Coronary artery disease is the number one cause of adult mortality dueto a medical illness in the United States. Exciting new studies are looking at the role transient ischemiamay play in preconditioning the myocardium to reduce the degree of infarction following a sustained ischemicinsult. In this speculative review, we surmise ischemic preconditioning and the resulting protectionafforded by it in response to abnormal insults arises from an already existing physiological processthat may be associated with exercise. A brief ischemic episode mimics the cells response to normal dipsin ATP levels caused by metabolic demand. In so doing, via constitutive nitric oxide synthase derivednitric oxide, it temporarily down regulates a cells excitatory state, thus protecting it from the nextinsult. Within this context, opiate and opioid actions can be incorporated into the protection scenario,as can other signal molecules since they may release nitric oxide. Instead of ischemia inducing nitricoxide release via a drop of ATP levels, various signal molecules, such as opiate alkaloids, have theircell surface receptors coupled to constitutive nitric oxide synthase thereby releasing nitric oxide,initiating associated cell activity dampening action. In conclusion, it appears as though endogenousnitric oxide stimulators offer their selective preconditioning protection by joining an already existingprocess that limits activation following normal physical exertion.

Keywords: Research Support, U.S. Gov