Hyland R H, Krastins I R, Aspin N, Mansell A L, Zamel N
Am Rev Respir Dis. 1978 Jun;117(6):1045-53. doi: 10.1164/arrd.1978.117.6.1045.
We measured carbon monoxide diffusion capacity (DLCO) in the sitting and supine position in 73 apparently normal subjects (41 nonsmokers and 32 smokers). The coefficient of DLCO standardized for alveolar volume (KCO) was less in the smokers than in the nonsmokers (P less than 0.05) in the sitting position, but the separation was wider in the supine posture (P less than 0.01). The per cent changes between supine and sitting KCO (deltaKCO) were shown to be age dependent in both nonsmokers and smokers, but this age dependence was more accentuated in the latter group. Only 3 smokers were below the 95 per cent confidence limit of nonsmokers for KCO in the sitting position, but there were 7 smokers below that limit for deltaKCO. An attempt was made, using intravenous injection of xenon-133, to study the mechanism of this impairment. Persons who failed to increase KCO in the supine posture showed an ability to increase apical blood flow in that position. The mechanisms of impairment in deltaKCO remain to be explained and may be due either to a predominant apical defect or to a widespread abnormality of the pulmonary capillary bed.
我们对73名看似健康的受试者(41名不吸烟者和32名吸烟者)在坐位和仰卧位时的一氧化碳弥散量(DLCO)进行了测量。以肺泡容积标准化的DLCO系数(KCO),在坐位时吸烟者低于不吸烟者(P<0.05),但在仰卧位时二者差异更大(P<0.01)。仰卧位和坐位KCO的百分比变化(ΔKCO)在不吸烟者和吸烟者中均显示出与年龄相关,但在后一组中这种年龄依赖性更为明显。在坐位时,只有3名吸烟者的KCO低于不吸烟者的95%置信限,但有7名吸烟者的ΔKCO低于该限值。我们尝试通过静脉注射氙-133来研究这种损害的机制。在仰卧位时未能增加KCO的人在该体位显示出增加肺尖血流的能力。ΔKCO受损的机制仍有待解释,可能是由于主要的肺尖缺陷或肺毛细血管床的广泛异常。