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

Background-Brief antecedent periods of coronary artery occlusion improve su bsequent vessel patency in damaged and stenotic coronary arteries via relea se of adenosine from ischemic/reperfused myocardium and resultant adenosine receptor stimulation. However, the site of receptor stimulation-circulatin g blood-borne elements (ie, platelets) versus vessel-wall components of the culprit artery-remains unclear. If platelet adenosine receptors are involv ed, then the benefits of brief coronary occlusion (1) should be manifested systemically and improve patency at a remote site and (2) should be inhibit ed 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. Methods and Results-In Protocol 1, anesthetized rabbits received 5 minutes of transient coronary occlusion, 5 minutes of transient bilateral carotid o cclusion (purported to cause negligible adenosine release from the brain), or no intervention. All rabbits then underwent injury plus stenosis of the left carotid artery, resulting in repeated cyclic variations in carotid blo odflow (CFVs). Carotid patency during the initial 2 hours after stenosis (a ssessed by quantifying the nadir of the CFVs and area of the flow-time prof ile) was significantly enhanced with antecedent coronary-but not carotid-oc clusion versus controls. In Protocol 2, improvement in carotid patency afte r brief coronary occlusion was corroborated in anesthetized dogs. However, the benefits of brief coronary occlusion were abrogated by the A(2)/A(1) an tagonist CGS 15943. Conclusions-Brief antecedent coronary artery occlusion enhanced vessel pate ncy in remote, damaged, and stenotic carotid arteries, largely due to adeno sine receptor stimulation on circulating elements.