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Preconditioning the myocardium: from cellular physiology to clinical cardiology.
The understanding of the mechanisms associated with preconditioning are unravelled can look forward to the development of new therapeutic agents with novel mechanisms of action that can supplement current treatment options for patients threatened with acute myocardial infarction.
Protection Against Infarction Afforded by Preconditioning is Mediated by A1 Adenosine Receptors in Rabbit Heart
Adenosine released during the preconditioning occlusion stimulates cardiac A 1 receptors, which leaves the heart protected against infarction even after the adenosine has been withdrawn.
Opening of Mitochondrial KATP Channels Triggers the Preconditioned State by Generating Free Radicals
Mito KATP channels are not the end effectors of protection, but rather their opening before ischemia generates free radicals that trigger entrance into a preconditioned state and activation of kinases, indicating that diazoxide triggers protection through free radicals.
Oxygen radicals released during ischemic preconditioning contribute to cardioprotection in the rabbit myocardium.
O oxygen radicals contribute to ischemic preconditioning in the rabbit and appear to do so via activation of PKC, and the fact that MPG could not block protection by PC4 suggests that oxygen radicals act in concert with other triggers of preconditionsing such as adenosine and bradykinin.
Ischemic preconditioning: from adenosine receptor to KATP channel.
Current evidence indicates that mitochondrial adenosine 5'-triphosphate-sensitive K+ channels open, and the latter may be the final mediator of protection for ischemic preconditioning.
Protein Kinase G Transmits the Cardioprotective Signal From Cytosol to Mitochondria
Ischemic and pharmacological preconditioning can be triggered by an intracellular signaling pathway in which Gi-coupled surface receptors activate a cascade including phosphatidylinositol 3-kinase,
Signaling pathways in ischemic preconditioning
The reperfused heart requires the support of the protective signals for only about an hour after which the ischemic injury is repaired and the signals are no longer needed.
Preconditioning protects ischemic rabbit heart by protein kinase C activation.
Activation of protein kinase C with 4 beta-phorbol 12-myristate 13-acetate (PMA) or with 1-oleyl-2-acetyl glycerol (OAG) mimicked preconditioning in buffer-perfused hearts, which blocked protection from ischemic preconditionsing in isolated heart.
The pH Hypothesis of Postconditioning: Staccato Reperfusion Reintroduces Oxygen and Perpetuates Myocardial Acidosis
Postconditioning prevents MPTP formation by maintaining acidosis during the first minutes of reperfusion as reoxygenated myocardium produces reactive oxygen species that activate protective signaling to inhibitMPTP formation after pH normalization.