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慢性高原病的病理生理学与流行病学

Pathophysiology and epidemiology of chronic mountain sickness.

作者信息

Monge-C C, Arregui A, León-Velarde F

机构信息

Department of Physiological Sciences, Universidad Peruana Cayetano Heredia, Lima, Perú.

出版信息

Int J Sports Med. 1992 Oct;13 Suppl 1:S79-81. doi: 10.1055/s-2007-1024603.

Abstract

Chronic mountain sickness, which affects permanent residents of high altitudes, is the outcome of a progressive loss of ventilatory rate which naturally occurs with age and resulting in excessive hypoxemia and polycythemia. A theoretical model predicts the progressive failure of homeostatic control of the hemoglobin concentration when the values increase above those found at sea level. This is confirmed by lack of feedback mechanism between high altitude erythrocytosis and serum erythropoietin. The results of epidemiological studies are in agreement with the physiological findings. In a male population living at 4,300 m, an increase with age of the prevalences of excessive erythrocytosis (Hb > 213 g/l), blood oxygen saturation < 83%, headaches and a high score of symptoms of chronic mountain sickness has been found. The studies suggest the possibility that in addition to an accentuated hypoxemia, the excessive erythrocytosis may also result from an overreaction of the bone marrow to a fixed level of hypoxemia in ageing individuals.

摘要

慢性高山病影响高海拔地区的常住居民,它是随着年龄增长自然发生的通气率逐渐丧失的结果,会导致过度低氧血症和红细胞增多症。一个理论模型预测,当血红蛋白浓度值高于海平面时的值时,体内平衡控制血红蛋白浓度会逐渐失效。高海拔红细胞增多症与血清促红细胞生成素之间缺乏反馈机制证实了这一点。流行病学研究结果与生理学发现一致。在生活在4300米的男性人群中,已发现红细胞增多症(血红蛋白>213克/升)、血氧饱和度<83%、头痛以及慢性高山病症状高分的患病率随年龄增加。研究表明,除了加重的低氧血症外,红细胞增多症可能还源于老年个体骨髓对固定水平低氧血症的过度反应。

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