title: [Preconditioning--endogenous defence mechanisms of the heart during ischemia].
abstract: BACKGROUND
  The term "preconditioning" refers to the paradoxical phenomenon that pretreatment with a potential noxious stress-stimulus can increase cellular tolerance to subsequent noxious stress-stimuli. This was first described in an experimental model in dog hearts in which short-lasting periods of myocardial ischaemia resulted in reduced infarction during a subsequent long-lasting ischaemic period. Similar observations are made in other organs and species. Preconditioning is also used to describe pretreatment with other physical stress-stimuli or pharmacological agents that can increase resistance against cellular damage. This phenomenon probably represents a general adaptive response to cellular stress.
  
  
  METHODS
  This review focuses on preconditioning in the heart and the possible endogenous mechanisms involved. The potential clinical role of preconditioning is also discussed.
  
  
  RESULTS
  It is shown that preconditioning can reduce myocardial infarction in patients. However, protection against reduced contractility without infarction ("stunning") and arrhythmia is more uncertain. Several mechanisms might be involved; these are not fully clarified.
  
  
  CONCLUSIONS
  Preconditioning is of great interest because its effect is vigorous and reproducible, with a potential for use in patients with coronary heart disease. Preconditioning also illustrates how activation of endogenous defence mechanisms can increase cellular tolerance to ischaemia or other stress stimuli.
authors.affiliation: Institutt for eksperimentell medisinsk forskning, Ullevål Sykehus 0407 Oslo. hilchen.sommerschild@ioks.uio.no
authors.forename: H T
authors.initials: HT
authors.lastname: Sommerschild
mesh_terms: D000222:Adaptation, Physiological; D000818:Animals; D016923:Cell Death; D004285:Dogs; D006321:Heart / Q000502:physiology*; D006801:Humans; D019157:Ischemic Preconditioning, Myocardial; D008955:Models, Cardiovascular; D017202:Myocardial Ischemia / Q000378:metabolism / Q000473:pathology / Q000503:physiopathology*; D017682:Myocardial Stunning; D009206:Myocardium / Q000378:metabolism / Q000473:pathology*; D013312:Stress, Physiological