Importance of mechanical factors in ischemic and reperfusion injury

Acute myocardial cell death is associated with complex biochemical and morphological changes which depend upon the type of cell injury sustained by the myocardium. Of the many changes associated with acute ischemic or anoxic myocardial cell death, intracellular calcium overload is a prominent feature of ischemia-reperfusion injury as has been shown in many experimental models. Consequently, early hypotheses and investigative research regarding acute myocardial death centered around calcium overload and determining the events and/or series of events which lead to cellular calcium overload. During our investigations of the mechanism(s) of cell damage associated with cellular injury, evidence appeared that cellular contracture and/or physical stress may be involved with acute cellular death in some experimental systems. Recently there is a growing body of evidence to suggest that cells irreversibly injured by hypoxia or ischemia may become fragile and therefore not able to withstand physical stresses associated with reperfusion or reoxygenation. This suggests that calcium overload may not be the primary cause of cell death. This chapter will evolve a discussion of the role of mechanical factors in the development of irreversible myocardial cellular injury and cell death.