title: Mild type 2 diabetes mellitus improves remote endothelial dysfunction after acute myocardial infarction.
abstract: OBJECTIVE
  Myocardial infarction (MI) is a common cause of mortality in patients with diabetes mellitus (DM) and vascular dysfunction is a major component of diabetic cardiomyopathy. We investigated the systemic influence of acute MI on the diabetes-induced pathogenic changes in the rat aorta.
  
  
  METHODS
  Nondiabetic Wistar (W) and type-2 diabetic Goto-Kakizaki (GK) rats underwent 45min of left anterior descending coronary artery occlusion followed by 24h of reperfusion. Isometric force was measured using organ bath.
  
  
  RESULTS
  Plasma glucose-levels were significantly higher in diabetic rats (GK+sham: 13±2mM; GK+MI: 19±2mM) compared to nondiabetic rats (W+sham: 8±0mM; W+MI: 8±1mM). Acetylcholine-induced relaxation was significantly weaker in rings from W+MI and GK+MI rats compared to corresponding sham-operated animals. Myocardial reperfusion injury was smaller in GK+MI than W+MI rats, and the concentration-response curves to acetylcholine were significantly enhanced in rings from GK+MI than W+MI rats. Nevertheless, the relaxation response to acetylcholine was similar in W+sham and GK+sham. Densitometric analysis of bands for endothelial nitric oxide synthase showed a significant decrease in W+MI rats compared to W+sham and GK+sham animals. Aortas from both GK+sham and GK+MI rats showed impaired contractile responses to phenylephrine in comparison with the nondiabetics.
  
  
  CONCLUSIONS
  For the first time we showed that short-term and mild type-2 DM improved remote endothelial dysfunction after reperfused acute MI.
authors.affiliation: Department of Cardiac Surgery, University of Heidelberg, Heidelberg, Germany. Electronic address: korkmaz@uni-heidelberg.de.
authors.forename: Sevil
authors.initials: S
authors.lastname: Korkmaz-Icöz
authors.affiliation: Department of Cardiac Surgery, University of Heidelberg, Heidelberg, Germany. Electronic address: adrianvater@gmx.de.
authors.forename: Adrian
authors.initials: A
authors.lastname: Vater
authors.affiliation: Department of Cardiac Surgery, University of Heidelberg, Heidelberg, Germany. Electronic address: lishiliangcom@hotmail.com.
authors.forename: Shiliang
authors.initials: S
authors.lastname: Li
authors.affiliation: Department of Cardiac Surgery, University of Heidelberg, Heidelberg, Germany. Electronic address: alice-lehner@web.de.
authors.forename: Alice
authors.initials: A
authors.lastname: Lehner
authors.affiliation: Heart Center, Semmelweis University, Budapest, Hungary. Electronic address: radovitstamas@yahoo.com.
authors.forename: Tamás
authors.initials: T
authors.lastname: Radovits
authors.affiliation: Department of Cardiac Surgery, University of Heidelberg, Heidelberg, Germany; Heart Center, Semmelweis University, Budapest, Hungary. Electronic address: phegedues@gmail.com.
authors.forename: Péter
authors.initials: P
authors.lastname: Hegedűs
authors.affiliation: Department of Cardiac Surgery, University of Heidelberg, Heidelberg, Germany; Heart Center, Semmelweis University, Budapest, Hungary. Electronic address: ruppertmis@gmail.com.
authors.forename: Mihály
authors.initials: M
authors.lastname: Ruppert
authors.affiliation: Department of Cardiac Surgery, University of Heidelberg, Heidelberg, Germany. Electronic address: paigebrlecic@yahoo.com.
authors.forename: Paige
authors.initials: P
authors.lastname: Brlecic
authors.affiliation: Department of Internal Medicine I, University of Heidelberg, Heidelberg, Germany. Electronic address: Markus.Zorn@med.uni-heidelberg.de.
authors.forename: Markus
authors.initials: M
authors.lastname: Zorn
authors.affiliation: Department of Cardiac Surgery, University of Heidelberg, Heidelberg, Germany. Electronic address: Matthias.karck@med.uni-heidelberg.de.
authors.forename: Matthias
authors.initials: M
authors.lastname: Karck
authors.affiliation: Department of Cardiac Surgery, University of Heidelberg, Heidelberg, Germany. Electronic address: gabor.szabo@med.uni-heidelberg.de.
authors.forename: Gábor
authors.initials: G
authors.lastname: Szabó
mesh_terms: D000818:Animals; D001011:Aorta; D001786:Blood Glucose / Q000032:analysis; D003924:Diabetes Mellitus, Type 2 / Q000150:complications* / Q000378:metabolism / Q000473:pathology / Q000503:physiopathology; D003925:Diabetic Angiopathies / Q000150:complications* / Q000503:physiopathology; D058065:Diabetic Cardiomyopathies / Q000150:complications* / Q000503:physiopathology; D060467:Disease Resistance; D004351:Drug Resistance; D004730:Endothelium, Vascular / Q000187:drug effects / Q000378:metabolism / Q000473:pathology / Q000503:physiopathology*; D008297:Male; D009203:Myocardial Infarction / Q000150:complications* / Q000503:physiopathology; D015428:Myocardial Reperfusion Injury / Q000209:etiology / Q000517:prevention & control*; D052250:Nitric Oxide Synthase Type III / Q000378:metabolism*; D010766:Phosphorylation; D011499:Protein Processing, Post-Translational; D051381:Rats; D011919:Rats, Inbred Strains; D017208:Rats, Wistar; D014661:Vasoconstriction / Q000187:drug effects; D014662:Vasoconstrictor Agents / Q000494:pharmacology; D014664:Vasodilation / Q000187:drug effects; D014665:Vasodilator Agents / Q000494:pharmacology
chemical_list: D001786:Blood Glucose; D014662:Vasoconstrictor Agents; D014665:Vasodilator Agents; D052250:Nitric Oxide Synthase Type III; C496316:Nos3 protein, rat
keywords: Acute Myocardial Dysfunction; Aorta; Contractile Response; Endothelial Dysfunction; Type 2 Diabetes mellitus