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Low concentrations of adenosine receptor blocker decrease protection by hypoxic preconditioning in ischemic rat

M Tani1, Y Suganuma, M Takayama

  • 1Department of Geriatrics, Keio University School of Medicine, 35 Shinanomachi, Shinjuku-Ku, Tokyo 160, Japan.

Journal of Molecular and Cellular Cardiology
|May 9, 1998
PubMed
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Hypoxic preconditioning (HP) protects rat hearts by activating adenosine receptors, improving cardiac function but not fully preventing cellular damage. This suggests a partial role for adenosine in HP-mediated myocardial protection.

Area of Science:

  • Cardiology
  • Physiology
  • Biochemistry

Background:

  • Adenosine's role in ischemic and hypoxic preconditioning is established in many species but debated in rats.
  • Inconsistent experimental designs contribute to conflicting data regarding adenosine's function in rat myocardial protection.

Purpose of the Study:

  • To investigate the specific role of adenosine in the protective mechanisms of hypoxic preconditioning (HP) against myocardial ischemia in rats.

Main Methods:

  • Isolated Sprague-Dawley rat hearts underwent hypoxic perfusion followed by global ischemia and reperfusion.
  • Adenosine receptor antagonist 8-(p-sulfophenyl)-theophylline (8SPT) was used at low concentrations (0.5 or 1.0 µmol/L) to assess its impact.
  • Evaluated effects on left-ventricular function, energy metabolites, and cardiac enzyme release (creatine kinase, lactate dehydrogenase).

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Main Results:

  • Hypoxic preconditioning (HP) enhanced recovery of left-ventricular function and creatine phosphate levels.
  • HP reduced the release of creatine kinase and lactate dehydrogenase during reperfusion.
  • The adenosine receptor antagonist 8SPT (1.0 µmol/L) partially reversed the functional improvement from HP but did not fully prevent the reduction in enzyme release.

Conclusions:

  • Adenosine receptor(s) mediate the protective effects of HP on myocardial contractile function in rats.
  • Adenosine may not be the primary mediator for reducing cellular damage caused by ischemia/reperfusion under HP.
  • Low concentrations of adenosine receptor antagonists can inhibit HP's beneficial effects on cardiac function.