It　has　been　convincingly　demonstrated　that　remote　ischemic　preconditioning　(RIPC)　can　make　the　myocardium　resistant　to　the　subsequent　ischemia　reperfusion　injury　(IRI),　which　causes　severe　damages　by　mainly　generating　cell　death.　However,　the　cardioprotective　effects　of　the　hepatic　RIPC,　which　is　the　largest　metabolic　organ　against　I/R,　have　not　been　fully　studied.　The　aim　of　our　research　is　whether　remote　liver　RIPC　may　provide　cardioprotective　effects　against　the　I/R-induced　injury.　Here,　we　generated　an　I/R　mice　model　in　four　groups　to　analyze　the　effect.　The　control　group　is　the　isolated　hearts　with　140-min　perfusion.　I/R　group　added　ischemia　in　30　min　following　90-min　reperfusion.　The　third　group　(sham)　was　subjected　to　the　same　procedure　as　the　latter　group.　The　animals　in　the　fourth　group　selected　as　the　treatment　group,　underwent　a　hepatic　RIPC　by　three　cycles　of　5-min　occlusion　of　the　portal　triad　and　then　followed　by　induction　of　I/R　in　the　isolated　heart.　The　level　of　myocardial　infarction　and　the　preventive　effects　of　RIPC　were　assessed　by　pathological　characteristics,　namely,　infarct,　enzyme　releases,　pressure,　and　cardiac　mechanical　activity.　Subjected　to　I/R,　the　hepatic　RIPC　minimized　the　infarct　size　(17.7　+/-　4.96　vs.　50.06　+/-　5,　p　＜　0.001)　and　improved　the　left　ventricular-developed　pressure　(from　47.42　+/-　6.27　to　91.62　+/-　5.22　mmHg)　and　the　mechanical　activity.　Release　of　phosphocreatine　kinase-myocardial　band　(73.86　+/-　1.95　vs.　25.93　+/-　0.66　IUL-1)　and　lactate　dehydrogenase　(299.01　+/-　10.7　vs.　152.3　+/-　16.7　IUL-1)　was　also　decreased　in　the　RIPC-treated　group.　These　results　demonstrate　the　cardioprotective　effects　of　the　hepatic　remote　preconditioning　against　the　injury　caused　by　I/R　in　the　isolated　perfused　hearts.