Magee F, Wright J L, Wiggs B R, Paré P D, Hogg J C
University of British Columbia Pulmonary Research Laboratory, St Paul's Hospital, Vancouver, Canada.
Thorax. 1988 Mar;43(3):183-9. doi: 10.1136/thx.43.3.183.
Cardiac catheterization data from eight patients with severe chronic obstructive lung disease and pulmonary hypertension at rest (greater than 25 mm Hg) were compared with those obtained from 14 patients with mild to moderate disease whose pulmonary artery pressure was within the normal range at rest (mean 15 (SEM 1) mm Hg), but increased with exercise (30 (2) mm Hg). We obtained lung sections from necropsy material from the group with severe disease, and from surgical specimens in the group with mild to moderate disease, and compared the structure of the vasculature in these groups with that obtained from surgical specimens in a non-smoking control group of seven patients. Oxygen administration either at rest or during exercise did not greatly affect the pulmonary arterial pressures. When cardiac index was plotted against pulmonary artery pressure at rest and during exercise and extrapolated to the axis there was no evidence for a critical closing pressure in either group. The vessels in the groups with mild to moderate and severe chronic obstructive lung disease showed intimal thickening (each 19% (SD 0.5%)) by comparison with the non-smoking group (16% (0.5%]. The group with severe disease, in addition, had medial hypertrophy (27% (0.5%) versus 24% (SD 1%) in the non-smoking group). These data are consistent with the idea that the diseased vessels are distorted and rigid. The lack of effect of breathing oxygen on the vascular response at rest and during exercise suggests that hypoxic vasoconstriction has a minimal role in the pulmonary hypertension of chronic obstructive lung disease. The data suggest that the intimal changes could narrow the vessel calibre in those patients with mild to moderate disease, and that the thickened media present in the vessels from patients with severe disease may act in concert with the enlarged intima to produce more severe vascular obstruction.
对8例重度慢性阻塞性肺疾病且静息时伴有肺动脉高压（大于25mmHg）患者的心脏导管插入术数据，与14例轻至中度疾病患者的数据进行了比较，后者静息时肺动脉压在正常范围内（平均15（标准误1）mmHg），但运动时升高（30（2）mmHg）。我们从重症组尸检材料以及轻至中度疾病组手术标本中获取肺组织切片，并将这些组的脉管系统结构与7例非吸烟对照组患者手术标本的结构进行比较。静息或运动时吸氧对肺动脉压影响不大。当绘制静息和运动时心脏指数与肺动脉压的关系图并外推至坐标轴时，两组均未发现临界关闭压的证据。与非吸烟组（16%（0.5%））相比，轻至中度和重度慢性阻塞性肺疾病组的血管内膜增厚（分别为19%（标准差0.5%））。此外，重症组有中膜肥厚（27%（0.5%），非吸烟组为24%（标准差1%））。这些数据与患病血管扭曲且僵硬的观点一致。静息和运动时吸氧对血管反应无影响，提示低氧性血管收缩在慢性阻塞性肺疾病肺动脉高压中作用极小。数据表明，内膜改变可能使轻至中度疾病患者的血管管径变窄，而重症患者血管中膜增厚可能与内膜增大共同作用，导致更严重的血管阻塞。
