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

机译:用实验诱导多发性多发性脓毒症评估兔心肌肌钙蛋白I的心肌肌钙蛋白I

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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.
机译:败血症是一种潜在的生命危及生命的病症,它经常被心肌损伤复杂化。兔遗传结扎和穿刺(CLP)模型的心肌损伤数据有限,但众多动物模型已被用于研究败血症相关的心肌损伤。本研究旨在通过测量血清心肌肌钙蛋白I(CTNI)浓度的CLP对心肌的影响,并通过检测兔心肌细胞的组织病理学变化和CTNI免疫反应性。在兔子中进行CLP后,血液样品从颈静脉以0,4,8和12小时取出,用于血液学和生化分析。在实验结束时,所有兔子都被安乐死,以检查心肌组织中的组织病理学变化和CTNI免疫反应性。在0和4小时的实验组(例如)或对照组(Cg)中没有观察到血清CTNI浓度的变化。在例如,平均血清CTNI浓度分别为0.230±0.209和1.177±0.971ng / ml,分别为8和12 h。在Cg中,平均血清CTNI浓度分别为8和12小时,分别为0.032±0.014和0.031±0.021ng / ml。此外,细胞质CTNI免疫反应性在例如CG中的比较下降(P <0.01)。结果表明,CLP诱导全身炎症反应并引起兔子心肌损伤。

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