Burkun A A, Nemirovskaia I N
Arkh Patol. 1975;37(4):37-43.
In experiments on 105 white rats using histological, histochemical, and morphometric methods the state of the lungs following daily "rises" in a pressure chamber to the "hight" of 5000--9000 m at verious time intervals--from 1 day to 9 weeks was studied. In 18 animals "ascents" were preceded by sinistral pulmonectomy. In parallel, the heart was investigated by the method of separate weighing. At initial stages changes in the lungs were characterized predominantly by impairment of the blood- and lymphocirculation. Subsequently, disorders of the microcirculation were observed to diminish and compensatory-hypertrophic changes in the lung tissue and vessels were noted. As the effect of hypoxia continued, sclerotic processes appeared, and extensive focal emphysema developed. These changes were manifested in a greater degree and appeared sooner with an increase in the extent of rarification of the atmosphere. Possibilities for adaptation to hypoxia in animals with the one lung were considerably lower as compared with normal ones. Hypercapnia produced an effect similar to that of hypoxia, making its influence on the structural elements of the lungs graver. Prolonged hypoxia led to hypertrophy of the right ventricle of the heart; the main factor in development of which the authors considered the elevation of the tonus and subsequent structural rearrangement of small vessels in the form of myoelastosis and myoelastofibrosis of the walls with narrowing of the lumen.
在对105只白鼠进行的实验中,运用组织学、组织化学和形态测量学方法,研究了在不同时间间隔(从1天到9周),每天在压力舱内将压力升至5000 - 9000米“高度”后肺部的状态。在18只动物中,“上升”前先进行了左肺切除术。同时,通过单独称重的方法对心脏进行了研究。在初始阶段,肺部的变化主要表现为血液循环和淋巴循环受损。随后,观察到微循环紊乱有所减轻,并注意到肺组织和血管出现代偿性肥大变化。随着缺氧作用的持续,硬化过程出现,广泛的局灶性肺气肿形成。这些变化在大气稀薄程度增加时表现得更为明显且出现得更早。与正常动物相比,单肺动物适应缺氧的可能性要低得多。高碳酸血症产生的影响与缺氧相似,使其对肺部结构成分的影响更为严重。长期缺氧导致心脏右心室肥大;作者认为其主要发展因素是张力升高以及随后小血管的结构重排,表现为血管壁的肌弹性组织增生和肌弹性纤维增生,管腔狭窄。