title: Is hyperglycemia bad for the heart during acute ischemia?
abstract: OBJECTIVE
  This study investigates the impact of diabetes on myocardium in the setting of acute ischemia-reperfusion in a porcine model.
  
  
  METHODS
  In normoglycemic (ND group) and alloxan-induced diabetic (DM group) male Yucatan pigs, the left anterior descending coronary artery territory was made ischemic and then reperfused. Hemodynamic values and myocardial function were measured. Monastryl blue and triphenyl tetrazolium chloride staining were used to assess size of the areas at risk and infarction. Glycogen content was assessed using periodic acid-Schiff staining. Cell death and survival signaling pathways were assessed by immunoblotting.
  
  
  RESULTS
  Mean arterial pressure and developed left ventricular pressure were lower in the DM group (P < .05). Whereas global left ventricular function was worse in the DM group (P < .05), regional function in the area at risk was improved on the horizontal axis (P < .05). Mean infarct size was smaller in the DM versus the ND group (19% vs 43%; P < .05), whereas the area at risk was similar in both groups (34% vs 36%; P = .7). Ischemic myocardium in the DM group displayed more prominent staining for glycogen compared with the ND group. In the area at risk, expression of cell survival proteins including phosphorylated endothelial nitric oxide synthase (0.17 ± 0.04 vs 0.04 ± 0.01; P < .05), heat shock protein 27 (0.7 ± 0.2 vs 0.3 ± 0.1; P < .05), nuclear factor-κB (0.14 ± 0.02 vs 0.03 ± 0.01; P < .05), and mammalian target of rapamycin (0.35 ± 0.05 vs 0.15 ± 0.02; P < .05) were higher in DM animals, whereas in nonischemic tissue, expression of these proteins was similar or lower in the DM group.
  
  
  CONCLUSIONS
  Although type I diabetes worsens global left ventricular function, it is protective in the ischemic area, leading to increased expression of cell survival proteins and decreased infarct size.
authors.affiliation: Department of Surgery, Beth Israel Deaconess Medical Center, Harvard Medical School, Boston, Mass, USA.
authors.forename: Louis M
authors.initials: LM
authors.lastname: Chu
authors.forename: Robert M
authors.initials: RM
authors.lastname: Osipov
authors.forename: Michael P
authors.initials: MP
authors.lastname: Robich
authors.forename: Jun
authors.initials: J
authors.lastname: Feng
authors.forename: Shizu
authors.initials: S
authors.lastname: Oyamada
authors.forename: Cesario
authors.initials: C
authors.lastname: Bianchi
authors.forename: Frank W
authors.initials: FW
authors.lastname: Sellke
mesh_terms: D000704:Analysis of Variance; D000818:Animals; D017209:Apoptosis; D015153:Blotting, Western; D003921:Diabetes Mellitus, Experimental / Q000473:pathology*; D006439:Hemodynamics; D008297:Male; D019950:Mitogen-Activated Protein Kinase 1 / Q000378:metabolism; D009203:Myocardial Infarction / Q000473:pathology*; D009206:Myocardium / Q000473:pathology*; D015398:Signal Transduction; D013194:Staining and Labeling; D013552:Swine
chemical_list: D019950:Mitogen-Activated Protein Kinase 1