Donate Help Contact The AHA Sign In Home
American Heart Association
Arteriosclerosis, Thrombosis, and Vascular Biology
Search: search_blue_button Advanced Search
Arteriosclerosis, Thrombosis, and Vascular Biology. 1989;9:299-307

This Article
Right arrow Full Text (PDF)
Right arrow Submit a response
Right arrow Alert me when this article is cited
Right arrow Alert me when eLetters are posted
Right arrow Alert me if a correction is posted
Services
Right arrow Email this article to a friend
Right arrow Similar articles in this journal
Right arrow Similar articles in PubMed
Right arrow Alert me to new issues of the journal
Right arrow Download to citation manager
Right arrowRequest Permissions
Citing Articles
Right arrow Citing Articles via HighWire
Right arrow Citing Articles via Google Scholar
Google Scholar
Right arrow Articles by Manderson, J. A.
Right arrow Articles by Campbell, G. R.
Right arrow Search for Related Content
PubMed
Right arrow PubMed Citation
Right arrow Articles by Manderson, J. A.
Right arrow Articles by Campbell, G. R.
Right arrowPubmed/NCBI databases
*Compound via MeSH
*Substance via MeSH
Hazardous Substances DB
*METHOXAMINE HYDROCHLORIDE
*POTASSIUM CHLORIDE

Arteriosclerosis, Vol 9, 299-307, Copyright © 1989 by American Heart Association


ARTICLES

Balloon catheter injury to rabbit carotid artery. II. Selective increase in reactivity to some vasoconstrictor drugs

JA Manderson, TM Cocks and GR Campbell
Department of Anatomy, University of Melbourne, Parkville, Victoria, Australia.

The present study examined the changes in reactivity to a variety of vasoconstrictor drugs of the rabbit carotid artery during development of an intimal thickening induced by injury with an inflated balloon catheter. The injured and the unoperated contralateral carotid arteries were studied at 2 and 6 weeks after the operation. To differentiate areas of the injured artery lined by modified smooth muscle cells from areas lined by regenerated endothelial cells, each rabbit was injected with Evans blue dye before sacrifice. Ring segments (3 mm length) from the control and injured arteries were mounted in organ baths to record the circumferential isometric force with a technique that ensured that all rings were set to equivalent initial resting conditions of passive transmural stretch. Compared with the controls, the experimental arteries had a significantly decreased maximum contraction (Emax) in response to KCl at both 2 and 6 weeks. The experimental arteries were also significantly less sensitive to the alpha 1-adrenoceptor agonist, methoxamine, at both 2 weeks (approximately sevenfold) and 6 weeks (fourfold), with a marked decrease in Emax at 2 weeks, which returned to control values at 6 weeks. There was no change in Emax to either serotonin or the thromboxane A2-mimetic, U46619, in the experimental arteries at either time. There was, however, a small but significant increase in the sensitivity to both drugs. There was no difference in response to any of the constrictor agents between the white and blue regions of the experimental vessels.(ABSTRACT TRUNCATED AT 250 WORDS)


This article has been cited by other articles:


Home page
Cardiovasc ResHome page
B. E. Rolfe, S. Stamatiou, C. J. World, L. Brown, A. C. Thomas, J. A. Bingley, N. F. Worth, and J. H. Campbell
Leukaemia inhibitory factor retards the progression of atherosclerosis
Cardiovasc Res, April 1, 2003; 58(1): 222 - 230.
[Abstract] [Full Text] [PDF]


Home page
VASC ENDOVASCULAR SURGHome page
M. K. O'Donohoe, Z. S. Radic, A. D. Stein, L. B. Schwartz, R. L. McCann, and P.-O. Hagen
Loss of Tachyphylaxis and Increased Sensitivity to Angiotensin II in Experimental Vein Grants
Vascular and Endovascular Surgery, May 1, 1991; 25(4): 281 - 288.
[Abstract] [PDF]