Skip Navigation

Cardiovascular Research 1996 32(3):604-612; doi:10.1016/S0008-6363(96)00126-5
© 1996 by European Society of Cardiology
This Article
Right arrow FREE Full Text (PDF) Freely available
Right arrow E-letters: Submit a response
Right arrow Alert me when this article is cited
Right arrow Alert me when E-letters 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 Add to My Personal Archive
Right arrow Download to citation manager
Right arrowRequest Permissions
Right arrow Disclaimer
Google Scholar
Right arrow Articles by Fujikawa, H.
Right arrow Articles by Shimada, K.
Right arrow Search for Related Content
PubMed
Right arrow PubMed Citation
Right arrow Articles by Fujikawa, H.
Right arrow Articles by Shimada, K.
Social Bookmarking
 Add to CiteULike   Add to Connotea   Add to Del.icio.us  
What's this?

Copyright © 1996, European Society of Cardiology

Endothelin-1 production in coronary circulation in a new canine model of coronary thrombosis

Hideyuki Fujikawa*, Ken-ichi Kawasaki, Hiromichi Sekiguchi, Hideaki Mito, Yuji Hayashi, Hiroshi Funayama and Kazuyaki Shimada

Department of Cardiology, Jichi Medical School, Minamikawachi-machi, Kawachi-gun, Tochigi 329-04, Japan

* Corresponding author. Tel.: (+81-285) 44-2111; fax: (+81-285) 44-5317.

Objective: The purpose of this study was to investigate whether endogenous endothelin-1 (ET-1) production in coronary circulation is associated with acute coronary thrombotic events in vivo. To achieve this goal, we have designed a new experimental canine model of coronary thrombosis.Methods: In vivo occlusive thrombus was induced by the intracoronary application of radiofrequency energy (660 kHz, 50 W) in closed-chest dogs. Pathological and immunohistochemical examinations of thrombosed coronary artery were performed. In 12 dogs, plasminogen activator was administered intravenously and serial measurements of ET-1, thromboxane B2 (TXB2) and thrombin-antithrombin HI complex (TAT) levels in plasma from the coronary sinus, aortic root and inferior vena cava were examined.Results: Occlusive platelet-rich thrombi were attached to the deeply injured intimal surface. TAT and TXB2 increased rapidly soon after the intimal injury and declined after successful thrombolysis. In contrast, ET-1 in the coronary sinus was elevated after reperfusion and was significantly higher than in the aorta. Net ET-1 production in the coronary circulation showed a significant positive correlation with the peak TAT levels (r = 0.69, P < 0.05), but not with TXBf2 or total occlusion time as an index of ischemic severity.Conclusions: Deep intimal injury leads to occlusive coronary thrombus. Thrombus formation and its subsequent lysis is associated with the activation and deactivation, respectively, of the coagulation cascade and platelets. Thrombin generation may stimulate ET-1 production in the coronary endothelium in acute coronary thrombotic events.

KEYWORDS Coronary blood flow; Endothelium; Thrombolysis; Endothelin-1; Thrombin; Tissue-type plasminogen activator; Dog; Coronary artery


Add to CiteULike CiteULike   Add to Connotea Connotea   Add to Del.icio.us Del.icio.us    What's this?


This article has been cited by other articles:


Home page
Cardiovasc ResHome page
M Mansaray, P.R Belcher, I Vergroesen, Z.M Wright, J.W Hynd, A.J Drake-Holland, and M.I.M Noble
Downstream resistance effects of intracoronary thrombosis in the stenosed canine coronary artery
Cardiovasc Res, April 1, 1999; 42(1): 193 - 200.
[Abstract] [Full Text] [PDF]



Disclaimer: Please note that abstracts for content published before 1996 were created through digital scanning and may therefore not exactly replicate the text of the original print issues. All efforts have been made to ensure accuracy, but the Publisher will not be held responsible for any remaining inaccuracies. If you require any further clarification, please contact our Customer Services Department.