Enzi G, Bevilacqua M, Crepaldi G
Bull Eur Physiopathol Respir. 1976 May-Jun;12(3):433-42.
Carbon monoxide diffusion (DLCO), blood gas analysis at rest and after exercise, distribution of ventilation and perfusion by Xenon 133 were carried out in 43 hyperlipidemic patients, Fredrickson's types I, IIA, IIB, and IV. DLCO was significantly reduced in hypertriglyceridemic and to a lesser degree in hypercholesterolemic patients. A significant negative correlation was found between DLCO and triglyceride values. Significantly lower basal PaO2 values, which improved after exercise, were observed in both type IIA and type IV hyperlipemic patients. The ventilation/perfusion ratio distribution (V/Q) did not increase from the basal to the apical segments of the lungs in hyperlipidemic patients as it did in normals. The hypothesis of an alteration in pulmonary surface-active lipoprotein, directly related to hyperlipoproteinemia or indirectly caused by fat microembolism, may explain the reduced DLCO, the loss of V/Q gradient, and the decrease in PaO2 (which improves after exercise) observed in hyperlipemic patients. Disturbances in pulmonary gas exchange and PaO2 reduction could play an important role in the pathogenesis of both angina pain due to ischaemic heart disease, which is frequently observed in hyperlipemic patients, and the postprandial angina syndrome.
对43例弗雷德里克森I型、IIA型、IIB型和IV型高脂血症患者进行了一氧化碳弥散量（DLCO）、静息及运动后的血气分析，以及用氙133进行通气和灌注分布的检测。高甘油三酯血症患者的DLCO显著降低，高胆固醇血症患者的降低程度较小。DLCO与甘油三酯值之间存在显著的负相关。在IIA型和IV型高脂血症患者中均观察到基础PaO₂值显著较低，运动后有所改善。高脂血症患者肺通气/灌注比分布（V/Q）从肺底部到顶部未像正常人那样增加。肺表面活性脂蛋白改变的假说，直接与高脂蛋白血症相关或由脂肪微栓塞间接引起，可能解释了高脂血症患者中观察到的DLCO降低、V/Q梯度丧失以及PaO₂降低（运动后改善）。肺气体交换障碍和PaO₂降低可能在高脂血症患者中常见的缺血性心脏病所致心绞痛以及餐后心绞痛综合征的发病机制中起重要作用。
