Heat-shock proteins (HSPs) are a family of gene products that are expressed in response to stress in every living cell. This name was derived from early observations demonstrating their synthesis in fruit flies following elevations in temperature. More recently, a number of other environmental and pathological events have been observed to increase the expression of HSPs; consequently, they are also referred to as stress proteins. After expression of the stress genes, cells become resistant to subsequent stresses. This phenomenon has been termed "stress tolerance." The mechanisms by which stress tolerance is achieved are still poorly understood. Recent evidence suggests that stress tolerance is, at least in part, due to the stabilization of cellular processes such as protein synthesis. Expression of HSPs has been observed during clinically relevant situations, especially under conditions in which the delivery of oxygen is diminished (e.g., hemorrhage, ischemia). Since the expression of HSPs is part of the cellular defense system protecting cells from harmful conditions, the regulation of their expression may be useful as a preventative measure prior to surgical manipulations, such as organ transplantation.