| Autor: |
Wright JL; Department of Pathology, University of British Columbia, Vancouver, British Columbia, Canada. jlwright@interchange.ubc.ca, Tai H, Dai J, Churg A |
| Jazyk: |
angličtina |
| Zdroj: |
Laboratory investigation; a journal of technical methods and pathology [Lab Invest] 2002 Oct; Vol. 82 (10), pp. 1391-8. |
| DOI: |
10.1097/01.lab.0000032806.45023.08 |
| Abstrakt: |
The pathogenesis of cigarette smoke-induced pulmonary hypertension is not well characterized. We used RT-PCR to examine gene expression of nitric oxide synthase 2 (NOS-2), nitric oxide synthase 3 (NOS-3), endothelin, and vascular endothelial growth factor (VEGF) and its flk-1 receptor (VEGF-R) in main pulmonary arteries and in intraparenchymal arteries microdissected from alcohol-fixed paraffin blocks. The main pulmonary artery and intraparenchymal vessels responded in a similar fashion, with up-regulation of endothelin, VEGF, and VEGF-R gene expression evident by 2 hours after smoke exposure. Up-regulation of gene expression was still present at 24 hours after exposure, and at this time there was also a small increase in NOS-2. As a comparison, we examined the trachea and microdissected intraparenchymal airways and found up-regulation of endothelin and NOS-2 at 2 hours and additional up-regulation of NOS-3 at 24 hours. These findings suggest that the pulmonary vasculature very rapidly responds to cigarette smoke with up-regulation of mediators that control vascular cell proliferation and vascular constriction. These changes support the idea that pulmonary hypertension in cigarette smokers reflects a direct effect of smoke on the vasculature. The pattern of response in the vessels is distinctly different from that in the airways. |
| Databáze: |
MEDLINE |
| Externí odkaz: |
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