title: Reversible pulmonary trunk banding. VI: Glucose-6-phosphate dehydrogenase activity in rapid ventricular hypertrophy in young goats.
abstract: OBJECTIVE
  Increased myocardial glucose-6-phosphate dehydrogenase (G6PD) activity occurs in heart failure. This study compared G6PD activity in 2 protocols of right ventricle (RV) systolic overload in young goats.
  
  
  METHODS
  Twenty-seven goats were separated into 3 groups: sham (no overload), continuous (continuous systolic overload), and intermittent (four 12-hour periods of systolic overload paired with a 12-hour resting period). During a 96-hour protocol, systolic overload was adjusted to achieve a 0.7 RV/aortic pressure ratio. Echocardiographic and hemodynamic evaluations were performed before and after systolic overload every day postoperatively. After the study period, the animals were humanely killed for morphologic and G6PD tissue activity assessment.
  
  
  RESULTS
  A 92.1% and 46.5% increase occurred in RV and septal mass, respectively, in the intermittent group compared with the sham group; continuous systolic overload resulted in a 37.2% increase in septal mass. A worsening RV myocardial performance index occurred in the continuous group at 72 hours and 96 hours, compared with the sham (P < .039) and intermittent groups at the end of the protocol (P < .001). Compared with the sham group, RV G6PD activity was elevated 130.1% in the continuous group (P = .012) and 39.8% in the intermittent group (P = .764).
  
  
  CONCLUSIONS
  Continuous systolic overload for ventricle retraining causes RV dysfunction and upregulation of myocardial G6PD activity, which can elevate levels of free radicals by NADPH oxidase, an important mechanism in the pathophysiology of heart failure. Intermittent systolic overload promotes a more efficient RV hypertrophy, with better preservation of myocardial performance and and less exposure to hypertrophic triggers.
authors: Heart Institute, University of São Paulo Medical School, São Paulo, Brazil. rsassad@cardiol.br
authors: Renato S
authors: RS
authors: Assad
authors: Fernando A
authors: FA
authors: Atik
authors: Fernanda S
authors: FS
authors: Oliveira
authors: Miriam H
authors: MH
authors: Fonseca-Alaniz
authors: Maria C D
authors: MC
authors: Abduch
authors: Gustavo J J
authors: GJ
authors: Silva
authors: Gustavo G
authors: GG
authors: Favaro
authors: Jose E
authors: JE
authors: Krieger
authors: Noedir A G
authors: NA
authors: Stolf
mesh_terms: D000367:Age Factors; D000818:Animals; D001011:Aorta / Q000503:physiopathology; D001794:Blood Pressure; D004195:Disease Models, Animal; D004734:Energy Metabolism; D005954:Glucosephosphate Dehydrogenase / Q000378:metabolism*; D006041:Goats; D017380:Hypertrophy, Right Ventricular / Q000000981:diagnostic imaging / Q000201:enzymology* / Q000209:etiology / Q000503:physiopathology; D008026:Ligation; D009206:Myocardium / Q000201:enzymology* / Q000473:pathology; D011651:Pulmonary Artery / Q000601:surgery*; D013997:Time Factors; D014463:Ultrasonography; D018497:Ventricular Dysfunction, Right / Q000000981:diagnostic imaging / Q000201:enzymology* / Q000209:etiology / Q000503:physiopathology; D016278:Ventricular Function, Right; D017725:Ventricular Pressure; D020257:Ventricular Remodeling
chemical_list: D005954:Glucosephosphate Dehydrogenase