Open AccessJournal Article
Hypoxia-induced structural changes in the media and adventitia of the rat hilar pulmonary artery and their regression.
B Meyrick,L Reid +1 more
TLDR
Hypoxia causes a doubling in thickness of the medial and adventitial coats of the hilar muscular pulmonary artery, which with recovery regain near normal thickness but whose structure is altered.Abstract:
Chronic hypobaric hypoxia induces structural features characteristic of pulmonary hypertension, but little is known of their reversal. In the present study, rats have been exposed to hypobaric hypoxia for 10 days and subsequently allowed to recover in room air for 3, 14, 28, or 70 days. With the use of 1-mu sections and electron-microscopic and point-counting techniques, the regression of the medial and adventitial changes in the rat hilar intrapulmonary artery has been followed. In the media, 10-day hypoxia causes more than a doubling in thickness due to 1) hypertrophy of smooth muscle cells, particularly of rough sarcoplasmic reticulum and Golgi apparatus; 2) an increase in extracellular connective tissue, microfibrils, collagen fibers, and elastin, and 3) edemalike fluid. In addition, the elestic laminas are doubled in thickness, and myofilamentous processes of the hypertrophied smooth muscle cells contact them. After just 3 days' recovery, some cells have already returned to normal diameter, although medial thickening is unchanged. By Day 14 and at Days 28 and 70 of recovery, medial thickness and cell diameter are within the normal range, and by recovery Day 70, there is a significant increase in the relative areal proportion of extracellular collagen fibers and a decrease in elastin (P less than 0.001). Hypoxia also produces a more than twofold increase in adventitial thickness. Hypertrophy of fibroblasts and an increase in their number contribute to the thickening, as does as increase in collagen fibers. During 3-70 days of recovery, thickness is gradually reduced to normal levels, although it is still significantly above normal at Days 3, 14, and 28. The increases in thickness at these times are due mainly to the accumulation of collagen fibers, which are still apparent after 70 days of recovery. Thus, hypoxia causes a doubling in thickness of the medial and adventitial coats of the hilar muscular pulmonary artery, which with recovery regain near normal thickness but whose structure is altered. The increase in collagen fibers contributes to contracture and reduced distensibility in these vessels, which is apparent in arteriograms as narrowed lumen diameter.read more
Citations
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Inhibition of the VEGF receptor 2 combined with chronic hypoxia causes cell death-dependent pulmonary endothelial cell proliferation and severe pulmonary hypertension
Laimute Taraseviciene-Stewart,Yasunori Kasahara,Lori Alger,Peter Hirth,Gerald Mc Mahon,Johannes Waltenberger,Norbert F. Voelkel,Rubin M. Tuder +7 more
TL;DR: It is demonstrated here that VEGFR‐2 blockade with SU5416 in combination with chronic hypobaric hypoxia causes severe pulmonary hypertension associated with precapillary arterial occlusion by proliferating endothelial cells.
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Cellular and molecular mechanisms of pulmonary vascular remodeling
TL;DR: This review discusses vascular development in the lung and the cellular responses occurring in pulmonary hypertension; special attention is given to heterogeneity of responses within cell populations and reiteration of developmental processes.
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Endothelial cell responses to hypoxic stress.
TL;DR: Changes in the environmental oxygen tension to which cells are exposed in vivo result in physiological and sometimes pathological consequences that are associated with differential expression of specific genes.
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Induction of interleukin 6 (IL-6) by hypoxia in vascular cells. Central role of the binding site for nuclear factor-IL-6
Shi Fang Yan,Isabella Tritto,David J. Pinsky,Hui Liao,James Huang,Gerald Fuller,Jerold Brett,Lester May,David M. Stern +8 more
TL;DR: Data indicate that hypoxia induces expression of IL-6, most likely a result of hypoxic activation at the NF-IL-6 site, and suggest that other genes with regulatory NF-il-6 sites may also be induced by a similar mechanism.
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Molecular and cellular basis of pulmonary vascular remodeling in pulmonary hypertension
TL;DR: This review focuses on the latest advances in knowledge of vascular remodeling processes as they relate to specific forms of pulmonary hypertension and particularly in the light of recent genetic studies that have identified specific pathways involved in the pathogenesis of severe pulmonary hypertension.
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Journal Article
The effect of continued hypoxia on rat pulmonary arterial circulation. An ultrastructural study.
B Meyrick,L Reid +1 more
TL;DR: The extreme narrowing of the lumen caused by thickened endothelial cells and by encroachment of new muscle as well as the finding of capillaries that are no longer patent doubtless explain the reduction in small peripheral areteries.
Journal ArticleDOI
WOUND HEALING AND COLLAGEN FORMATION : V. Quantitative Electron Microscope Radioautographic Observations of Proline-H3 Utilization by Fibroblasts
Russell Ross,Earl P. Benditt +1 more
TL;DR: Morphologic observations of regions in the fibroblast interpretable as possible sites of communication between the ergastoplasm and the extracellular space, together with kinetic studies, permit the suggestion of an alternate pathway of passage of at least some of the synthesized protein directly from the ergastsoplasmic cisternae to the cell exterior.
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The effect of continued hypoxia on rat pulmonary arterial circulation. An ultrastructural study.
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