Ischaemic preconditioning of myocardium.
Myocardium has the innate potential to adapt to transient sublethal ischaemia so that it becomes more resistant to a subsequent, more severe, ischaemic insult. The response is called ischaemic preconditioning and protection of the myocardium is manifested by a slowing of adenosine triphosphate decline, limitation of ischaemic necrosis and a reduction in dysrhythmia severity. Protection conferred by preconditioning occurs in two distinct temporal phases. An early phase of protection is observed immediately but wanes within two to three hours (classic preconditioning). This is followed many hours later by a second window of protection (delayed preconditioning). The cellular mechanisms underpinning both forms of protection are currently being intensively investigated. There is evidence that human myocardium can be preconditioned ex vivo and also in situ during elective procedures such as angioplasty and coronary artery bypass grafting. Furthermore, evidence points to the possibility that preconditioning occurs naturally in some ischaemic syndromes, particularly warm-up angina and preinfarction angina. Ultimately, investigation of the mechanisms of preconditioning may contribute to the development of rational therapies for protecting the ischaemic myocardium and, perhaps more importantly, enhance our understanding of the molecular basis of ischaemic heart disease.
Baxter
G F
GF
The Hatter Institute for Cardiovascular Studies, London, UK. g.baxter@ucl.ac.uk
D000222:Adaptation, Physiological; D000241:Adenosine / Q000502:physiology; D015906:Angioplasty, Balloon, Coronary; D000818:Animals; D001026:Coronary Artery Bypass; D006801:Humans; D019157:Ischemic Preconditioning, Myocardial; D009203:Myocardial Infarction / Q000503:physiopathology; D011494:Protein Kinases / Q000502:physiology; D013997:Time Factors
D011494:Protein Kinases; D000241:Adenosine