title: Recovery after cardioplegia in the hypertrophic rat heart.
abstract: BACKGROUND
  Enhanced recovery after cardioplegic arrest has been observed in rat hearts with hypertrophy induced by hemodynamic overload. We hypothesize that this is related to altered characteristics of hypertrophied myocardium-reflected by increased V(3) isomyosin and glycolytic potential-other than increased left ventricular mass.
  
  
  METHODS
  Isolated hearts from age-matched nonoperated and sham-operated control rats and from aortic-banded, hyperthyroid, and hypothyroid rats-groups in which hypertrophy and V(3) as a percentage of left ventricular myosin vary independently-underwent 2 h of multidose cardioplegic arrest at 8 degrees C followed by reperfusion at 37 degrees C. Left ventricular V(3) isomyosin was evaluated after separation by gel electrophoresis.
  
  
  RESULTS
  Moderate left ventricular hypertrophy was produced by aortic banding or hyperthyroidism and atrophy by hypothyroidism. V(3) isomyosin was increased in banded (28%) and hypothyroid (75%) rats compared to control (12%) and hyperthyroid rats (7%). Myocardial glycogen content closely paralleled %V(3). At 30 min of working reperfusion, functional recovery (assessed as percentage prearrest cardiac output) was 66 +/- 4 and 68 +/- 5% in control and hyperthyroid hearts and 81 +/- 2 and 80 +/- 5% in hearts from banded and hypothyroid rats (each P < 0.05 vs controls), respectively. At 30 min, hearts from banded and hypothyroid rats were also more efficient (as indexed by cardiac output at constant mean aortic pressure/myocardial oxygen consumption) than control and hyperthyroid hearts.
  
  
  CONCLUSIONS
  The data suggest that recovery is related not to increased mass but to other changes in overload hypertrophy. Increased percentage V(3) isomyosin and glycogen reflect these changes and may themselves contribute to improved functional recovery after cardioplegic arrest, as may increased postischemic efficiency.
authors.affiliation: Department of Surgery, Massachusetts General Hospital, Boston, Massachusetts 02114, USA.
authors.forename: J A
authors.initials: JA
authors.lastname: Lahorra
authors.forename: D F
authors.initials: DF
authors.lastname: Torchiana
authors.forename: C
authors.initials: C
authors.lastname: Hahn
authors.forename: C A
authors.initials: CA
authors.lastname: Bashour
authors.forename: A G
authors.initials: AG
authors.lastname: Denenberg
authors.forename: J S
authors.initials: JS
authors.lastname: Titus
authors.forename: W M
authors.initials: WM
authors.lastname: Daggett
authors.forename: G A
authors.initials: GA
authors.lastname: Geffin
mesh_terms: D000818:Animals; D006324:Heart Arrest, Induced; D006439:Hemodynamics; D017379:Hypertrophy, Left Ventricular / Q000503:physiopathology*; D007037:Hypothyroidism / Q000503:physiopathology; D008297:Male; D009206:Myocardium / Q000378:metabolism; D010101:Oxygen Consumption; D010477:Perfusion; D051381:Rats; D017207:Rats, Sprague-Dawley