Invited Symposium: Cardiac Ischemia Reperfusion
Kennedy, SP (Cardiovascular and Metabolic Diseases, Pfizer Central Research, Groton, CT, USA)
Knight, DR (Cardiovascular and Metabolic Diseases, Pfizer Central Research, Groton, CT, USA)
Hill, RJ (Cardiovascular and Metabolic Diseases, Pfizer Central Research, Groton, CT, USA)
Ischemic preconditioning is a phenomenon in which a brief ischemic event protects the myocardium from a subsequent prolonged ischemic insult. Numerous humoral agents have been proposed to either mediate or mimic ischemic preconditioning, but a significant amount of attention has focused on adenosine and its analogues. Within the last decade, the role of adenosine A1 and A3 receptors in providing cardioprotection from ischemic injury has begun to emerge. Recent evidence indicates that although stimulation of either receptor subtype can elicit cardioprotection, it is unlikely A3 receptors play a major role in mediating adenosine's actions in ischemic preconditioning. However, in pharmacological preconditioning, stimulation of A3 receptors has an advantage over A1 receptor stimulation in that A3 receptors do not cause unwanted cardiac/hemodynamic side-effects. Studies performed in our laboratories and others have demonstrated that both moderately (IB-MECA) and highly (CB-MECA) selective A3 receptor agonists provide significant cardioprotection both in vitro and in vivo. Although these agents appear to cardioprotect via PKC activation and the opening of KATP channels, further study is necessary to clearly delineate their full mechanism of action.
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|Tracey, WR; Kennedy, SP; Knight, DR; Hill, RJ; (1998). Identification of Adenosine A3 Receptors as a Target for Providing Cardioprotection from Ischemia-Reperfusion Injury. Presented at INABIS '98 - 5th Internet World Congress on Biomedical Sciences at McMaster University, Canada, Dec 7-16th. Invited Symposium. Available at URL http://www.mcmaster.ca/inabis98/lukas/tracey0350/index.html|
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