title: Altered susceptibility to ischemia-reperfusion injury in isolated-perfused hearts of short-term diabetic rats associated with changes in non-enzymatic antioxidants.
abstract: The effects of short-term (2-week) diabetes on myocardial ischemia-reperfusion (I-R) injury and associated changes in myocardial non-enzymatic antioxidant level were examined. Isolated-perfused hearts prepared from control and diabetic rats were subjected to increasing periods of ischemia and reperfusion, and myocardial I-R injury was assessed by measuring the extent of lactate dehydrogenase (LDH) leakage and contractile force recovery. While a brief period (20 min) of post-ischemic reperfusion caused a smaller extent of LDH leakage, the prolonged period (40 min) of reperfusion produced a greater degree of I-R injury in diabetic hearts, as indicated by the impaired recovery of contractile force. The apparent protection against I-R injury in diabetic hearts during the early phase of post-ischemic reperfusion was associated with increases in myocardial reduced glutathione/ascorbic acid and a-tocopherol levels, with the effect on a-tocopherol being most prominent. Insulin treatment could reverse the diabetes-associated changes in susceptibility to myocardial I-R injury and antioxidant response. The ensemble of results indicates that the myocardium isolated from short-term diabetic rat can produce a beneficial antioxidant response to I-R challenge, which may, in turn, be attributable to the decreased susceptibility to I-R injury observable during the early phase of reperfusion.
authors.affiliation: Department of Biochemistry, The Hong Kong University of Science & Technology, Kowloon, China. bcrko@ust.hk
authors.forename: K M
authors.initials: KM
authors.lastname: Ko
authors.forename: D H
authors.initials: DH
authors.lastname: Mak
authors.forename: M K
authors.initials: MK
authors.lastname: Poon
authors.forename: H Y
authors.initials: HY
authors.lastname: Yiu
mesh_terms: D000818:Animals; D000975:Antioxidants / Q000378:metabolism*; D001205:Ascorbic Acid / Q000378:metabolism*; D003921:Diabetes Mellitus, Experimental / Q000378:metabolism* / Q000473:pathology / Q000517:prevention & control; D004198:Disease Susceptibility; D005260:Female; D005978:Glutathione / Q000378:metabolism*; D007004:Hypoglycemic Agents / Q000627:therapeutic use; D066298:In Vitro Techniques; D007328:Insulin / Q000627:therapeutic use; D007770:L-Lactate Dehydrogenase / Q000378:metabolism; D015428:Myocardial Reperfusion Injury / Q000209:etiology* / Q000378:metabolism* / Q000473:pathology / Q000517:prevention & control; D051381:Rats; D017207:Rats, Sprague-Dawley; D024502:alpha-Tocopherol / Q000378:metabolism*
chemical_list: D000975:Antioxidants; D007004:Hypoglycemic Agents; D007328:Insulin; D007770:L-Lactate Dehydrogenase; D005978:Glutathione; D024502:alpha-Tocopherol; D001205:Ascorbic Acid