ABSTRACT
Th e role of hypoxia reperfusion (HR) injury has been well recognized in the pathogenesis of many kinds of organ dysfunction. Despite the complexity of the mechanism of HR injury, the investigations in last couple of decades have made our understanding more clear about these phenomena. Th e pathogenesis of HR represents a complex interaction between biochemical, cellular, vascular endothelial and tissue-specifi c factors, infl ammation being a common feature. In recent years there has been a specifi c focus on describing the mechanism of HR injury. With advances in technology and a better understanding of organization of cellular structures, it is now possible to describe the details of this convoluted phenomenon, to which is attributed the pathogenesis of many kinds of organ dysfunction. Th is chapter focuses on the cascade of events that occur during HR injury and the factors responsible in the expression and upregulation of adhesion molecules on neutrophil, platelet and vascular cells and their mechanism of tissue injury. Ischaemia itself can cause direct cell death, in which case damage may lead to activation of many degenerative systems in a rapid and uncontrolled fashion. Th is form of cell death is called ischaemic or necrotic cell death. It is essential to restore the blood supply of an ishcaemic organ, but reperfusion itself can augment tissue injury. Temporary ischaemic damage causes cells to undergo reperfusion injury when blood fl ow is re-established. Th e tissue insult caused by this injury is not restricted locally but also causes damage to distant organs. Th us, HR injury may extend beyond the ischaemic area at risk to include injury of a remote, nonischaemic organ. Of much clinical and scientifi c interest is the minimizing of additional loss of tissue that occurs during reperfusion following ischaemia.
