In　most　previous　studies,　ischaemiareperfusion　(I/R)-induced　vascular　injury　referred　to　injury　in　the　tissue　or　blood　vessel　that　was　directly　subjected　to　I/R.　However,　less　attention　has　been　focused　on　remote　vascular　injury　that　might　be　caused　by　cardiac　I/R.　In　the　present　study,　we　aimed　to　assess　whether　cardiac　I/R　could　affect　vasoconstriction　and　vasodilatation　in　mesenteric　arteries　from　SpragueDawley　rats.　Left　anterior　descending　coronary　arteries　from　adult　male　SpragueDawley　rats　were　occluded　(60　min)　and　then　reperfused　(120　min).　Changes　in　haemodynamic　parameters　indicated　that　this　procedure　caused　evident　cardiac　dysfunction.　In　mesenteric　arteries　isolated　from　the　animals,　cardiac　I/R　significantly　increased　the　maximal　contractions　in　response　to　KCl,　5-hydroxytryptamine,　phenylephrine　and　U46619　and　decreased　the　maximal　relaxation　in　response　to　acetylcholine,　but　not　to　sodium　nitroprusside,　compared　with　sham-operated　animals.　The　nitric　oxide　synthase　inhibitor　l-NAME　abolished　differences　of　contractile　responses　to　phenylephrine　between　sham-operated　and　I/R　rats.　The　antioxidant　N-acetyl-l-cysteine　reversed　the　impairment　of　acetylcholine-stimulated　vasodilatation　induced　by　regional　cardiac　I/R.　However,　l-NAME　caused　a　similar　degree　of　inhibition　of　acetylcholine-stimulated　relaxation　in　mesenteric　arteries　from　sham-operated　and　I/R　rats.　Electron　microscopy　revealed　that　mesenteric　arterial　endothelial　structure　was　degraded　in　the　I/R　group　and　that　N-acetyl-l-cysteine　treatment　prevented　this　structural　damage.　In　conclusion,　regional　cardiac　I/R　caused　by　transient　occlusion　and　reperfusion　of　the　left　anterior　descending　coronary　artery　results　in　peripheral　vascular　endothelial　dysfunction.