ABSTRACT

Ischemic preconditioning (IPC) is a cardioprotective phenomenon in which a single or multiple brief period of coronary artery occlusion results in an increased tolerance to a subsequent more prolonged period of ischemia [1]. This phenomenon occurs in two phases temporally-an acute or early phase in which the cardioprotective effect lasts for 1-3 h, and a delayed phase or second window of protection which reappears 24-48 h after the acute phase and may last for 72 h [2].There has been considerable interest in the triggers and/or mediators of this phenomenon since identification of a mechanism responsible might lead to a powerful new therapeutic approach to treating patients with ischemic heart disease at risk for a myocardial infarction. Adenosine, bradykinin, and opioid receptors have all been identified as potential targets for drug development since occupation and activation of

all three of these G protein-coupled receptors have been shown to trigger IPC in a number of animalmodels and species [2]. The purpose of this chapter then will be to focus on the evidence which suggests that delta opioid receptor activation is an important component of both early and delayed IPC and potential mechanisms by which delta opioid receptor agonists produce a direct cardioprotective effect on the cardiac myocyte. We will also discuss possible clinical implications of this approach to cardioprotection.