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黏液性水肿中水肿形成的机制——蛋白质外渗增加和淋巴引流相对缓慢。

Mechanisms of edema formation in myxedema--increased protein extravasation and relatively slow lymphatic drainage.

作者信息

Parving H H, Hansen J M, Nielsen S L, Rossing N, Munck O, Lassen N A

出版信息

N Engl J Med. 1979 Aug 30;301(9):460-5. doi: 10.1056/NEJM197908303010902.

Abstract

We assessed extravascular accumulation of albumin and fluid in primary myxedema by measuring metabolic turnover and transcapillary escape of 131I-labeled human albumin in seven patients. In the hypothyroid state, we found a low plasma volume (P less than 0.05), a reduced rate of albumin synthesis and catabolism (P less than 0.01), an increased transcapillary escape rate of albumin (P less than 0.01), a remarkable increase in the extravascular mass of albumin (1500 micronmol; P less than 0.01) and a longer mean transit time through the extravascular spaces in primary myxedema than in other states of generalized edema (P less than 0.05). All variables returned to normal during l-thyroxine treatment. The extravascular accumulation of albumin, and presumably of all other plasma proteins, is important in the generalized edema typically found in myxedema. Inadequate lymphatic drainage may also explain the formation of exudates in the serous cavities that are well known in myxedema.

摘要

我们通过测量7例原发性黏液性水肿患者体内131I标记的人白蛋白的代谢转换和毛细血管通透性,评估了血管外白蛋白和液体的蓄积情况。在甲状腺功能减退状态下,我们发现血浆容量降低(P<0.05),白蛋白合成和分解代谢速率降低(P<0.01),白蛋白的毛细血管通透性增加(P<0.01),血管外白蛋白质量显著增加(1500微摩尔;P<0.01),且原发性黏液性水肿患者血管外间隙的平均通过时间比其他全身性水肿状态更长(P<0.05)。在左甲状腺素治疗期间,所有变量均恢复正常。白蛋白以及可能所有其他血浆蛋白的血管外蓄积在黏液性水肿中常见的全身性水肿中起重要作用。淋巴管引流不足也可能解释了黏液性水肿中常见的浆膜腔渗出液的形成。

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