Lungs and hypoxia: a review of the literature

Anatomy Pub Date : 2021-04-01 DOI:10.2399/ana.21.841001
M. Sargon
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Abstract

Acute, intermittent or chronic hypoxia have negative effects on lung maturation during the embryological period which has been shown by many experimental models designed on animal studies. The receptors responsible from the development of lungs in fetal period are affected from hypoxia. Hypoxia also affects the morphometry, anatomy and microscopy of lung tissue in the adults. In acute phase of hypoxia; lung parenchyma showed destructive oxidative changes. However, in later phases repair and proliferative processes were observed in the lung tissue. Damage to the lining layer of alveoli, accumulation of alveolar macrophages, oedematous changes in the lung parenchyma, mild oedema, inflammatory cell infiltration, increased number of type II pneumocytes and pulmonary fibrosis are the main findings in cases of hypoxia. Chronic hypoxia accentuates lung growth by increasing the lung parenchyma. Decrease of capillary volume and suppression of elastin repair in lung fibroblasts are other clinically important microscopic findings in hypoxia. Many molecular studies found in the literature revealed micro-RNAs to be involved in modulation of hypoxia-induced pulmonary hypertension. In animal models submitted to acute hypobaric hypoxia; the researchers detected an increase in eNOS mRNA which is responsible of the immediate response, producing nitric oxide that caused vasodilation and bronchodilation in lung tissue. In other molecular studies; suppression of many immune molecules, major changes at the levels of various enzymes and growth factors were detected in the researches. Additionally; hypoxia causes to an increase in the amount of lung cancer cells and therefore; induces the metastases of lung cancer cells to brain tissues.
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肺与缺氧:文献综述
急性、间歇性或慢性缺氧对胚胎期肺成熟有负面影响,这已被许多动物实验模型所证实。胎儿期肺发育的受体受到缺氧的影响。缺氧也会影响成人肺组织的形态学、解剖学和显微检查。急性缺氧期;肺实质出现破坏性氧化改变。然而,在后期,在肺组织中观察到修复和增殖过程。肺泡内层损伤、肺泡巨噬细胞积聚、肺实质水肿改变、轻度水肿、炎性细胞浸润、II型肺细胞增多、肺纤维化是缺氧的主要表现。慢性缺氧通过增加肺实质来促进肺的生长。肺成纤维细胞毛细血管体积减小和弹性蛋白修复抑制是缺氧时其他重要的临床显微镜表现。在文献中发现的许多分子研究表明,微rna参与了缺氧诱导的肺动脉高压的调节。在急性低气压缺氧的动物模型中;研究人员检测到eNOS mRNA的增加,这种mRNA负责即时反应,产生一氧化氮,导致肺组织血管舒张和支气管扩张。在其他分子研究中;在研究中发现许多免疫分子受到抑制,各种酶和生长因子水平发生重大变化。另外;缺氧会导致肺癌细胞数量的增加,因此;诱导肺癌细胞向脑组织转移。
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