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暴发性肝衰竭时肺循环的结构改变

Structural alterations to the pulmonary circulation in fulminant hepatic failure.

作者信息

Williams A, Trewby P, Williams R, Reid L

出版信息

Thorax. 1979 Aug;34(4):447-53. doi: 10.1136/thx.34.4.447.

Abstract

Like patients with chronic liver disease, those with coma due to fulminant hepatic failure may show arterial hypoxaemia even in the absence of pulmonary complications, and in both it is attributed to increased intrapulmonary arteriovenous admixture. This study is concerned with the structural alterations in the pulmonary circulation of patients who have died from fulminant hepatic failure. Precise quantitative morphometric techniques applied to the injected and inflated lung have shown the major abnormality to be a diffuse dilatation of the pulmonary vascular bed affecting arteries and veins of all structural types. At an intra-acinar level the diameter of arteries accompanying respiratory bronchioles was 232.97 micron (+/-SD 46.35) compared with 177.76 micron (+/-SD 30.43) in controls (P less than 0.01). In two-thirds of the patients pleural spider naevi were seen and, throughout the lung, similar significant dilatation of precapillary vessels; but in only one patient were precapillary anastomoses shown. While intrapulmonary venous admixture undoubtedly contributes to hypoxia in fulminant hepatic failure, its exact relation to the structural changes is not yet determined.

摘要

与慢性肝病患者一样,暴发性肝衰竭所致昏迷患者即使没有肺部并发症也可能出现动脉血氧不足,两者均归因于肺内动静脉混合增加。本研究关注死于暴发性肝衰竭患者肺循环的结构改变。应用于注入空气并膨胀的肺的精确定量形态测量技术显示,主要异常是肺血管床弥漫性扩张,累及所有结构类型的动脉和静脉。在腺泡内水平,呼吸性细支气管伴行动脉的直径为232.97微米(±标准差46.35),而对照组为177.76微米(±标准差30.43)(P<0.01)。三分之二的患者可见胸膜蜘蛛痣,且全肺毛细血管前血管有类似的明显扩张;但仅1例患者显示有毛细血管前吻合。虽然肺内静脉混合无疑是暴发性肝衰竭患者缺氧的原因之一,但其与结构改变的确切关系尚未确定。

https://cdn.ncbi.nlm.nih.gov/pmc/blobs/ca1b/471095/39e83507e69a/thorax00166-0020-a.jpg

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