaco, Wardhana Ardyan, Ghea Cornelia

机构信息

Department of Cardiology and Vascular Medicine, Faculty of Medicine, Universitas Airlangga, Surabaya, Indonesia.

Department of Cardiology and Vascular Medicine, Dr. Soetomo General Hospital, Surabaya, Indonesia.

出版信息

Vet World. 2019 Sep;12(9):1448-1453. doi: 10.14202/vetworld.2019.1448-1453.

DOI:10.14202/vetworld.2019.1448-1453
PMID:31749580
原文链接:https://pmc.ncbi.nlm.nih.gov/articles/PMC6813610/
Abstract

BACKGROUND AND AIM

Several difficulties are involved in creating models for myocardial infarction (MI) in animals, such as low survival rates after acute MI, complicated techniques in creating animal models, complexities in confirming acute MI incidence, and complex surgical tools needed in the process. This study aimed to develop an animal model for acute MI using Wistar rats utilizing simple instruments that are readily available in standard animal laboratories.

MATERIALS AND METHODS

We induced MI in 48 Wistar rats using the left anterior descending coronary artery ligation modification technique without tracheal incision and ventilator. This ligation technique was performed 1-2 mm distal to the left atrial appendage. MI occurrence was evaluated using heart enzyme parameters 24 h post-ligation and histological studies of the infarcted area 6 weeks after the ligation. Rats were divided into the coronary artery ligation group and sham group.

RESULTS

Of the 48 rats, 24 (50%) died within 24 h post-ligation, but no further deaths occurred in the next follow-up period of 6 weeks. The average infarct size in six rats within 24 h of ligation was 35%±5.7%. The serum glutamic oxaloacetic transaminase level of the group treated with coronary artery ligation was statistically significantly higher than that of the sham group (p=0.000).

CONCLUSION

We developed an MI rat model with consistent infarction size, in which the long-term death of rats was not observed. Our ligation technique for an MI rat model can be a reference for experimental settings without ventilators for small animals.

摘要

背景与目的

在动物中创建心肌梗死(MI)模型存在诸多困难,例如急性心肌梗死后存活率低、创建动物模型的技术复杂、确认急性心肌梗死发生率的复杂性以及该过程所需的复杂手术工具。本研究旨在利用标准动物实验室中易于获得的简单器械,为Wistar大鼠开发一种急性心肌梗死动物模型。

材料与方法

我们采用左冠状动脉前降支结扎改良技术,在48只Wistar大鼠中诱导心肌梗死,无需气管切开和呼吸机。该结扎技术在左心耳远端1 - 2毫米处进行。在结扎后24小时使用心脏酶参数评估心肌梗死的发生情况,并在结扎后6周对梗死区域进行组织学研究。将大鼠分为冠状动脉结扎组和假手术组。

结果

48只大鼠中,24只(50%)在结扎后24小时内死亡,但在接下来的6周随访期内没有进一步死亡。结扎后24小时内6只大鼠的平均梗死面积为35%±5.7%。冠状动脉结扎组的血清谷氨酸草酰乙酸转氨酶水平显著高于假手术组(p = 0.000)。

结论

我们开发了一种梗死面积一致的心肌梗死大鼠模型,未观察到大鼠的长期死亡。我们的心肌梗死大鼠模型结扎技术可为无呼吸机的小动物实验设置提供参考。

https://cdn.ncbi.nlm.nih.gov/pmc/blobs/35c0/6813610/e24229862833/Vetworld-12-1448-g004.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/35c0/6813610/15a6087520d7/Vetworld-12-1448-g001.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/35c0/6813610/1ea416005150/Vetworld-12-1448-g002.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/35c0/6813610/3d66c35bba74/Vetworld-12-1448-g003.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/35c0/6813610/e24229862833/Vetworld-12-1448-g004.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/35c0/6813610/15a6087520d7/Vetworld-12-1448-g001.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/35c0/6813610/1ea416005150/Vetworld-12-1448-g002.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/35c0/6813610/3d66c35bba74/Vetworld-12-1448-g003.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/35c0/6813610/e24229862833/Vetworld-12-1448-g004.jpg

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本文引用的文献

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Guidelines for experimental models of myocardial ischemia and infarction.心肌缺血和梗死实验模型指南。
Am J Physiol Heart Circ Physiol. 2018 Apr 1;314(4):H812-H838. doi: 10.1152/ajpheart.00335.2017. Epub 2018 Jan 12.
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Toll-like receptor 9 prevents cardiac rupture after myocardial infarction in mice independently of inflammation.Toll样受体9可独立于炎症反应预防小鼠心肌梗死后心脏破裂。
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Early matrix metalloproteinase-9 inhibition post-myocardial infarction worsens cardiac dysfunction by delaying inflammation resolution.
心肌梗死后早期抑制基质金属蛋白酶-9会因延迟炎症消退而加重心脏功能障碍。
J Mol Cell Cardiol. 2016 Nov;100:109-117. doi: 10.1016/j.yjmcc.2016.10.005. Epub 2016 Oct 13.
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Early matrix metalloproteinase-12 inhibition worsens post-myocardial infarction cardiac dysfunction by delaying inflammation resolution.早期抑制基质金属蛋白酶-12会因延迟炎症消退而加重心肌梗死后的心功能障碍。
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Complete thymectomy in adult rats with non-invasive endotracheal intubation.采用非侵入性气管插管对成年大鼠进行完整胸腺切除术。
J Vis Exp. 2014 Dec 29(94):52152. doi: 10.3791/52152.
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A murine model of myocardial ischemia-reperfusion injury through ligation of the left anterior descending artery.一种通过结扎左冠状动脉前降支建立的心肌缺血再灌注损伤小鼠模型。
J Vis Exp. 2014 Apr 10(86):51329. doi: 10.3791/51329.
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J Stem Cells Regen Med. 2009 Apr 8;5(1):30-6. doi: 10.46582/jsrm.0501006. eCollection 2009.
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Quantitation of acute necrosis after experimental myocardial infarction.实验性心肌梗死后急性坏死的定量分析。
Methods Mol Biol. 2013;1004:115-33. doi: 10.1007/978-1-62703-383-1_9.
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