title: The effects of dynamic cardiac compression on ventricular mechanics and energetics. Role of ventricular size and contractility.
abstract: The purpose of this study was to determine the role of ventricular size or contractility in the effectiveness of dynamic cardiac compression in terms of the pressure-volume relationship and myocardial oxygen consumption. In 10 isolated cross-circulated dog hearts, the ventricle was directly compressed during systole. For the volume run, measurements for slope of the end-systolic pressure-volume relation, pressure-volume area, external work, coronary blood flow, and myocardial oxygen consumption were achieved before and during a fixed amount of dynamic cardiac compression. Left ventricular volume was then increased while stroke volume was kept constant, and measurements were repeated. For the contractility run, after the control measurements were taken, left ventricular contractility was significantly increased or decreased by infusion of either dobutamine or propranolol into the coronary circulation. Measurements were repeated before and during dynamic cardiac compression at the control level of end-diastolic and stroke volumes. Dynamic cardiac compression significantly increased slope of the end-systolic pressure-volume relation, pressure-volume area, and external work (p < 0.01), whereas coronary blood flow and myocardial oxygen consumption were not affected. The increase in pressure-volume area caused by dynamic cardiac compression was greater with the larger volume. Despite the significant differences in the native left ventricular contractility, the increases in slope of the end-systolic pressure-volume relation, pressure-volume area, and external work did not differ among the three groups. We conclude that dynamic cardiac compression enhances left ventricular systolic function independent of ventricular contractility and without affecting coronary blood flow or myocardial oxygen consumption. Mechanical enhancement is more effective in the dilated heart.
authors.affiliation: Department of Cardiovascular Dynamics, National Cardiovascular Center Research Institute, Osaka, Japan.
authors.forename: O
authors.initials: O
authors.lastname: Kawaguchi
authors.forename: Y
authors.initials: Y
authors.lastname: Goto
authors.forename: S
authors.initials: S
authors.lastname: Futaki
authors.forename: Y
authors.initials: Y
authors.lastname: Ohgoshi
authors.forename: H
authors.initials: H
authors.lastname: Yaku
authors.forename: H
authors.initials: H
authors.lastname: Suga
mesh_terms: D000818:Animals; D001243:Assisted Circulation / Q000379:methods*; D003326:Coronary Circulation / Q000502:physiology; D003427:Cross Circulation; D004280:Dobutamine / Q000494:pharmacology; D004285:Dogs; D017379:Hypertrophy, Left Ventricular / Q000503:physiopathology*; D009200:Myocardial Contraction / Q000187:drug effects / Q000502:physiology*; D009206:Myocardium / Q000378:metabolism*; D010101:Oxygen Consumption / Q000502:physiology; D011433:Propranolol / Q000494:pharmacology; D016277:Ventricular Function, Left / Q000187:drug effects / Q000502:physiology*
chemical_list: D004280:Dobutamine; D011433:Propranolol