title: Improved protection of the hypertrophied left ventricle by histidine-containing cardioplegia.
abstract: BACKGROUND
  Myocardial hypertrophy has been shown to lead to increased susceptibility to ischemia with accelerated loss of high-energy nucleotides, greater accumulation of H+ and lactate, and earlier onset of contracture.
  
  
  RESULTS
  To determine whether promoting anaerobic glycolysis during ischemia by buffering H+ results in improved preservation of the hypertrophied heart, we studied the effect of a histidine-containing solution (HBS) on recovery of contractile function and energetic state. Hypertrophied rabbit hearts (aortic banding at 10 days) were subjected to 40 minutes of 37 degrees C ischemia and reperfusion in an isolated Langendorff model. This group was compared with groups receiving St Thomas solution and high-potassium Krebs buffer solution (KCl). Although both phosphocreatine (PCr) and ATP were lower in hypertrophied hearts by end-ischemia compared with nonhypertrophied age-matched controls, there was significantly higher PCr, ATP, and intracellular pH in the HBS group compared with the St Thomas and KCl groups. Recovery of left ventricular developed pressure was best in the HBS group (91% of preischemic values) as was end-diastolic pressure after 30 minutes of reperfusion. Lactate production was also significantly greater in the HBS group, suggesting augmentation of anaerobic glycolysis.
  
  
  CONCLUSIONS
  We concluded that administration of histidine-containing cardioplegia promotes anaerobic glycolysis and improves recovery of high-energy phosphates and contractile function in hypertrophied myocardium.
authors.affiliation: Department of Cardiac Surgery, Children's Hospital, Harvard Medical School, Boston, Mass 02115, USA.
authors.forename: K
authors.initials: K
authors.lastname: Takeuchi
authors.forename: P
authors.initials: P
authors.lastname: Buenaventura
authors.forename: H
authors.initials: H
authors.lastname: Cao-Danh
authors.forename: P
authors.initials: P
authors.lastname: Glynn
authors.forename: E
authors.initials: E
authors.lastname: Simplaceanu
authors.forename: F X
authors.initials: FX
authors.lastname: McGowan
authors.forename: P J
authors.initials: PJ
authors.lastname: del Nido
mesh_terms: D000818:Animals; D006332:Cardiomegaly / Q000503:physiopathology*; D004734:Energy Metabolism; D006321:Heart / Q000187:drug effects / Q000503:physiopathology; D006324:Heart Arrest, Induced; D006639:Histidine / Q000494:pharmacology*; D006863:Hydrogen-Ion Concentration; D017379:Hypertrophy, Left Ventricular / Q000503:physiopathology; D066298:In Vitro Techniques; D007425:Intracellular Membranes / Q000378:metabolism; D007773:Lactates / Q000096:biosynthesis; D019344:Lactic Acid; D009206:Myocardium / Q000378:metabolism; D010710:Phosphates / Q000378:metabolism; D011817:Rabbits; D016277:Ventricular Function, Left / Q000187:drug effects*
chemical_list: D007773:Lactates; D010710:Phosphates; D019344:Lactic Acid; D006639:Histidine