title: Superior recovery of hypertrophied rat myocardium after cardioplegic arrest.
abstract: BACKGROUND
  Although cardioplegic protection of the hypertrophied heart remains a clinical challenge, we have previously observed enhanced recovery in rat hearts with pressure-overload hypertrophy induced by aortic banding. We investigated whether this unexpected result is found in other models of hypertrophy.
  
  
  METHODS
  Hearts with hypertrophy induced by aortic banding or administration of desoxycorticosterone acetate were each compared with age-matched sham-operated and nonoperated controls. Spontaneously hypertensive rats and Wistar-Kyoto controls were also compared. We evaluated left ventricular isomyosin distribution by gel electrophoresis and recovery of isolated working rat hearts arrested at 8 degrees C for 2 hours.
  
  
  RESULTS
  The percentage of V3 isomyosin in hearts with hypertrophy from aortic banding or administration of desoxycorticosterone acetate was increased compared with the control groups. Recovery of aortic flow in all three groups of hypertrophied hearts was at least as good or better than their respective controls. There were no significant differences in ATP or glycogen between hypertrophied and control hearts before or after arrest.
  
  
  CONCLUSIONS
  Enhanced recovery of hypertrophied hearts is not specific to a single model. This level of recovery may be supported by induction of a "fetal genetic program," exemplified in the rat by the shift in isomyosin from predominantly V1 to the more efficient V3 isoform, which occurs in pressure-overloaded hearts.
authors.affiliation: Department of Surgery, Massachusetts General Hospital and Harvard Medical School, Boston 02114, USA.
authors.forename: S D
authors.initials: SD
authors.lastname: Blank
authors.forename: J A
authors.initials: JA
authors.lastname: Lahorra
authors.forename: R S
authors.initials: RS
authors.lastname: McDonald
authors.forename: A G
authors.initials: AG
authors.lastname: Denenberg
authors.forename: J S
authors.initials: JS
authors.lastname: Titus
authors.forename: D F
authors.initials: DF
authors.lastname: Torchiana
authors.forename: W M
authors.initials: WM
authors.lastname: Daggett
authors.forename: G A
authors.initials: GA
authors.lastname: Geffin
mesh_terms: D000255:Adenosine Triphosphate / Q000032:analysis; D000818:Animals; D001012:Aorta, Abdominal; D002314:Cardioplegic Solutions; D002851:Chromatography, High Pressure Liquid; D003900:Desoxycorticosterone; D004195:Disease Models, Animal; D004591:Electrophoresis, Polyacrylamide Gel; D006003:Glycogen / Q000032:analysis; D006321:Heart / Q000503:physiopathology*; D006324:Heart Arrest, Induced; D006439:Hemodynamics; D017379:Hypertrophy, Left Ventricular / Q000209:etiology / Q000378:metabolism / Q000503:physiopathology*; D066298:In Vitro Techniques; D008026:Ligation; D009206:Myocardium / Q000378:metabolism; D009218:Myosins / Q000378:metabolism; D009392:Nephrectomy; D010725:Phosphocreatine / Q000032:analysis; D051381:Rats; D011918:Rats, Inbred SHR; D011921:Rats, Inbred WKY; D017207:Rats, Sprague-Dawley
chemical_list: D002314:Cardioplegic Solutions; D010725:Phosphocreatine; D003900:Desoxycorticosterone; D000255:Adenosine Triphosphate; D006003:Glycogen; D009218:Myosins