Ligand triggers of classical preconditioning and postconditioning

The cardioprotection afforded by ischemic preconditioning (IPC) and ischemic postconditioning (PC) are receptor mediated. In this review, we will focus on the major ligand classes and receptors that contribute to IPC and PC-induced cardioprotection. Ligand classes discussed include adenosine, bradyk...

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Bibliographic Details
Published in:	Cardiovascular research 2006-05, Vol.70 (2), p.212-221
Main Authors:	GROSS, Eric R, GROSS, Garrett J
Format:	Article
Language:	eng
Subjects:	Adenosine - metabolism Adenosine - therapeutic use Adrenergic Agents - metabolism Adrenergic Agents - therapeutic use Biological and medical sciences Bradykinin - metabolism Bradykinin - therapeutic use Cardiology. Vascular system Cholinergic Agents - metabolism Cholinergic Agents - therapeutic use Erythropoietin - metabolism Erythropoietin - therapeutic use Humans Ischemic Preconditioning, Myocardial Ligands Medical sciences Myocardial Ischemia - drug therapy Myocardial Ischemia - metabolism Myocardial Reperfusion Injury - metabolism Myocardial Reperfusion Injury - prevention & control Myocardium - metabolism Narcotics - metabolism Narcotics - therapeutic use Protein Binding
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Summary:	The cardioprotection afforded by ischemic preconditioning (IPC) and ischemic postconditioning (PC) are receptor mediated. In this review, we will focus on the major ligand classes and receptors that contribute to IPC and PC-induced cardioprotection. Ligand classes discussed include adenosine, bradykinin, opioids, erythropoietin, adrenergics and muscarinics. The cardioprotective therapeutic window of each ligand class will also be summarized, with particular focus as to whether ligands are protective when administered at or close to the time of reperfusion. Information will primarily be directed at studies in which infarct size reduction is the gold standard to assess the efficacy of IPC and PC. Myocardial stunning is a less robust endpoint for assessing cardioprotection and the use of this endpoint is only limited to studies with human tissue where infarct size assessment is not possible. Receptor cross-talk between ligands and the common signaling pathways involved for these ligands will also be briefly discussed.
ISSN:	0008-6363 1755-3245