| Abstrakt: |
Myocardial ischemia remains the largest single factor contributing to death in the Western hemisphere. It arises in many guises, such as regional ischemia in evolving myocardial infarction and induced whole heart ischemia in cardiac surgery and transplantation. Ischemia initiates a sequence of progressively more severe cellular events that, unless interrupted by early reperfusion, will culminate in cell death and tissue necrosis. Early reperfusion is not always possible, and therefore attempts have been made to develop procedures to slow the rate of progression of ischemic injury so that less irreversible injury occurs and more tissue is available for salvage at the time of reperfusion. Developing and successfully applying such protective interventions requires a detailed knowledge of the complex temporal, spatial, cellular, and molecular characteristics of the ischemic process. Further complications are added by the possibility that reperfusion, although an absolute prerequisite for the survival of ischemic tissue, may not be without hazard. Reperfusion injury may subtract from the obvious benefit of the restoration of coronary flow and, as such, merits consideration as a possible target in the development of myocardial protective strategies. In addition to the conventional pharmacological approach to cardioprotection, there is intense interest in exploiting the ability of the heart to use adaptive processes, such as preconditioning and the expression of stress proteins, to control the ravages of ischemia. Myocardial protection has achieved great success in cardiac surgery through the development of cardioplegic solutions but is yet to make a major impact on the control of injury during evolving infarction. [ABSTRACT FROM AUTHOR] |
