Targeted deletion of the A3 adenosine receptor confers resistance to myocardial ischemic injury and does not prevent early preconditioning

Yiru Guo, Roberto Bolli, Weike Bao, Wen Jian Wu, Richard G. Black, Sidney S. Murphree, Christopher A. Salvatore, Marlene A. Jacobson, John A. Auchampach

Research output: Contribution to journalArticlepeer-review


We used mice with genetic disruption of the A3 adenosine receptor (AR) gene (A3AR-1-mice) to assess the in vivo role of me A3AR in modulating myocardial ischemia/reperfusion injury and preconditioning (PC). Surprisingly, infarct size induced by 30 rain of coronary artery occlusion and 24 h of reperfusion was 35% smaller in A3AR-/- compared to wild-type mice (A3AR +/+). The reduction in infarct size was not the result of differences in heart rate. body temperature or increased cardiac expression of A1ARs. However, neutrophil infiltration within infarcted regions was less in A3AR-/- mice. Furthermore, ischemic PC induced by either a single episode (one 5 min occlusion) or multiple episodes (six 4 min occlusions) of ischemia produced equivalent reductions in infarct size in A3AR-/- and A3AR+/+ mice. These results indicate that, in the mouse. (i) A3ARs play an injurious role during acute myocardial ischemia/ reperfusion injury, possibly by exacerbating the inflammatory response, and (ii) A3ARs are not necessary for the development of the early phase of ischemic PC.

Original languageEnglish (US)
Pages (from-to)825-830
Number of pages6
JournalJournal of Molecular and Cellular Cardiology
Issue number4
StatePublished - 2001


  • Adenosine receptor
  • Heart
  • Ischemia/reperfusion
  • Knock-out mice
  • Preconditioning

ASJC Scopus subject areas

  • Molecular Biology
  • Cardiology and Cardiovascular Medicine


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