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实验性空气栓塞后肺动脉病变的发展与消退。一项光镜和电镜研究。

Development and regression of pulmonary arterial lesions after experimental air embolism. A light and electronmicroscopic study.

作者信息

Balk A G, Mooi W J, Dingemans K P, Wagenvoort C A

出版信息

Virchows Arch A Pathol Anat Histopathol. 1985;406(2):203-12. doi: 10.1007/BF00737086.

Abstract

Repeated systemic venous air embolism produces pulmonary vascular lesions, the nature of which is still a subject of controversy. We investigated the pulmonary arterial lesions produced by repeated air embolism in rabbits, both at light and electron microscopic level. We found that they form a remarkable histopathological entity, consisting of initial pronounced vasoconstriction, combined with severe intimal inflammatory changes. Within 4 days after the last injection of air, peculiar sheet-like structures consisting of oedematous tissue and lined by endothelium, projected into the lumen. These structures probably resulted from the shearing stress of the blood, streaming over the severely oedematous intima. They subsequently became thinner and disappeared after two weeks. Various types of blood-borne and mesenchymal cells were present in the thickened intima and within the sheets. The origin of the latter cells remained undecided. They may originate from medial smooth muscle cells penetrating the internal elastic lamina as well as by transition from blood-borne cells into mesenchymal cells, or both.

摘要

反复发生的系统性静脉空气栓塞会导致肺血管病变,其性质仍存在争议。我们在光镜和电镜水平上研究了家兔反复空气栓塞所产生的肺动脉病变。我们发现这些病变形成了一个显著的组织病理学实体,包括最初明显的血管收缩,并伴有严重的内膜炎症变化。在最后一次注射空气后的4天内,由水肿组织构成并内衬内皮的特殊片状结构向管腔内突出。这些结构可能是由于血液对严重水肿的内膜产生剪切力所致。两周后,它们随后变薄并消失。增厚的内膜和片状结构内存在各种类型的血源性细胞和间充质细胞。后者的细胞来源尚未确定。它们可能起源于穿透内弹性膜的中膜平滑肌细胞,也可能由血源性细胞转变为间充质细胞,或者两者皆有。

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