Heat stress proteins and myocardial protection: experimental model or potential clinical tool?

Heat stress proteins (hsp) are induced by a variety of stimuli including el evated temperature, ischaemia, hypoxia, pressure overload and some chemical s. They help to maintain the metabolic and structural integrity of the cell , as a protective response to external stresses. They are known to protect the myocardium from the damaging effects of ischaemia and reperfusion. The heat stress response results in accumulation of heat stress proteins. The b eneficial effects associated with their expression include improved endothe lial and mechanical recovery of the ischaemic heart. In addition, preservat ion of high energy phosphates and reduction in infarct size. Tt has also be en shown that critical amounts of hsp70 are necessary to ensure protection of the myocardium. However, questions remain regarding the biochemical mech anisms underlying this protective effect, Alterations in the cell metabolis m and chaperone function of cells expressing heat shook proteins, are thoug ht to be responsible, Despite the obvious clinical benefits related to the heat stress response i n a clinical setting, the application of this phenomena remains limited. He at, both quantitatively and qualitatively is one of the best inducers of he at stress proteins. However, the effects of heat stress are nonspecific and intracellular damage is a common occurrence. The search for alternative st imuli, particularly within the fields of pharmacotherapy or genetic manipul ation may offer more viable options, if the heat stress response is take it s place as an established strategy for myocardial protection. (C) 1999 Else vier Science Ltd, All rights reserved.