Repeated short coronary occlusions trigger probably more than one pathway leading to increased tolerance toward ischemia. Adenosine plays probably a very important but not an exclusive role. It may act via opening of A1-receptor-operated K(+)-channels that lead to hyperpolarization of the cell, and it has antiadrenergic actions. A proposed action of adenosine via protein kinase C is not confirmed. Trophic factors are expressed during short periods of ischemia and contribute to survival, probably via inhibition of apoptosis.