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

UMMS Affiliation

Department of Emergency Medicine; Department of Physiology; Department of Medicine, Division of Cardiology

Publication Date


Document Type



Adenosine; Animals; *Blood Transfusion; Coronary Circulation; Coronary Vessels; Ischemic Preconditioning; Models, Cardiovascular; Myocardial Infarction; Myocardial Ischemia; Myocardial Reperfusion; Norepinephrine; Perfusion; Rabbits; Time Factors; Ventricular Function, Left


Life Sciences | Medicine and Health Sciences


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.

DOI of Published Version



Am J Physiol. 1999 Dec;277(6 Pt 2):H2451-7.

Journal/Book/Conference Title

The American journal of physiology

Related Resources

Link to article in PubMed

PubMed ID