During hibernation, animals enter torpor, a reversible physiological state typically characterised by reductions in core temperature, heart rate and oxygen consumption. Species that enter this hypothermic and hypometabolic state are highly tolerant of ischaemia-reperfusion injury. Consequently, there is a growing interest in utilizing aspects of torpor for clinical applications, such as protection from ischaemia-reperfusion injury during stroke or myocardial infarction. It is currently unknown, however, if a torpor-like state is protective in animals that do not naturally enter torpor. Using viral-vector mediated chemogenetics in the medial preoptic area of the hypothalamus, we induced synthetic torpor in the rat, a species that does not naturally enter torpor. We demonstrate this state is cardioprotective in an ex-vivo ischaemia-reperfusion injury model. Synthetic torpor induced cardioprotection of the normothermic, isolated heart is not dependent on hypothermia during synthetic torpor. These findings provide important insights into synthetic torpor states in novel species, and demonstrate feasibility for future clinical translation in humans.