Abstract
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.
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- Albert R. K., Muramoto A., Caldwell J., Koepsell T., Butler J. Increases in intrathoracic pressure do not explain the rise in left ventricular end-diastolic pressure that occurs during exercise in patients with chronic obstructive pulmonary disease. Am Rev Respir Dis. 1985 Sep;132(3):623–627. doi: 10.1164/arrd.1985.132.3.623. [DOI] [PubMed] [Google Scholar]
- BURTON A. C., PATEL D. J. Effect on pulmonary vascular resistance of inflation of the rabbit lungs. J Appl Physiol. 1958 Mar;12(2):239–246. doi: 10.1152/jappl.1958.12.2.239. [DOI] [PubMed] [Google Scholar]
- Emirgil C., Sobol B. J., Campodonico S., Herbert W. H., Mechkati R. Pulmonary circulation in the aged. J Appl Physiol. 1967 Nov;23(5):631–640. doi: 10.1152/jappl.1967.23.5.631. [DOI] [PubMed] [Google Scholar]
- Hale K. A., Ewing S. L., Gosnell B. A., Niewoehner D. E. Lung disease in long-term cigarette smokers with and without chronic air-flow obstruction. Am Rev Respir Dis. 1984 Nov;130(5):716–721. doi: 10.1164/arrd.1984.130.5.716. [DOI] [PubMed] [Google Scholar]
- Lockhart A., Sestier F., Sentissi M., Gauthier J. J., Schrijen F. Effects of exercise and postural changes on pulmonary haemodynamics in patients with chronic lung diseases. Scand J Respir Dis Suppl. 1971;77:77–81. [PubMed] [Google Scholar]
- Mink S. N., Unruh H. W., Oppenheimer L. Vascular and interstitial mechanics in canine pulmonary emphysema. J Appl Physiol (1985) 1985 Dec;59(6):1704–1715. doi: 10.1152/jappl.1985.59.6.1704. [DOI] [PubMed] [Google Scholar]
- PERMUTT S., RILEY R. L. HEMODYNAMICS OF COLLAPSIBLE VESSELS WITH TONE: THE VASCULAR WATERFALL. J Appl Physiol. 1963 Sep;18:924–932. doi: 10.1152/jappl.1963.18.5.924. [DOI] [PubMed] [Google Scholar]
- Reid L. M. Structure and function in pulmonary hypertension. New perceptions. Chest. 1986 Feb;89(2):279–288. doi: 10.1378/chest.89.2.279. [DOI] [PubMed] [Google Scholar]
- Thurlbeck W. M., Dunnill M. S., Hartung W., Heard B. E., Heppleston A. G., Ryder R. C. A comparison of three methods of measuring emphysema. Hum Pathol. 1970 Jun;1(2):215–226. doi: 10.1016/s0046-8177(70)80035-1. [DOI] [PubMed] [Google Scholar]
- Timms R. M., Khaja F. U., Williams G. W. Hemodynamic response to oxygen therapy in chronic obstructive pulmonary disease. Ann Intern Med. 1985 Jan;102(1):29–36. doi: 10.7326/0003-4819-102-1-29. [DOI] [PubMed] [Google Scholar]
- Weitzenblum E., Sautegeau A., Ehrhart M., Mammosser M., Pelletier A. Long-term oxygen therapy can reverse the progression of pulmonary hypertension in patients with chronic obstructive pulmonary disease. Am Rev Respir Dis. 1985 Apr;131(4):493–498. doi: 10.1164/arrd.1985.131.4.493. [DOI] [PubMed] [Google Scholar]
- Williams I. P., Boyd M. J., Humberstone A. M., Wilson A. G., Millard F. J. Pulmonary arterial hypertension and emphysema. Br J Dis Chest. 1984 Jul;78(3):211–216. [PubMed] [Google Scholar]
- Wright J. L., Barry W., Paré P. D., Hogg J. C. Ranking the severity of emphysema on whole lung slices. Concordance of upper lobe, lower lobe, and entire lung ranks. Am Rev Respir Dis. 1986 May;133(5):930–931. [PubMed] [Google Scholar]
- Wright J. L., Lawson L., Paré P. D., Hooper R. O., Peretz D. I., Nelems J. M., Schulzer M., Hogg J. C. The structure and function of the pulmonary vasculature in mild chronic obstructive pulmonary disease. The effect of oxygen and exercise. Am Rev Respir Dis. 1983 Oct;128(4):702–707. doi: 10.1164/arrd.1983.128.4.702. [DOI] [PubMed] [Google Scholar]

