Role of opioids in acute and delayed preconditioning. J Mol Cell Cardiol 2003 Jul;35(7):709-18
Date
06/24/2003Pubmed ID
12818560DOI
10.1016/s0022-2828(03)00135-4Scopus ID
2-s2.0-0038123105 (requires institutional sign-in at Scopus site) 129 CitationsAbstract
A number of endogenous mediators, including opioids, adenosine and bradykinin, which act on cardiac cell membrane receptors have been demonstrated to trigger the phenomenon termed ischemic preconditioning (IPC). IPC is an endogenous protective mechanism, whereby a brief period of ischemia or hypoxia protects a cell or organ, in this review the heart, against injury from a subsequent more prolonged stressful insult. Recent data suggest that opioid receptors are important triggers and/or mediators of this protective response. Selective pharmacological antagonists of the delta-or kappa-opioid receptor have been shown to block IPC, and agonists of these same receptors have been shown to mimic IPC in intact animals, isolated hearts or isolated cardiomyocytes. This review will summarize the current state of knowledge, which exists defining the role and cellular signaling pathways by which endogenously or exogenously administered opioids produce their cardioprotective response. The potential clinical application and evidence to suggest that opioids produce a similar protective effect in man will also be discussed.
Author List
Gross GJMESH terms used to index this publication - Major topics in bold
AnimalsCryoprotective Agents
Humans
Ischemic Preconditioning, Myocardial
Narcotics
Receptors, Opioid, delta
Receptors, Opioid, kappa
Signal Transduction
