title: Mechanical, energetic, and biochemical changes in long-term pressure overload of rabbit heart.
abstract: The mechanical and energetic consequences of long-term pressure-overload (POL) hypertrophy have been investigated in rabbits and compared with sham-operated controls (SOC). Hypertrophy was induced by banding the pulmonary artery of young rabbits and examining the mechanical, biochemical, and energetic properties of the compensated heart 10-16 wk later. Experiments were undertaken on papillary muscles from the hypertrophic hearts. At 27 degrees C and a stimulus frequency of 1 Hz there was a modest depression of peak stress development but no significant changes in isometric rise times and one-half widths or in isotonic maximum velocity of shortening and power output. The inverse relationship between peak stress and cross-sectional area (CSA) was practically identical in the POL and SOC groups. Both polarographic and myothermic investigations were made on papillary muscles. Hypertrophy nearly halved basal metabolism, and in isometric contractions there was increased isometric economy due to a combination of a lower stress cost and a reduced activation heat. Hypertrophy did significantly depress the extent of shortening leading to a reduced work output per beat. In isotonic contractions the reduced work output was offset by a reduced energy output such that there was no significant change in suprabasal mechanical efficiency. Biochemical studies showed that the transition of myosin isoenzymes to the V3 form was essentially complete in the POL group, but that the SOC group was also predominantly V3 when the animals were killed. There was a significant 30% decline in the Ca2(+)-stimulated adenosinetriphosphatase activity of the sarcoplasmic reticulum. It is concluded that in long-term compensated hypertrophy of rabbit hearts there are only a few mechanical and energetic differences between control and hypertrophic muscles. The changes that can be detected appear to predominantly reflect disturbances in cellular Ca2+ regulation.
authors: Department of Physiology, Monash University, Clayton, Victoria, Australia.
authors: C L
authors: CL
authors: Gibbs
authors: I R
authors: IR
authors: Wendt
authors: G
authors: G
authors: Kotsanas
authors: I R
authors: IR
authors: Young
authors: G
authors: G
authors: Woolley
mesh_terms: D000818:Animals; D000252:Calcium-Transporting ATPases / Q000378:metabolism; D004558:Electric Stimulation; D004734:Energy Metabolism; D006321:Heart / Q000503:physiopathology*; D006358:Hot Temperature; D006973:Hypertension / Q000378:metabolism / Q000503:physiopathology*; D009200:Myocardial Contraction; D009206:Myocardium / Q000378:metabolism*; D009218:Myosins / Q000378:metabolism; D010101:Oxygen Consumption; D011048:Polarography; D011817:Rabbits; D013997:Time Factors
chemical_list: D009218:Myosins; D000252:Calcium-Transporting ATPases