Background: The clinical hallmarks of hibernating myocardium include hypocontractility whilst retaining an inotropic reserve (using dobutamine echocardiography), having normal or increased ¹⁸FDG6P accumulation associated with decreased coronary flow (flow-metabolism mismatch by positron revascularization. In this paper, we investigate an emission tomography, PET) and recovering completely post-isolated rat heart model of hibernation using experimental equivalents of these clinical techniques. Methods and Results: Rat hearts (n=5/group) were perfused with Krebs-Henseleit buffer for 40 minutes at 100% flow, 3 hours at 10% flow and reperfused at 100% flow for 30 minutes (paced at 300bpm throughout). LV developed pressure fell to 30 ± 8 % during 10% flow and recovered to 90 ± 7% after reperfusion. In an additional group, this recovery of function was found to be preserved over 2 hours of reperfusion. Electron microscopic examination of hearts fixed at the end of the hibernation period demonstrated a lack of ischemic injury and an accumulation of glycogen granules, a phenomenon observed clinically. In a further group, hearts were challenged with dobutamine during the low-flow period. Hearts demonstrated an inotropic reserve at the expense of increased lactate leakage, with no appreciable creatine kinase release. PET studies used the same basic protocol in both dual- and globally-perfused hearts (with 250MBq ¹⁸FDG in Krebs, +/- 0.4 mmol/l oleate). PET data showed flow - metabolism "mis-match", whether regional or global, ¹⁸FDG6P accumulation in ischemic tissue was the same as (glucose only) or significantly higher than (glucose + oleate) control tissue (0.023 ± 0.002 vs. 0.011 ± 0.002 normalised cps/g/min p<0.05) despite receiving 10% of the flow. Conclusions: This isolated rat heart model of acute hibernation exhibits many of the same characteristics demonstrated clinically in hibernating myocardium.