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Research Article Free access | 10.1172/JCI109502

Reflex Cardiovascular Depression during Unilateral Lung Hyperinflation in the Dog

Sharon S. Cassidy, William L. Eschenbacher, and Robert L. Johnson Jr.

Pauline and Adolph Weinberger Laboratory for Cardiopulmonary Research, Department of Internal Medicine, University of Texas Health Science Center at Dallas, Dallas, Texas 75235

Find articles by Cassidy, S. in: PubMed | Google Scholar

Pauline and Adolph Weinberger Laboratory for Cardiopulmonary Research, Department of Internal Medicine, University of Texas Health Science Center at Dallas, Dallas, Texas 75235

Find articles by Eschenbacher, W. in: PubMed | Google Scholar

Pauline and Adolph Weinberger Laboratory for Cardiopulmonary Research, Department of Internal Medicine, University of Texas Health Science Center at Dallas, Dallas, Texas 75235

Find articles by Johnson, R. in: PubMed | Google Scholar

Published August 1, 1979 - More info

Published in Volume 64, Issue 2 on August 1, 1979
J Clin Invest. 1979;64(2):620–626. https://doi.org/10.1172/JCI109502.
© 1979 The American Society for Clinical Investigation
Published August 1, 1979 - Version history
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Abstract

We have examined whether lung hyperinflation in the anesthetized dog reflexly depresses cardiac output, stroke volume, heart rate, and blood pressure and whether these changes persist for more than a minute. To eliminate any mechanical restriction to venous return and pulmonary blood flow during lung hyperinflation, a model was developed in which all pulmonary artery blood flow and all ventilation were directed to the right lung in dogs with widely open chest and the left lung was hyperinflated before and after left cervical vagotomy. Heart rate, stroke volume, and blood pressure decreased by 24, 20, and 27%, respectively, within 15 s of left lung inflation to 30 cm H2O. Heart rate increased to preinflation levels by 1 min, but stroke volume and blood pressure remained depressed during lung hyperinflation for at least 15 min. Upon deflation, stroke volume and blood pressure returned to control levels within 1 min. Division of the left vagosympathetic trunk at the neck interrupted all autonomic afferent and efferent nerves of the left lung, but left intact the right vagal sympathetic and parasympathetic afferent and efferent nerves of the heart. After left cervical vagotomy the transient fall in heart rate, stroke volume, and blood pressure during left lung hyperinflation was greatly reduced or eliminated. These results suggest that unilateral lung hyperinflation reflexly depresses heart rate and blood pressure, which are partially compensated with time, and reflexly depresses stroke volume, which persists uncompensated until the lung is deflated. These findings may explain the depressed cardiovascular function observed during regional lung overdistention especially when it occurs during positive pressure ventilation.

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