title: Ventricular fibrillation does not depress postfibrillatory contractility in blood-perfused dog hearts.
abstract: We studied whether ventricular fibrillation depresses ventricular contractility in a blood-perfused heart. In 12 excised, cross-circulated dog hearts, we measured left ventricular pressure and myocardial oxygen consumption at a middle left ventricular volume as control and induced ventricular fibrillation electrically. Six hearts were subjected to 20 minutes of ventricular fibrillation (group A), and the other six hearts were subjected to 40 minutes of ventricular fibrillation (group B). Then we defibrillated the heart with direct current shock and measured left ventricular pressure, left ventricular volume, and myocardial oxygen consumption immediately, 10 minutes, 20 minutes, and 30 minutes after the defibrillation. Coronary perfusion pressure was maintained normal (around 100 mm Hg) by the arterial pressure of the support dog throughout each experiment. Ventricular contractility was quantified by the maximum value for the instantaneous pressure/volume ratio (Emax). Pooled data of both groups A and B showed that Emax immediately after defibrillation increased to 116% +/- 28% (p less than 0.05) of control level and Emax 10 minutes after defibrillation decreased to 84% +/- 17% (p less than 0.05) of control level. Then Emax recovered to the control level: 95% +/- 18% (p greater than 0.05) of control level at 20 minutes and 100% +/- 20% (p greater than 0.05) of control level at 30 minutes after defibrillation. Emax of group A was not different from that of group B at comparable measurement times after defibrillation. Changes in myocardial oxygen consumption per beat were in proportion to the changes in Emax. We conclude that ventricular fibrillation per se for 20 to 40 minutes does not depress postfibrillatory contractility when coronary blood perfusion is maintained normal in the dog left ventricle.
authors.affiliation: Department of Cardiovascular Dynamics, National Cardiovascular Center Research Institute, Osaka, Japan.
authors.forename: H
authors.initials: H
authors.lastname: Yaku
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: O
authors.initials: O
authors.lastname: Kawaguchi
authors.forename: H
authors.initials: H
authors.lastname: Suga
mesh_terms: D000818:Animals; D001790:Blood Physiological Phenomena; D003427:Cross Circulation; D004285:Dogs; D004562:Electrocardiography; D006352:Heart Ventricles / Q000503:physiopathology; D006439:Hemodynamics; D009200:Myocardial Contraction / Q000502:physiology*; D009206:Myocardium / Q000378:metabolism; D010101:Oxygen Consumption; D010477:Perfusion / Q000379:methods; D014693:Ventricular Fibrillation / Q000503:physiopathology*