An adenosine A1 receptor agonist, R(-)-N-(2-phenylisopropyl)-adenosine (PIA), but not adenosine itself, acts as a therapeutic preconditioning-mimetic agent in rabbits

Cardiovasc Res. 1993 Dec;27(12):2140-5. doi: 10.1093/cvr/27.12.2140.

Abstract

Objective: A preconditioning mimetic agent could be useful therapy for cardiac ischaemic events; stimulation of adenosine receptors has been proposed as a preconditioning mediator. The ability of adenosine-receptor activation to mimic ischaemic preconditioning was tested in an in vivo rabbit model.

Methods: Adenosine (15 mg, a maximally tolerated dose, n = 10) was infused over six minutes via a coronary artery and compared with saline (n = 12) in anaesthetised rabbits. Five minutes after infusion, a coronary artery was occluded for 40 minutes followed by three hours of reperfusion. In a second study, preischaemic intravenous treatment with adenosine (25 mg.kg-1, n = 9), or an A1-adenosine agonist, R(-)-N-(2-phenylisopropyl)-adenosine (PIA, 900 micrograms.kg-1, n = 12), were compared with saline (n = 12), when given before 40 minutes of coronary artery ligation and three hours of reperfusion in anaesthetised rabbits.

Results: Intracoronary adenosine reduced mean arterial pressure during infusion (48(3) v 80(4) mm Hg, control, p < 0.001); however, infusion regional myocardial blood flow was significantly higher in adenosine treated hearts (5.00(0.90) v 2.30(0.26) ml.min-1 x g-1, p < 0.02) in the region later to become ischaemic. During occlusion ischaemic blood flow was similar in both groups as was the size of the ischaemic risk region, expressed as a % of the left ventricle (42(3)% adenosine and 37(3)% control, NS). Intracoronary adenosine treatment failed to reduce infarct size (52(5)% of the risk zone v 57(7)% in controls, NS). In the second protocol, heart rate immediately after treatment was reduced by both intravenous denosine (26%) and PIA (22%) v control, indicating atrial A1 receptor activation. Treatment with PIA resulted in a significant reduction in ultimate infarct size compared with saline (38(5)% of risk region v 57(5)%, p < 0.05). Adenosine, however, failed to reduce infarct size (50(8)%, NS v saline). There were no differences between area at risk or myocardial blood flow among groups.

Conclusion: The adenosine agonist PIA but not adenosine itself might be a useful adjunctive therapy.

Publication types

  • Comparative Study

MeSH terms

  • Adenosine / pharmacology
  • Animals
  • Blood Pressure / drug effects
  • Coronary Circulation / drug effects
  • Disease Models, Animal
  • Dose-Response Relationship, Drug
  • Heart Rate / drug effects
  • Male
  • Myocardial Infarction / pathology
  • Myocardial Infarction / prevention & control*
  • Myocardial Ischemia / metabolism*
  • Myocardial Ischemia / pathology
  • Myocardium / pathology
  • Phenylisopropyladenosine / pharmacology*
  • Rabbits
  • Receptors, Purinergic P1*

Substances

  • Receptors, Purinergic P1
  • Phenylisopropyladenosine
  • Adenosine