title: Glucose metabolism, energetics, and function of rat hearts exposed to ischemic preconditioning and oxygenated cardioplegia.
abstract: We examined changes induced during ischemia-reperfusion on myocardial metabolism and function by oxygenated warm cardioplegia (CP) and ischemic preconditioning (IP). The postischemic hemodynamic recovery was comparable and significantly better in IP and CP groups, than in untreated hearts (e.g., LVDP recovery was threefold that of the control). The IP hearts reached a pH plateau earlier during ischemia and at considerably higher pH value (pH approximately 6) compared to the other groups (pH approximately 5.5). Postischemic phosphocreatine (PCr) and ATP recoveries were comparable and better in protected groups (approximately 72% and approximately 30% vs approximately 25% and approximately 10% in control, p < 0.0001). Preischemic glycogen was significantly reduced in IP to 49% and increased in CP hearts to 127%. However, the lactate levels at the end of ischemia were similar in all the groups, indicating glucose utilization from extracellular space during ischemia in IP hearts. Thus, similar hemodynamic protection by CP and IP is observed despite increased energy depletion during ischemia in IP. IP and CP protection is expressed through better energetic status and by higher recovery of the TCA cycle activity or enhanced mitochondria-cytosol transport of alpha-ketoglutarate on reperfusion in addition to metabolic changes during ischemia. Glycogen store recovered significantly better in IP than in CP and Control. These results exhibit similar and improved postischemic hemodynamic protection by CP and IP. Increased recovery of postischemic glycogen pool is a protective feature of IP, whereas slightly higher lactate metabolism during reperfusion is a protection component of CP.
authors.affiliation: Human Biology Research Center, Hadassah University Hospital, Jerusalem, Israel.
authors.forename: Abira
authors.initials: A
authors.lastname: Olivson
authors.forename: Elisha
authors.initials: E
authors.lastname: Berman
authors.forename: Ester
authors.initials: E
authors.lastname: Houminer
authors.forename: Joseph B
authors.initials: JB
authors.lastname: Borman
authors.forename: Gideon
authors.initials: G
authors.lastname: Merin
authors.forename: Matthias
authors.initials: M
authors.lastname: Karck
authors.forename: Axel
authors.initials: A
authors.lastname: Haverich
authors.forename: Roland
authors.initials: R
authors.lastname: Chisin
authors.forename: Herzl
authors.initials: H
authors.lastname: Schwalb
mesh_terms: D000255:Adenosine Triphosphate / Q000378:metabolism; D000818:Animals; D050260:Carbohydrate Metabolism; D004734:Energy Metabolism / Q000502:physiology*; D005947:Glucose / Q000378:metabolism*; D006321:Heart / Q000502:physiology*; D006324:Heart Arrest, Induced; D006439:Hemodynamics / Q000502:physiology; D006863:Hydrogen-Ion Concentration; D019157:Ischemic Preconditioning, Myocardial; D008297:Male; D023421:Models, Animal; D008955:Models, Cardiovascular; D017202:Myocardial Ischemia / Q000378:metabolism / Q000503:physiopathology* / Q000628:therapy*; D015425:Myocardial Reperfusion; D010725:Phosphocreatine / Q000378:metabolism; D011184:Postoperative Period; D051381:Rats; D020127:Recovery of Function / Q000502:physiology*; D013997:Time Factors; D016896:Treatment Outcome; D014233:Tricarboxylic Acids / Q000378:metabolism
chemical_list: D014233:Tricarboxylic Acids; D010725:Phosphocreatine; D000255:Adenosine Triphosphate; D005947:Glucose