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人类和猪急性自发性心肌梗死后心脏节点的形态计量学和组织学变化

Morphometric and histological changes in cardiac nodes after acute spontaneous myocardial infarction in humans and pigs.

作者信息

Gómez-Torres Fabián, Ballesteros-Acuña Luis Ernesto, Molina-Aguilar Pilar, Ríos-Navarro César, Ruíz-Sauri Amparo

机构信息

Department of Basic Sciences, School of Medicine, Universidad Industrial de Santander, Cra 32 # 29-31, 68002, Bucaramanga, Colombia.

Department of Pathology, Faculty of Medicine and Odontology, University of Valencia, Av. de Blasco Ibáñez, 15. 46010. Valencia, Spain.

出版信息

Vet World. 2024 Dec;17(12):2880-2888. doi: 10.14202/vetworld.2024.2880-2888. Epub 2024 Dec 19.

Abstract

BACKGROUND AND AIM

The sinoatrial node is responsible for the intrinsic electrical activation that in mammals leads to coordinated rhythmic contractions of the heart, from where it is distributed through the atrial tissue to the atrioventricular node. This study aimed to conduct a histological and morphometric study of the components and cells in cardiac nodes altered by myocardial infarction (MI) and compare them with normal tissues in humans and pigs.

MATERIALS AND METHODS

We analyzed 10 human hearts and 10 pig hearts that died from MI and compared them with 10 healthy control hearts from each species. Histological sections of 5 μm thickness were obtained using a microtome and stained with hematoxylin-eosin and Masson's trichrome. The identification and assessment of the percentage of connective tissue and cellularity in the cardiac nodes were performed.

RESULTS

We observed a decreased size of cardiac nodes in humans and pigs, as well as an increased percentage of fibrosis inside the nodes, and changes in the size of the nodal cells and surrounding cardiomyocytes (decrease or hypertrophy) were observed. Cartilaginous metaplasia was also found in the cardiac skeleton of all pig samples.

CONCLUSION

In the present study, a significant increase in collagen fibers and a decrease in cellularity were found in cardiac nodes in samples from humans and pigs with MI. These findings would explain the presence of arrhythmias, which often lead to death.

摘要

背景与目的

窦房结负责内在电激活,在哺乳动物中,这种激活会导致心脏协调的节律性收缩,并从窦房结通过心房组织传导至房室结。本研究旨在对因心肌梗死(MI)而改变的心脏节点中的成分和细胞进行组织学和形态计量学研究,并将其与人类和猪的正常组织进行比较。

材料与方法

我们分析了10例死于心肌梗死的人类心脏和10例猪心脏,并将它们与每种物种的10个健康对照心脏进行比较。使用切片机获得5μm厚的组织学切片,并用苏木精-伊红和马松三色染色法进行染色。对心脏节点中的结缔组织百分比和细胞密度进行识别和评估。

结果

我们观察到人类和猪的心脏节点尺寸减小,以及节点内纤维化百分比增加,并且观察到节点细胞和周围心肌细胞的大小发生变化(减小或肥大)。在所有猪样本的心脏骨骼中也发现了软骨化生。

结论

在本研究中,在患有心肌梗死的人类和猪的样本的心脏节点中发现胶原纤维显著增加且细胞密度降低。这些发现可以解释心律失常的存在,而心律失常常常导致死亡。

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