Advertisement
Research Article Free access | 10.1172/JCI105523
Department of Physiology and Biophysics, University of Washington, Seattle, Wash.
†Address requests for reprints to Dr. Richard H. Martin, Dept. of Medicine, University of Missouri School of Medicine, Columbia, Mo.
‡Present address: Dept. of Physiology, University of California San Francisco Medical Center, San Francisco, Calif.
*Submitted for publication August 1, 1966; accepted October 20, 1966.
Supported by a grant (HE-08433) from the National Institutes of Health and grants from the American Heart Association, the Washington State Heart Association, and the Northeastern Chapter of the Washington State Heart Association.
Presented in part at the National Meeting, American Federation for Clinical Research, Atlantic City, N.J., May 1, 1966.
Find articles by Martin, R. in: JCI | PubMed | Google Scholar
Department of Physiology and Biophysics, University of Washington, Seattle, Wash.
†Address requests for reprints to Dr. Richard H. Martin, Dept. of Medicine, University of Missouri School of Medicine, Columbia, Mo.
‡Present address: Dept. of Physiology, University of California San Francisco Medical Center, San Francisco, Calif.
*Submitted for publication August 1, 1966; accepted October 20, 1966.
Supported by a grant (HE-08433) from the National Institutes of Health and grants from the American Heart Association, the Washington State Heart Association, and the Northeastern Chapter of the Washington State Heart Association.
Presented in part at the National Meeting, American Federation for Clinical Research, Atlantic City, N.J., May 1, 1966.
Find articles by Lim, S. in: JCI | PubMed | Google Scholar
Department of Physiology and Biophysics, University of Washington, Seattle, Wash.
†Address requests for reprints to Dr. Richard H. Martin, Dept. of Medicine, University of Missouri School of Medicine, Columbia, Mo.
‡Present address: Dept. of Physiology, University of California San Francisco Medical Center, San Francisco, Calif.
*Submitted for publication August 1, 1966; accepted October 20, 1966.
Supported by a grant (HE-08433) from the National Institutes of Health and grants from the American Heart Association, the Washington State Heart Association, and the Northeastern Chapter of the Washington State Heart Association.
Presented in part at the National Meeting, American Federation for Clinical Research, Atlantic City, N.J., May 1, 1966.
Find articles by Citters, R. in: JCI | PubMed | Google Scholar
Published February 1, 1967 - More info
The effects of atrial fibrillation were studied in 12 healthy unanesthetized dogs, 9 to 49 days after surgical implantation of transducers for measurement of aortic flow and left ventricular diameter. Atrial fibrillation and pacing at comparable ventricular rates were induced by electrical stimulation of the right atrial appendage, and their effects were compared with observations made during sinus rhythm in each dog. At rest, cardiac output and mean arterial pressure were not significantly different during sinus rhythm, atrial fibrillation, and atrial pacing. After beta-adrenergic blockade with propranolol, cardiac output during fibrillation was significantly less than that during pacing at comparable ventricular rates. Arterial pressure was not detectably altered. During moderately severe treadmill exercise by six dogs, cardiac output fell significantly upon induction of fibrillation. After pentobarbital anesthesia fibrillation caused decrements in cardiac output and arterial pressure that were accentuated after thoracotomy.
These observations suggest the existence of compensatory mechanisms that maintain an essentially constant cardiac output when atrial fibrillation is induced in healthy unanesthetized dogs at rest. These mechanisms appear to fail during moderately severe exercise, beta-adrenergic blockade, and pentobarbital anesthesia.
Images.