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评价实验性多微生物脓毒症兔血清和心肌中心肌钙蛋白 I。

Evaluation of cardiac troponin I in serum and myocardium of rabbits with experimentally induced polymicrobial sepsis.

机构信息

Department of Internal Medicine, Faculty of Veterinary Medicine, Firat University, 23200, Elazığ, Turkey.

Department of Pathology, Faculty of Veterinary Medicine, Firat University, 23200, Elazığ, Turkey.

出版信息

Exp Anim. 2020 Jan 29;69(1):54-61. doi: 10.1538/expanim.19-0046. Epub 2019 Aug 29.

DOI:10.1538/expanim.19-0046
PMID:31462610
原文链接:https://pmc.ncbi.nlm.nih.gov/articles/PMC7004812/
Abstract

Sepsis is a potentially life-threatening condition, and it is frequently complicated by myocardial damage. Data on myocardial damage in rabbit caecal ligation and puncture (CLP) models are limited, although numerous animal models have been used to study sepsis-associated myocardial damage. This study aimed to investigate the effect of CLP on cardiac muscle by measuring serum cardiac troponin I (cTnI) concentrations and by detecting both histopathological changes and cTnI immunoreactivity in cardiomyocytes in rabbits. After CLP was performed in rabbits, blood samples were taken from the jugular vein at 0, 4, 8, and 12 h for haematological and biochemical analyses. At the end of the experiment, all of the rabbits were euthanised to examine the histopathological changes and the cTnI immunoreactivity in cardiac muscle tissue. No changes in serum cTnI concentration were observed in the experimental group (EG) or control group (CG) at 0 and 4 h. In EG, the mean serum cTnI concentrations were 0.230 ± 0.209 and 1.177 ± 0.971 ng/ml at 8 and 12 h, respectively. In CG, the mean serum cTnI concentrations were 0.032 ± 0.014 and 0.031 ± 0.021 ng/ml at 8 and 12 h, respectively. Moreover, cytoplasmic cTnI immunoreactivity decreased in EG compared with that in CG (P<0.01). The results demonstrated that CLP induced a systemic inflammatory response and caused myocardial damage in rabbits.

摘要

脓毒症是一种潜在的危及生命的病症,常伴有心肌损伤。尽管有许多动物模型被用于研究与脓毒症相关的心肌损伤,但关于兔盲肠结扎穿刺(CLP)模型中心肌损伤的数据有限。本研究旨在通过测量血清心肌肌钙蛋白 I(cTnI)浓度,并检测心肌细胞的组织病理学变化和 cTnI 免疫反应性,来研究 CLP 对心肌的影响。在兔实施 CLP 后,于 0、4、8 和 12 h 从颈静脉采集血液样本进行血液学和生化分析。实验结束时,所有兔子均被安乐死,以检查心肌组织的组织病理学变化和 cTnI 免疫反应性。在实验组(EG)和对照组(CG)中,在 0 和 4 h 时,血清 cTnI 浓度均无变化。在 EG 中,血清 cTnI 浓度分别在 8 和 12 h 时为 0.230±0.209 和 1.177±0.971ng/ml。在 CG 中,血清 cTnI 浓度分别在 8 和 12 h 时为 0.032±0.014 和 0.031±0.021ng/ml。此外,与 CG 相比,EG 中的细胞质 cTnI 免疫反应性降低(P<0.01)。结果表明,CLP 诱导了全身性炎症反应,并导致兔心肌损伤。

https://cdn.ncbi.nlm.nih.gov/pmc/blobs/30dd/7004812/cde47634c323/expanim-69-054-g003.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/30dd/7004812/925f88212ac2/expanim-69-054-g001.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/30dd/7004812/468dd395a5d8/expanim-69-054-g002.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/30dd/7004812/cde47634c323/expanim-69-054-g003.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/30dd/7004812/925f88212ac2/expanim-69-054-g001.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/30dd/7004812/468dd395a5d8/expanim-69-054-g002.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/30dd/7004812/cde47634c323/expanim-69-054-g003.jpg

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[Myocardial cells and mitochondrial autophagy in sepsis mice induced by lipopolysaccharide].脂多糖诱导的脓毒症小鼠心肌细胞与线粒体自噬
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