Rabbit heart can be "preconditioned" via transfer of coronary effluent
Authors
Dickson, Eric W.Lorbar, Mojca
Porcaro, William A.
Fenton, Richard A.
Reinhardt, Christopher P.
Gysembergh, Anne
Przyklenk, Karin
UMass Chan Affiliations
Department of Medicine, Division of CardiologyDepartment of Physiology
Department of Emergency Medicine
Document Type
Journal ArticlePublication Date
1999-12-22Keywords
AdenosineAnimals
*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
Metadata
Show full item recordAbstract
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.Source
Am J Physiol. 1999 Dec;277(6 Pt 2):H2451-7.
DOI
10.1152/ajpheart.1999.277.6.H2451Permanent Link to this Item
http://hdl.handle.net/20.500.14038/38168PubMed ID
10600868Related Resources
ae974a485f413a2113503eed53cd6c53
10.1152/ajpheart.1999.277.6.H2451