| HOME | HELP | FEEDBACK | SUBSCRIPTIONS | ARCHIVE | SEARCH | TABLE OF CONTENTS |
American Journal of Pathology, Vol 146, 389-397, Copyright © 1995 by American Society for Investigative Pathology
REGULAR ARTICLES |
I Chazova, JE Loyd, VS Zhdanov, JH Newman, Y Belenkov and B Meyrick
Cardiology Research Centre, Academy of Medical Sciences, Moscow, Russia.
Primary pulmonary hypertension (PPH) is associated with a spectrum of structural changes in the pulmonary arteries: increased medial thickness, eccentric and concentric intimal thickening, obliteration and recanalization of arteries, and appearance of plexiform and dilatation lesions. The purpose of the present study was to further characterize these structural changes with particular emphasis on arterial adventitial thickness and alterations in the walls of the pulmonary veins. In addition, to determine whether the characteristic structural changes of PPH were size related, each was related to external diameter. With quantitative techniques, the pulmonary vasculature of 19 patients with PPH and 7 controls was examined by light microscopy. In all 19 patients, we found a striking increase in adventitial, as well as intimal and medial, thickness in arteries of all sizes when compared with controls (P < 0.05). In addition, we found intimal and adventitial thickening of pulmonary veins < 250 mu in diameter in approximately half of the PPH cases (P < 0.05). The frequency of arterial obliteration, concentric intimal thickening, and recanalization was 16, 18, and 11 of 19 cases, respectively. These changes were most prevalent in arteries less than 200 mu in diameter whereas eccentric intimal thickening and plexiform lesions occurred in 15 and 6 of the patients, respectively, and were most widespread in arteries > 200 mu. We conclude that remodeling of the pulmonary vasculature in PPH routinely includes thickening of the arterial adventitia and frequently also includes changes in the walls of the pulmonary veins. The finding that recanalization occurs predominantly in the smaller arteries whereas eccentric intimal thickening occurs mainly in the larger ones suggests that recanalization should not be considered a consequence of thromboemboli but may also occur at sites of more fibrotic intimal change.
This article has been cited by other articles:
![]() |
M. J. Haurani and P. J. Pagano Adventitial fibroblast reactive oxygen species as autacrine and paracrine mediators of remodeling: Bellwether for vascular disease? Cardiovasc Res, September 1, 2007; 75(4): 679 - 689. [Abstract] [Full Text] [PDF] |
||||
![]() |
W. Zhou, B. O. Ibe, and J. U. Raj Platelet-activating factor induces ovine fetal pulmonary venous smooth muscle cell proliferation: role of epidermal growth factor receptor transactivation Am J Physiol Heart Circ Physiol, June 1, 2007; 292(6): H2773 - H2781. [Abstract] [Full Text] [PDF] |
||||
![]() |
K. R. Stenmark, N. Davie, M. Frid, E. Gerasimovskaya, and M. Das Role of the Adventitia in Pulmonary Vascular Remodeling Physiology, April 1, 2006; 21(2): 134 - 145. [Abstract] [Full Text] [PDF] |
||||
![]() |
Y. Gao and J. U. Raj Role of veins in regulation of pulmonary circulation Am J Physiol Lung Cell Mol Physiol, February 1, 2005; 288(2): L213 - L226. [Abstract] [Full Text] [PDF] |
||||
![]() |
G. G. Pietra, F. Capron, S. Stewart, O. Leone, M. Humbert, I. M. Robbins, L. M. Reid, and R. M. Tuder Pathologic assessment of vasculopathies in pulmonary hypertension J. Am. Coll. Cardiol., June 16, 2004; 43(12_Suppl_S): 25S - 32S. [Abstract] [Full Text] [PDF] |
||||
![]() |
B. W. Fouty and D. M. Rodman Mevastatin Can Cause G1 Arrest and Induce Apoptosis in Pulmonary Artery Smooth Muscle Cells Through a p27Kip1-Independent Pathway Circ. Res., March 21, 2003; 92(5): 501 - 509. [Abstract] [Full Text] [PDF] |
||||
![]() |
J. R. Runo, C. L. Vnencak-Jones, M. Prince, J. E. Loyd, L. Wheeler, I. M. Robbins, K. B. Lane, J. H. Newman, J. Johnson, W. C. Nichols, et al. Pulmonary Veno-occlusive Disease Caused by an Inherited Mutation in Bone Morphogenetic Protein Receptor II Am. J. Respir. Crit. Care Med., March 15, 2003; 167(6): 889 - 894. [Abstract] [Full Text] [PDF] |
||||
![]() |
P. Fesler, A. Pagnamenta, J-L. Vachiery, S. Brimioulle, S. Abdel Kafi, A. Boonstra, M. Delcroix, R.N. Channick, L.J. Rubin, and R. Naeije Single arterial occlusion to locate resistance in patients with pulmonary hypertension Eur. Respir. J., January 1, 2003; 21(1): 31 - 36. [Abstract] [Full Text] [PDF] |
||||
![]() |
B. W. Fouty, B. Grimison, K. A. Fagan, T. D. Le Cras, J. W. Harral, M. Hoedt-Miller, R. A. Sclafani, and D. M. Rodman p27Kip1 Is Important in Modulating Pulmonary Artery Smooth Muscle Cell Proliferation Am. J. Respir. Cell Mol. Biol., November 1, 2001; 25(5): 652 - 658. [Abstract] [Full Text] [PDF] |
||||
![]() |
E. L. Greidinger, S. P. Gaine, R. A. Wise, C. Boling, T. Housten-Harris, and F. M. Wigley Primary Pulmonary Hypertension Is Not Associated With Scleroderma-Like Changes in Nailfold Capillaries Chest, September 1, 2001; 120(3): 796 - 800. [Abstract] [Full Text] [PDF] |
||||
![]() |
H. Takahashi, S. Soma, M. Muramatsu, M. Oka, and Y. Fukuchi Upregulation of ET-1 and its receptors and remodeling in small pulmonary veins under hypoxic conditions Am J Physiol Lung Cell Mol Physiol, June 1, 2001; 280(6): L1104 - L1114. [Abstract] [Full Text] [PDF] |
||||
![]() |
S. Archer and S. Rich Primary Pulmonary Hypertension : A Vascular Biology and Translational Research "Work in Progress" Circulation, November 28, 2000; 102(22): 2781 - 2791. [Abstract] [Full Text] [PDF] |
||||
| HOME | HELP | FEEDBACK | SUBSCRIPTIONS | ARCHIVE | SEARCH | TABLE OF CONTENTS |