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Brief myocardial ischemia attenuates platelet thrombosis in remote, damaged, and stenotic carotid arteries.

Authors: K Hata|||P Whittaker|||R A Kloner|||K Przyklenk

Journal: Circulation

Publication Type: Journal Article

Date: 1999

DOI: 10.1161/01.cir.100.8.843

ID: 10458721

Affiliations:

Affiliations

    Heart Institute, Good Samaritan Hospital, Department of Medicine University of Southern California, Los Angeles, CA, USA.|||||||||

Abstract

Brief antecedent periods of coronary artery occlusion improve subsequent vessel patency in damaged and stenotic coronary arteries via release of adenosine from ischemic/reperfused myocardium and resultant adenosine receptor stimulation. However, the site of receptor stimulation-circulating blood-borne elements (ie, platelets) versus vessel-wall components of the culprit artery-remains unclear. If platelet adenosine receptors are involved, then the benefits of brief coronary occlusion (1) should be manifested systemically and improve patency at a remote site and (2) should be inhibited by an antagonist of adenosine A(2) receptors, whereas, in contrast, (3) brief vascular occlusion not associated with appreciable adenosine release should be ineffective in improving vessel patency.


Chemical List

    Quinazolines|||Receptors, Purinergic P1|||Triazoles|||Adenosine|||9-chloro-2-(2-furyl)-(1,2,4)triazolo(1,5-c)quinazolin-5-imine