The classical picture of the polymorphonuclear leukocyte--antimicrobal activities and participation in the inflammatory reaction--appears now to be expanded. It has been recognized that this cell may be highly injurious to other cells, has a propensity to be trapped in the capillary network, and may occlude microvascular pathways. The classical hypothesis that the granulocytes appear in the ischemic or postischemic myocardium as response to the associated inflammatory reaction may have to be revised. Instead, the granulocyte may actually be the key factor causing the inflammation. An array of future studies is needed to clarify the events step by step. Important aspects are the activation and degranulation sequence in the ischemic myocardium, the form and extent of injury caused by the oxygen free radicals and lysosomal enzymes, the source and nature of chemotactic substances, particularly in human forms of myocardial ischemia, and the degree to which granulocytes cause or magnify the injury.