title: Reversible pulmonary trunk banding: IX. G6PD activity of adult goat myocardium submitted to ventricular retraining.
abstract: OBJECTIVE
  Increased glucose 6-phosphate dehydrogenase activity has been demonstrated in heart failure. This study sought to assess myocardial glucose 6-phosphate dehydrogenase activity in retraining of the subpulmonary ventricle of adult goats.
  
  
  METHODS
  Eighteen adult goats were divided into three groups: traditional (fixed banding), sham, and intermittent (adjustable banding, daily 12-hour systolic overload). Systolic overload (70% of systemic pressure) was maintained during a 4-week period. Right ventricle, pulmonary artery and aortic pressures were measured throughout the study. All animals were submitted to echocardiographic and hemodynamic evaluations throughout the protocol. After the study period, the animals were killed for morphological and glucose 6-phosphate dehydrogenase activity assessment.
  
  
  RESULTS
  A 55.7% and 36.7% increase occurred in the intermittent and traditional right ventricle masses, respectively, when compared with the sham group (P<0.05), despite less exposure of intermittent group to systolic overload. No significant changes were observed in myocardial water content in the 3 groups (P=0.27). A 37.2% increase was found in right ventricle wall thickness of intermittent group, compared to sham and traditional groups (P<0.05). Right ventricle glucose 6-phosphate dehydrogenase activity was elevated in the traditional group, when compared to sham and intermittent groups (P=0.05).
  
  
  CONCLUSIONS
  Both study groups have developed similar right ventricle hypertrophy, regardless less systolic overload exposure of intermittent group. Traditional systolic overload for adult subpulmonary ventricle retraining causes upregulation of myocardial glucose 6-phosphate dehydrogenase activity. It may suggest that the undesirable "pathologic systolic overload" is influenced by activation of penthose pathway and cytosolic Nicotinamide adenine dinucleotide phosphate availability. This altered energy substrate metabolism can elevate levels of free radicals by Nicotinamide adenine dinucleotide phosphate oxidase, an important mechanism in the pathophysiology of heart failure.
authors.forename: Renato Samy
authors.initials: RS
authors.lastname: Assad
authors.forename: Leonardo Augusto
authors.initials: LA
authors.lastname: Miana
authors.forename: Miriam Helena
authors.initials: MH
authors.lastname: Fonseca-Alaniz
authors.forename: Maria Cristina Donadio
authors.initials: MC
authors.lastname: Abduch
authors.forename: Gustavo José Justo da
authors.initials: GJ
authors.lastname: Silva
authors.forename: Fernanda Santos de
authors.initials: FS
authors.lastname: Oliveira
authors.forename: Luiz Felipe Pinho
authors.initials: LF
authors.lastname: Moreira
authors.forename: José Eduardo
authors.initials: JE
authors.lastname: Krieger
mesh_terms: D000818:Animals; D015415:Biomarkers / Q000378:metabolism; D001794:Blood Pressure; D004195:Disease Models, Animal; D004734:Energy Metabolism; D005954:Glucosephosphate Dehydrogenase / Q000378:metabolism*; D006041:Goats; D006352:Heart Ventricles / Q000201:enzymology / Q000503:physiopathology; D006439:Hemodynamics; D017380:Hypertrophy, Right Ventricular / Q000201:enzymology* / Q000503:physiopathology; D009206:Myocardium / Q000201:enzymology*; D011651:Pulmonary Artery / Q000601:surgery*; D013997:Time Factors; D014188:Transposition of Great Vessels / Q000601:surgery*; D018497:Ventricular Dysfunction, Right / Q000201:enzymology / Q000503:physiopathology
chemical_list: D015415:Biomarkers; D005954:Glucosephosphate Dehydrogenase