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Research Article Free access | 10.1172/JCI106893

Extent of Carotid Sinus Regulation of the Myocardial Contractile State in Conscious Dogs

Stephen F. Vatner, Charles B. Higgins, Dean Franklin, and Eugene Braunwald

Department of Medicine, University of California, San Diego, School of Medicine, California 92037

Scripps Clinic and Research Foundation, La Jolla, California 92037

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

Department of Medicine, University of California, San Diego, School of Medicine, California 92037

Scripps Clinic and Research Foundation, La Jolla, California 92037

Find articles by Higgins, C. in: PubMed | Google Scholar

Department of Medicine, University of California, San Diego, School of Medicine, California 92037

Scripps Clinic and Research Foundation, La Jolla, California 92037

Find articles by Franklin, D. in: PubMed | Google Scholar

Department of Medicine, University of California, San Diego, School of Medicine, California 92037

Scripps Clinic and Research Foundation, La Jolla, California 92037

Find articles by Braunwald, E. in: PubMed | Google Scholar

Published April 1, 1972 - More info

Published in Volume 51, Issue 4 on April 1, 1972
J Clin Invest. 1972;51(4):995–1008. https://doi.org/10.1172/JCI106893.
© 1972 The American Society for Clinical Investigation
Published April 1, 1972 - Version history
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Abstract

The effects of bilateral carotid artery occlusion (BCO) and carotid sinus nerve stimulation (CSNS) on left ventricular (LV) pressure (P), diameter (D), velocity of contraction (V), rate of change of pressure (dP/dt), and cardiac output were studied in conscious dogs instrumented with ultrasonic diameter gauges, miniature pressure gauges, and aortic electromagnetic flow transducers. The effects of BCO and CSNS were also studied after automatic blockade and were compared to similar alterations in pressure produced by norepinephrine, methoxamine, and nitroglycerin. When heart rate was maintained constant with atrial stimulation, BCO had little effect on ventricular contractility, increasing isolength systolic pressure (LV Piso) by 36% while isolength velocity of myocardial shortening (Viso) decreased by 12% and (dP/dt)/P fell by 8%. These effects could be explained largely by vasoconstriction, since elevating systolic pressure with methoxamine produced similar results, while norepinephrine increased Viso by 36% and (dP/dt)/P by 56%. CSNS produced directionally opposite results from BCO; it decreased Piso by 15%, Viso increased by 11%, while (dP/dt)/P remained almost constant. These effects may be explained largely by vasodilatation since reducing systolic pressure to the same level with nitroglycerin produced similar results. When peripheral vasoconstriction was minimized by phenoxybenzamine pretreatment. BCO produced a slight positive inotropic effect (Piso increased by 8%, Viso by 4%, and (dp/dt)/P by 10%), while CSNS produced a slight negative inotropic effect (Piso decreased by 3%, Viso decreased by 5%, and (dP/dt)/P by 7%).

Thus, in the normal, healthy, conscious dog, the carotid sinuses exert relatively little control of the inotropic state of the left ventricle; moreover, this small inotropic action is masked by the more powerful effects on peripheral resistance.

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