title: [Molecular mechanisms for protecting the heart].
abstract: Long lasting myocardial ischemia causes death of myocytes despite the restoration of coronary blood flow. Short period of ischemia and reperfusion transiently injures myocytes and is followed by the prolonged but reversible contractile dysfunction called myocardial stunning. Additionally, after a short time ischemia the postischemic myocardium shows enhanced tolerance towards subsequent, long time ischemia, so called ischemic preconditioning. The mechanisms responsible for both phenomena are not completely understood. Myocardial stunning is probably caused by injury to the heart at the molecular level (for example the transient inactivation or damage of proteins of the sarcoplasmic reticulum or the contractile machinery). Since contractility of stunned myocardium recovers, this injury is reversible. The presence of anti-oxidant enzymes system in the heart as well as endogenous protective substances like adenosine or bradykinin and synthesis of stress proteins like hsp 70, hsp 27 or ubiquitin might represent the molecular defense mechanisms against ischemia/reperfusion injury.
authors.affiliation: Katedra Anestezjologii i Intensywnej Terapii Collegium Medicum UJ w Krakowie.
authors.forename: J
authors.initials: J
authors.lastname: Andres
mesh_terms: D000241:Adenosine / Q000502:physiology; D000818:Animals; D000975:Antioxidants / Q000378:metabolism; D001920:Bradykinin / Q000502:physiology; D006360:Heat-Shock Proteins / Q000502:physiology; D006801:Humans; D017202:Myocardial Ischemia / Q000503:physiopathology*; D015428:Myocardial Reperfusion Injury / Q000503:physiopathology*; D017682:Myocardial Stunning / Q000503:physiopathology*
chemical_list: D000975:Antioxidants; D006360:Heat-Shock Proteins; D000241:Adenosine; D001920:Bradykinin