A NEW LOOK AT MYOCARDIAL PRECONDITIONING

An hypothesis for the sequence of events in myocardial ischaemic preco nditioning is presented. Comparisons are made with Ca-preconditioning and protection in the Ca-paradox. Ischaemic preconditioning is initiat ed by the stimulation of phospholipase C via the mediation of G protei ns and the diacylglycerol generated promotes the translocation of prot ein kinase C from the cytosol to the sarcolemma. Membrane-based protei n kinase C then promotes the phosphorylation of a transmembrane oxido- reductase and thereby inhibits the switching of this enzyme complex an d blocks the cellular damage pathway, so producing the early, classic preconditioning. Protein kinase C also triggers gene transcription and the consequent production of heat shock proteins which provide the se cond window of protection.