Heath D, Harris P, Sui G J, Liu Y H, Gosney J, Harris E, Anand I S
Department of Pathology, University of Liverpool, U.K.
Respir Med. 1989 Jan;83(1):77-81. doi: 10.1016/s0954-6111(89)80064-2.
A male infant of 16 months, of the Han race, died from subacute infantile mountain sickness in Lhasa (3600 m). At necropsy there was right ventricular hypertrophy secondary to muscularization of the pulmonary arteries and arterioles thought to have been induced by hypobaric hypoxia. In addition, there was intimal proliferation of myofibroblasts in the pulmonary arterioles, venules and veins. There were increased numbers within the bronchioles of pulmonary endocrine cells, containing calcitonin and bombesin, which could be related to hypoxia or trophic effects on the pulmonary vasculature. The relation of delayed effects of hypoxia to primary pulmonary hypertension is considered in this study.
一名16个月大的汉族男婴在拉萨(海拔3600米)死于亚急性婴儿高山病。尸检发现,肺动脉和小动脉肌化继发右心室肥厚,推测是由低压缺氧引起的。此外,肺小动脉、小静脉和静脉中有肌成纤维细胞内膜增生。细支气管内含有降钙素和蛙皮素的肺内分泌细胞数量增加,这可能与缺氧或对肺血管系统的营养作用有关。本研究探讨了缺氧延迟效应与原发性肺动脉高压的关系。