Rabbit heart can be “preconditioned” via transfer of coronary effluent

Abstract

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.

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“…While the mechanisms responsible for opioid-induced cardioprotection are not clear, it is possible that activation of opioid receptors within the central nervous system may contribute either directly or indirectly to cardioprotection. Recent studies also document cellular protection of the heart by postconditioning (ie, repetitive ischemia-reperfusion episodes after reopening the infarct-related artery) (65) and remote IPC, in which protection appears to be transduced from one organ to another (66,67) via humoral factors (68,69) or activation of the autonomic nervous system (70).…”

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“…This hypothesis was further supported by a study reporting that blood taken from a rabbit which had been subjected to simultaneous IPC of both the heart and kidney, could reduce a subsequent myocardial infarct size by 77% when transfused to an untreated rabbit [165], suggesting the transfer of one or more humoral cardioprotective factors. The same authors went onto demonstrate that coronary effluent from an isolated rabbit heart treated with a standard ischemic preconditioning protocol, could reduce myocardial infarct size by 69% [166] and improve recovery of left ventricular function [167] when used to perfuse an untreated isolated rabbit heart.…”