作者: Gerd Heusch
DOI: 10.1002/CPHY.C140075
关键词:
摘要: Timely reperfusion is the only way to salvage ischemic myocardium from impending infarction. However, also adds a further component myocardial injury such that ultimate infarct size result of both ischemia- and reperfusion-induced injury. Modification can attenuate thus reduce size. Ischemic postconditioning maneuver repeated brief interruption by short-lasting coronary occlusions which results in reduced Cardioprotection mediated through delayed reversal acidosis activation complex signal transduction cascade, including triggers as adenosine, bradykinin, opioids, mediators protein kinases and, notably, mitochondrial function effector. Inhibition permeability transition pore appears be final signaling step postconditioning. Several drugs recruit part steps induce cardioprotection, even when drug administered at reperfusion, is, there pharmacological have been translated patients with acute infarction proof-of-concept studies, but mechanistic insight needed optimize conditions algorithms cardioprotection