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Related Experiment Videos

Adenosine A(3)-receptor stimulation attenuates postischemic dysfunction through K(ATP) channels.

V H Thourani1, M Nakamura, R S Ronson

  • 1Division of Cardiothoracic Surgery, Department of Surgery, Crawford Long Hospital, Atlanta, Georgia 30365-2225, USA.

The American Journal of Physiology
|July 17, 1999
PubMed
Summary
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Selective adenosine A(3)-receptor stimulation protects heart function after ischemia by activating ATP-sensitive potassium (K(ATP)) channels. This A(3) agonist reduces cardiac dysfunction and enzyme release without causing vasodilation.

Area of Science:

  • Cardiology
  • Pharmacology
  • Physiology

Background:

  • Postischemic contractile dysfunction is a significant clinical concern.
  • Adenosine receptors play a role in cardiovascular regulation.
  • ATP-sensitive potassium (K(ATP)) channels are involved in cardioprotection.

Purpose of the Study:

  • To test if selective adenosine A(3)-receptor stimulation reduces postischemic contractile dysfunction via K(ATP) channel activation.
  • To evaluate the cardioprotective effects of the A(3) agonist Cl-IB-MECA.
  • To determine if these effects are mediated by K(ATP) channels.

Main Methods:

  • Isolated, buffer-perfused rat hearts were used.
  • Hearts were pretreated with adenosine A(3) agonist (Cl-IB-MECA), A(1) antagonist (KW-3902), K(ATP) channel blocker (glibenclamide), or combinations thereof.

Related Experiment Videos

  • Global normothermic ischemia was induced, followed by reperfusion.
  • Left ventricular developed pressure (LVDP), peak dP/dt, and creatine kinase (CK) release were measured.

    • Main Results:

    • Cl-IB-MECA significantly attenuated postischemic LVDP reduction and CK release compared to controls.
    • The protective effects of Cl-IB-MECA were reversed by glibenclamide, indicating K(ATP) channel involvement.
    • The A(1) antagonist KW-3902 did not reverse the effects of Cl-IB-MECA.
    • Coronary flow was not increased by Cl-IB-MECA, unlike adenosine.

    Conclusions:

    • Selective adenosine A(3)-receptor stimulation, via Cl-IB-MECA, provides cardioprotection against postischemic injury.
    • This protection appears to be mediated, at least in part, by the activation of K(ATP) channels.
    • Cl-IB-MECA is a potential pretreatment agent that attenuates cardiac dysfunction and CK release without vasodilator side effects.