The reduction of infarct size produced by brief ischemic episodes prio
r to a sustained occlusion of a coronary artery, called ischemic preco
nditioning, is a well known phenomenon that occurs in several species,
but its mechanism is still under investigation. Recent reports suppor
t the idea that this protection can also be obtained by non-ischemic m
aneuvers like distention of the left ventricle and metabolic stimulati
on of myocardial cells. The features of non-ischemic preconditioning (
temporal limitation, second window, tolerance development, remote prec
onditioning and efficiency of the protection), as opposed to those of
ischemic preconditioning, are still to be determined. Neither is it kn
own if non-ischemic preconditioning occurs in humans. From a physiolog
ical point of view the protective effect of an increase in metabolic r
ate of the heart means a constant feed-back mechanism in the myocardia
l cell that counteracts the presumptive damage consequent to the incre
ase in metabolism Therefore, in the presence of a sudden coronary occl
usion the metabolic rate of the heart immediately before the occlusion
would have a dual role of increasing the degree of ischemia and of pr
otecting against it.