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[慢性血容量过多时肺微循环床中气-血屏障与淋巴连接终末段的结构相互关系]

[Structural interrelations of the air-blood barrier and terminal sections of the lymphatic link in the pulmonary microcirculatory bed in chronic hypervolemia].

作者信息

Vikaliuk Iu F, Bisiarin Iu V

出版信息

Arkh Anat Gistol Embriol. 1987 Nov;93(11):67-73.

PMID:3328591
Abstract

The interalveolar septa of the human lungs are known to have no lymphatic capillaries. The topography of the pulmonary lymphatic system origin under conditions of chronic hypervolemia is still not investigated. Lungs of 24 corpses of persons, died from non-pulmonary pathology (control) and lungs of 34 corpses of persons, died from congenital and acquired heart disease accompanied with pre- and postcapillary forms of the pulmonary circulation hypertension, have been investigated. Decreased efficiency of the microcirculation, increased permeability of the blood capillary walls against the background of hypoxia result in an elevated production of lymph. Intensified collagen formation in the blood vessel walls and in the interalveolar septa is the prerequisite for reorganization of the pulmonary lymphatic bed. Lymphatic capillaries are found to grow into some sclerotic interalveolar septa and into deep structures of the blood capillary walls. This demonstrates a high plasticity of the lymphatic link terminal parts of the microcirculatory bed in pathologically changed lungs.

摘要

已知人类肺部的肺泡间隔没有淋巴管。慢性血容量过多情况下肺淋巴系统起源的地形学仍未得到研究。对24具死于非肺部疾病的尸体(对照组)的肺以及34具死于先天性和后天性心脏病并伴有毛细血管前和毛细血管后形式肺循环高压的尸体的肺进行了研究。在缺氧背景下,微循环效率降低、毛细血管壁通透性增加导致淋巴生成增加。血管壁和肺泡间隔中胶原蛋白形成增加是肺淋巴床重组的先决条件。发现淋巴管生长到一些硬化的肺泡间隔和毛细血管壁的深部结构中。这表明在病变肺中微循环床淋巴连接末端部分具有高度可塑性。

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