Delayed preconditioning with adenosine is mediated by opening of ATP-sensitive K+ channels in rabbit heart.

No abstract is available for this paper.

• Publication year

  1999

• Venue

  American Journal of Physiology. Heart and Circulatory Physiology

• Publication date

  1999-07-01

• Fields of study

  Medicine, Chemistry

• Identifiers
  DOI 10.1152/ajpheart.1999.277.1.H128PMID 10409190
• External record

  Open on Semantic Scholar

• Source metadata

  Semantic Scholar, PubMed

• No claims are published for this paper.

• No concepts are published for this paper.

• Delayed ischemic preconditioning is mediated by opening of ATP-sensitive potassium channels in the rabbit heart.

  1999cited by this paper
• Prolonging the delayed phase of myocardial protection: repetitive adenosine A1 receptor activation maintains rabbit myocardium in a preconditioned state.

  1998cited by this paper
• Whole body heat shock fails to protect mouse heart against ischemia/reperfusion injury: role of 72 kDa heat shock protein and antioxidant enzymes.

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• Dissociation of heat shock proteins expression with ischemic tolerance by whole body hyperthermia in rat heart.

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• Pharmacologic preconditioning with monophosphoryl lipid A is abolished by 5-hydroxydecanoate, a specific inhibitor of the K(ATP) channel.

  1998cited by this paper
• Mitochondrial ATP-dependent potassium channels: novel effectors of cardioprotection?

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• ATP-sensitive potassium channel mediates delayed ischemic protection by heat stress in rabbit heart.

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• Cardioprotective effect of diazoxide and its interaction with mitochondrial ATP-sensitive K+ channels. Possible mechanism of cardioprotection.

  1997cited by this paper
• The ischemia-selective KATP channel antagonist, 5-hydroxydecanoate, blocks ischemic preconditioning in the rat heart.

  1997cited by this paper
• Myocardial Ischemic Tolerance Following Heat Stress Is Abolished by ATP-Sensitive Potassium Channel Blockade

  1997cited by this paper
• Delayed preconditioning of cultured adult rat cardiac myocytes: role of 70- and 90-kDa heat stress proteins.

  1997cited by this paper
• KATP channels mediate late preconditioning against infarction produced by monophosphoryl lipid A.

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• KATP channels in rat heart: blockade of ischemic and acetylcholine-mediated preconditioning by glibenclamide.

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• Myocardial protection after monophosphoryl lipid A: studies of delayed anti‐ischaemic properties in rabbit heart

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• Direct preconditioning of cardiac ventricular myocytes via adenosine A1 receptor and KATP channel.

  1996cited by this paper
• Myocardial ischemia/reperfusion protection using monophosphoryl lipid A is abrogated by the ATP-sensitive potassium channel blocker, glibenclamide.

  1996cited by this paper
• Monophosphoryl lipid A induces pharmacologic ‘preconditioning’ in rabbit hearts without concomitant expression of 70-kDa heat shock protein

  1996cited by this paper
• Heat stress improves functional recovery and induces synthesis of 27- and 70-kDa heat shock proteins without preserving sarcoplasmic reticulum function in the ischemic rat heart.

  1996cited by this paper
• Cardioprotection with the KATP Opener Cromakalim Is Not Correlated with Ischemic Myocardial Action Potential Duration

  1995cited by this paper
• Overexpression of the rat inducible 70-kD heat stress protein in a transgenic mouse increases the resistance of the heart to ischemic injury.

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• Effects of the KATP channel opener bimakalim on coronary blood flow, monophasic action potential duration, and infarct size in dogs.

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• The anti-infarct effect of an adenosine A1-selective agonist is diminished after prolonged infusion as is the cardioprotective effect of ischaemic preconditioning in rabbit heart.

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• Heat-shock protein induction in rat hearts. A direct correlation between the amount of heat-shock protein induced and the degree of myocardial protection.

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• Adenosine Receptor Involvement in a Delayed Phase of Myocardial Protection 24 Hours After Ischemic Preconditioning

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• Oxidant stress increases heat shock protein 70 mRNA in isolated perfused rat heart.

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• Pretreatment with the adenosine A1 selective agonist, 2-chloro-N6-cyclopentyladenosine (CCPA), causes a sustained limitation of infarct size in rabbits.

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• The protection of ischaemic preconditioning can be reinstated in the rabbit heart after the initial protection has waned.

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• Cardiac stress protein elevation 24 hours after brief ischemia or heat stress is associated with resistance to myocardial infarction.

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• Delayed effects of sublethal ischemia on the acquisition of tolerance to ischemia.

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• Blockade of ATP-sensitive potassium channels prevents myocardial preconditioning in dogs.

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• Role of Myocardial ATP‐Sensitive Potassium Channels in Mediating Preconditioning in the Dog Heart and Their Possible Interaction With Adenosine A1‐Receptors

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• Protection Against Infarction Afforded by Preconditioning is Mediated by A1 Adenosine Receptors in Rabbit Heart

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• Coupling of ATP-sensitive K+ channels to A1 receptors by G proteins in rat ventricular myocytes.

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• Ischemic preconditioning reduces infarct size in swine myocardium.

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• Cardiac microdialysis to estimate interstitial adenosine and coronary blood flow.

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• Effects of glyburide on ischemia-induced changes in extracellular potassium and local myocardial activation: a potential new approach to the management of ischemia-induced malignant ventricular arrhythmias.

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• Preconditioning with ischemia: a delay of lethal cell injury in ischemic myocardium.

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• The Medical College of Virginia.

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  2007cites this paper
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  2007cites this paper
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