title: In vivo profile of myocardial energy metabolism of pressure-overloaded rat.
abstract: Cardiac energy metabolism of pressure-overloaded rat hearts was examined under in vivo and in vitro conditions. Two, 4 and 6 weeks after constriction of the abdominal artery, the hemodynamic and metabolic profiles of hearts in vivo and of perfused hearts were determined. Significant increases in left ventricular weight/body weight (30 to 45% increase relative to the sham group), systolic and diastolic blood pressure (22 to 33% increase) and pressure-rate product (31 to 33% increase) were observed 2, 4 and 6 weeks after the operation, and a slight but significant decrease in heart rate was observed at 2 weeks after the operation. Tissue hydroxyproline content increased (17 to 93%) with time after pressure-overload. These findings are indicators of pressure-overloaded cardiac hypertrophy. The total high-energy phosphates of the in vivo rat myocardium under artificial respiration were lower than those of sham-operated rat myocardium 2 (23%) and 4 weeks (21%), but not 6 weeks after aortic constriction. The maximal oxygen consumption rates of mitochondria, when determined in the skinned cardiac fibers, also decreased 2 (47%) and 4 weeks (36%), but reversed 6 weeks after pressure-overload. However, the myocardial ATP, a utilizing form of high-energy phosphate, of pressure-overloaded rat myocardium remained normal at all times after cardiac hypertrophy. This suggests that alterations in hemodynamic variables of in vivo pressure-overloaded rats may not be attributable to a reduction in the myocardial energy production. In the perfused hearts isolated from pressure-overloaded rats, tissue ATP levels were similar to those of sham-operated rats, although the tissue creatine phosphate tended to be reduced in the pressure-overloaded animals at all stages of cardiac hypertrophy examined. Only a marginal decrease in the tissue high-energy phosphate (13%) was observed 4 weeks after the operation relative to that of sham-operated rats. In contrast, the developed tension of the perfused pressure-overloaded rat hearts was consistently lower (27 to 36%) than that of the sham-operated rat hearts. The results suggest that the high-energy phosphate levels of pressure-overloaded rat myocardium in vitro are unlikely to account for the observed decline in cardiac contractile function. The reduction of myocardial high-energy phosphates of pressure overloaded rats may be due to an adaptative change rather than a causal events.
authors.affiliation: Department of Pharmacology, Tokyo College of Pharmacy, Japan.
authors.forename: S
authors.initials: S
authors.lastname: Takeo
authors.forename: K
authors.initials: K
authors.lastname: Tanonaka
authors.forename: M
authors.initials: M
authors.lastname: Aoki
authors.forename: Y
authors.initials: Y
authors.lastname: Nakai
authors.forename: A
authors.initials: A
authors.lastname: Sanbe
authors.forename: Y
authors.initials: Y
authors.lastname: Shizume
authors.forename: C
authors.initials: C
authors.lastname: Tanaka
authors.forename: K
authors.initials: K
authors.lastname: Miyake
authors.forename: K
authors.initials: K
authors.lastname: Hirai
authors.forename: N
authors.initials: N
authors.lastname: Ueda
mesh_terms: D000255:Adenosine Triphosphate / Q000378:metabolism; D000818:Animals; D001794:Blood Pressure; D006332:Cardiomegaly / Q000378:metabolism / Q000503:physiopathology; D003094:Collagen / Q000378:metabolism; D004734:Energy Metabolism; D006439:Hemodynamics; D006909:Hydroxyproline / Q000378:metabolism; D066298:In Vitro Techniques; D008297:Male; D008929:Mitochondria, Heart / Q000378:metabolism; D009206:Myocardium / Q000378:metabolism*; D010101:Oxygen Consumption; D010725:Phosphocreatine / Q000378:metabolism; D051381:Rats; D017208:Rats, Wistar
chemical_list: D010725:Phosphocreatine; D000255:Adenosine Triphosphate; D003094:Collagen; D006909:Hydroxyproline