title: Ischaemic preconditioning protects against ischaemia/reperfusion injury: emerging concepts.
abstract: BACKGROUND
  Ischaemic preconditioning (IP) has emerged as a powerful method of ameliorating ischaemia/reperfusion (I/R) injury to the myocardium. This review investigates whether this phenomenon is universally applicable in modulating I/R injury to other tissues.
  
  
  METHODS
  A Medline search was conducted to identify both animal and human studies that described IP-induced protection from I/R injury in a variety of non-cardiac organ systems. Particular emphasis was placed on elucidation of underlying physiological concepts.
  
  
  CONCLUSIONS
  IP utilises endogenous mechanisms in skeletal muscle, liver, lung, kidney, intestine and brain in animal models to convey varying degrees of protection from I/R injury. To date there are few human studies, but recent reports suggest that human liver, lung and skeletal muscle acquire similar protection after IP. Specifically, preconditioned tissues exhibit reduced energy requirements, altered energy metabolism, better electrolyte homeostasis and genetic re-organisation, giving rise to the concept of 'ischaemia tolerance'. IP also induces 'reperfusion tolerance' with less reactive oxygen species and activated neutrophils released, reduced apoptosis and better microcirculatory perfusion compared to non-preconditioned tissue. Systemic I/R injury is also diminished by preconditioning. IP is ubiquitous but more research is required to fully translate these findings to the clinical arena.
authors.affiliation: Vascular Surgical Unit, Leeds General Infirmary, Great George Street, Leeds, West Yorkshire LS1 3EX, UK. s_pasu@hotmail.com
authors.forename: S
authors.initials: S
authors.lastname: Pasupathy
authors.forename: S
authors.initials: S
authors.lastname: Homer-Vanniasinkam
mesh_terms: D000222:Adaptation, Physiological; D000818:Animals; D017209:Apoptosis; D015687:Cell Hypoxia; D006801:Humans; D019194:Ischemic Preconditioning; D015427:Reperfusion Injury / Q000517:prevention & control*