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慢性低压缺氧时肺脏的形态学研究

Morphological studies of the lungs in chronic hypobaric hypoxia.

作者信息

Sulkowska M

机构信息

Department of Pathological Anatomy, University Medical School, Białystok.

出版信息

Pol J Pathol. 1997;48(4):225-34.

PMID:9529928
Abstract

The aim of the present study was to evaluate the effect of hypobaric hypoxia on the changes observed within lung parenchyma, particularly in the surfactant system-forming structures. The experiment used male Wistar rats, 180-220g b.w. The animals were kept in a hypobaric chamber for 3, 10 and 30 days. Pressure in the chamber (380mm Hg) corresponded to air rarefaction at an altitude of 5500m. Control animals were kept in the same room near the chamber at normal atmospheric pressure. The changes observed in the lungs were evaluated basing on ultrastructural analysis by transmission electron microscopy. The present results indicate phasic character of the changes occurring within lung parenchyma, including the surfactant system-forming structures. In the early phase (3 days), destructive-exudative changes predominated (delamelation of type II pneumocytes; oedematous changes, damage to the alveolar lining layer, accumulation of alveolar macrophages). In the later phases, repair-proliferative processes were predominant (increased number of type II pneumocytes, focal intensification of fibroplasia). The changes within the surfactant system-forming structures were accompanied by the accumulation of granulocytes and monocytes (hypobaric conditions for 3 and 10 days) and blood platelets (hypobaric conditions for 30 days) in the vascular bed of the lungs. The pathomechanism of the changes observed in the surfactant system was discussed with regard to the vascular changes. The possibility of formation of blood platelets within the vascular system of the lungs was considered.

摘要

本研究的目的是评估低压缺氧对肺实质内观察到的变化的影响,特别是对形成表面活性剂系统的结构的影响。实验使用体重180 - 220克的雄性Wistar大鼠。将动物置于低压舱中3天、10天和30天。舱内压力(380毫米汞柱)相当于海拔5500米处的空气稀薄程度。对照动物在常压下饲养在靠近舱室的同一房间内。基于透射电子显微镜的超微结构分析评估肺内观察到的变化。目前的结果表明肺实质内发生的变化具有阶段性,包括形成表面活性剂系统的结构。在早期阶段(3天),以破坏性渗出性变化为主(II型肺细胞脱片;水肿性变化、肺泡衬里层损伤、肺泡巨噬细胞积聚)。在后期阶段,以修复增殖过程为主(II型肺细胞数量增加、局灶性纤维增生强化)。形成表面活性剂系统的结构内的变化伴随着肺血管床中粒细胞和单核细胞(低压条件3天和10天)以及血小板(低压条件30天)的积聚。关于血管变化讨论了表面活性剂系统中观察到的变化的发病机制。考虑了肺血管系统内形成血小板的可能性。

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