title: Cardiac ischemia and reperfusion in spontaneously diabetic rats with and without application of EGb 761: I. cardiomyocytes.
abstract: Diabetic cardiomyopathy is known to result in increased mortality after ischemic events. Permanently increased oxidative stress with formation of oxygen-free radicals plays a key role in the development of specific heart muscle disease. Associated lesions include structural alterations to cardiomyocytes. Antioxidative treatment in addition to the usual insulin substitution would seem sensible in preventing or delaying long-term diabetic complications and protecting the myocardium against acute ischemic events. We investigated the effects of radical scavenger Ginkgo biloba extract EGb 761 against diabetes-induced damage to cardiomyocytes and additional ischemia/reperfusion injury in spontaneously diabetic BioBreeding/Ottawa Karlsburg (BB/OK) rats, as a model of diabetic myocardium infarction. Morphological and morphometric parameters of heart muscles were analyzed by light and electron-microscopic techniques. We used immunohistochemistry to evaluate parameters of oxidative stress (superoxide dismutase [SOD]) and inducible nitric oxide synthase (iNOS) protein expression. Our results indicated that A) Diabetic myocardium appears more vulnerable to ischemia/reperfusion damage concerning ultrastructure of cardiomyocytes (sarcomeres, vacuoles, mitochondria), expression of antioxidative enzymes (CuZnSOD, MnSOD), and iNOS than normal myocardium; B) Pre-treatment of diabetic myocardium with EGb and additional ischemia/reperfusion leads to a relative improvement in myocardial ultrastructure compared to unprotected myocardium. In summary, EGb appears to be promising as an adjuvant therapeutic drug in diabetics with respect to ischemic myocardium injury. It may contribute to the prevention of late diabetic complications in diabetic cardiomyopathy.
authors.affiliation: Department of Surgery II, University of Leipzig, Germany. rick.schneider@medizin.uni-leipzig.de
authors.forename: Rick
authors.initials: R
authors.lastname: Schneider
authors.forename: Klaus
authors.initials: K
authors.lastname: Welt
authors.forename: Wolfram
authors.initials: W
authors.lastname: Aust
authors.forename: Heinz
authors.initials: H
authors.lastname: Löster
authors.forename: Günther
authors.initials: G
authors.lastname: Fitzl
mesh_terms: D000818:Animals; D002317:Cardiovascular Agents / Q000627:therapeutic use*; D003921:Diabetes Mellitus, Experimental; D004195:Disease Models, Animal; D016166:Free Radical Scavengers / Q000627:therapeutic use; D020441:Ginkgo biloba; D008297:Male; D015428:Myocardial Reperfusion Injury / Q000378:metabolism / Q000473:pathology / Q000517:prevention & control*; D032383:Myocytes, Cardiac / Q000187:drug effects* / Q000473:pathology / Q000648:ultrastructure; D052247:Nitric Oxide Synthase Type II / Q000378:metabolism; D018384:Oxidative Stress; D010936:Plant Extracts / Q000627:therapeutic use*; D051381:Rats; D011913:Rats, Inbred BB; D013482:Superoxide Dismutase; D000096983:Ginkgo Extract
chemical_list: D002317:Cardiovascular Agents; D016166:Free Radical Scavengers; D052247:Nitric Oxide Synthase Type II; D010936:Plant Extracts; D013482:Superoxide Dismutase; C063170:Ginkgo biloba extract; D000096983:Ginkgo Extract; C496318:Nos2 protein, rat