title: Mechanical, energetic, and biochemical changes in long-term volume overload of rabbit heart.
abstract: The mechanical and energetic consequences of long-term volume-overload (VOL) hypertrophy have been investigated in rabbits and compared with the consequence in sham-operated controls (SOC). Hypertrophy was induced by creating an aortocaval shunt, and the mechanical, biochemical, and energetic properties of the compensated heart were examined approximately 12 wk later. At 27 degrees C and a stimulus frequency of 1 Hz there were no significant changes in peak stress development, 10-90% rise times, shortening velocity, work, and mechanical power output. There was, however, a prolongation of contractile duration. The inverse relationship between peak stress and cross-sectional area was unchanged in the VOL and SOC groups. Polarographic and myothermic experiments were made on papillary muscles. Hypertrophy produced a small increment in basal metabolism. In isometric studies there were no significant changes in either the activation heat magnitude or the slope of the heat-stress relationship. In isotonic contractions there was no change in work output or total enthalpy (heat + work), and as a result mechanical efficiency was unchanged. A force-length-area (FLA) analysis of the isotonic data showed no significant change in intercept or FLA contractile efficiency. Biochemical studies showed no significant difference in the myosin isoenzyme profile at the time of death. The Ca(2+)-stimulated adenosinetriphosphatase activity of the sarcoplasmic reticulum was unchanged as were the enzymatic activities of mitochondrial citrate synthase and alpha-ketoglutarate dehydrogenase. Interestingly essentially the same data were obtained from the hearts of four animals in failure and from the hearts of seven compensated animals.(ABSTRACT TRUNCATED AT 250 WORDS)
authors.affiliation: Department of Physiology, Monash University, Clayton, Victoria, Australia.
authors.forename: C L
authors.initials: CL
authors.lastname: Gibbs
authors.forename: I R
authors.initials: IR
authors.lastname: Wendt
authors.forename: G
authors.initials: G
authors.lastname: Kotsanas
authors.forename: I R
authors.initials: IR
authors.lastname: Young
mesh_terms: D000818:Animals; D000252:Calcium-Transporting ATPases / Q000378:metabolism; D006332:Cardiomegaly / Q000503:physiopathology*; D002950:Citrate (si)-Synthase / Q000378:metabolism; D006321:Heart / Q000502:physiology / Q000503:physiopathology*; D066298:In Vitro Techniques; D007527:Isoenzymes / Q000302:isolation & purification / Q000378:metabolism; D007655:Ketoglutarate Dehydrogenase Complex / Q000378:metabolism; D008929:Mitochondria, Heart / Q000201:enzymology; D009200:Myocardial Contraction; D009206:Myocardium / Q000378:metabolism*; D009218:Myosins / Q000302:isolation & purification / Q000378:metabolism; D010101:Oxygen Consumption; D010210:Papillary Muscles / Q000502:physiology / Q000503:physiopathology*; D011048:Polarography; D011817:Rabbits; D012016:Reference Values; D012044:Regression Analysis; D012519:Sarcoplasmic Reticulum / Q000201:enzymology; D013816:Thermodynamics
chemical_list: D007527:Isoenzymes; D007655:Ketoglutarate Dehydrogenase Complex; D002950:Citrate (si)-Synthase; D009218:Myosins; D000252:Calcium-Transporting ATPases