Rabbit heart can be 'preconditioned' via transfer of coronary effluent

Eric W. Dickson, Mojca Lorbar, William A. Porcaro, Richard A. Fenton, Christopher P. Reinhardt, Anne Gysembergh, Karin Przyklenk

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163 Scopus citations


Brief myocardial ischemia not only evokes a local cardioprotective or 'preconditioning' effect but also can render remote myocardium resistant to sustained ischemia. We propose the following hypotheses: remote protection is initiated by a humoral trigger; brief ischemia-reperfusion will result in release of the humoral trigger (possibly adenosine and/or norepinephrine) into the coronary effluent; and transfer of this effluent to a virgin acceptor heart will elicit cardioprotection. To test these concepts, effluent was collected during normal perfusion from donor-control hearts and during preconditioning ischemia-reperfusion from donor-preconditioned (PC) hearts. After reoxygenation occurred and aliquots for measurement of adenosine and norepinephrine content were harvested, effluent was transfused to acceptor- control and acceptor-PC hearts. All hearts then underwent 40 min of global ischemia and 60 min of reperfusion, and infarct size was delineated by tetrazolium staining. Mean infarct size was smaller in both donor- and acceptor-PC groups (9% of left ventricle) than in donor- and acceptor-control groups (36% and 34%; P < 0.01). Protection in acceptor-PC hearts could not, however, be attributed to adenosine or norepinephrine. Thus preconditioning- induced cardioprotection can be transferred between rabbit hearts by transfusion of coronary effluent. Although adenosine and norepinephrine are apparently not responsible, these results suggest that remote protection is initiated by a humoral mechanism.

Original languageEnglish
Pages (from-to)H2451-H2457
JournalAmerican Journal of Physiology - Heart and Circulatory Physiology
Issue number6 46-6
StatePublished - Dec 1999


  • Adenosine
  • Myocardial infarction
  • Myocardial ischemia
  • Norepinephrine


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