Myocardial ischaemia remains a significant cause of morbidity and mort
ality due both to the initial ischaemic insult and also to subsequent
reperfusion injury. Inflammatory mediators contribute to this phenomen
on by a humoral cascade directly affecting myocytes, as well as by a c
ellular cascade activating the interactions between neutrophils, endot
helial cells and myocytes. Investigation of these cellular interaction
s reveals a complex process of adhesion molecule expression with subse
quent recruitment and activation of neutrophils to the site of ischaem
ia-induced inflammation. Understanding of mechanisms of cellular activ
ation and interaction is advancing rapidly, and its applications are b
eing recognised to have significant clinical potential. Although thera
peutic interventions directed against the ischaemia/reperfusion phenom
enon have traditionally involved modification of the insult, future th
erapeutics may more effectively target adhesion molecule expression or
availability, thus modifying the creation of the injury.