Preconditioning Against Myocardial Infarction—Its Features and Adenosine-Mediated Mechanism

  • Tetsuji Miura
Part of the Medical Intelligence Unit book series (MIU.LANDES)

Abstract

Myocardial infarction is the leading cause of mortality and morbidity in industrialized countries. Prognosis of the patients is determined primarily by the extent of infarct in the heart (i.e., infarct size).1 Because of this fact, for more than 20 years basic and clinical investigators have devoted much effort to limiting myocardial infarct size. There have been two approaches to this objective: early reperfusion and enhancement of myocardial resistance to ischemia. Several methodologies have been developed over a decade to recanalize the occluded coronary artery and it has been established that reperfusion improves hemodynamics, decreases infarct size, and improves prognosis.2 In contrast, attempts to enhance myocardial resistance against infarction by pharmacological agents3–7 has achieved only limited success in animal experiments. However, in 1986 Murry and co-workers8 found that exposing the myocardium to brief ischemia markedly limits the infarct size due to the subsequent 40 minutes of coronary occlusion in canine hearts. This cardioprotective effect, termed “preconditioning,” was not accompanied by alterations of coronary collateral flow, indicating that myocardial resistance to infarction was directly enhanced. In order to understand this novel form of cardioprotection against infarction, we undertook a series of studies to clarify the features and mechanisms of preconditioning.

Keywords

Propranolol Verapamil Theophylline Nucleoside Inositol 

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© Springer-Verlag Berlin Heidelberg 1996

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  • Tetsuji Miura

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