Hemodynamic mechanisms of increased cardiovascular response resulting from ganglioplegics and atropine

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Abstract
Continuous measurement of cardiac output and peripheral resistance in unrestrained dogs revealed that constant arterial pressure is maintained by a variable interplay of these factors in accord with the "mosaic theory" of blood pressure regulation. Equipressor responses to several vasoactive agents also depended on this variable interplay. Tetraethylammonium and chlorisondamine had inconstant effects but usually caused an initial decrease in total peripheral resistance and an increase in heart rate. Augmentation of pressor responses by these ganglioplegics was due to larger increases in cardiac output and/or peripheral resistance depending mainly on the primary site of action of the pressor drug. Following tetraethylammonium, norepinephrine caused greater increases in both cardiac output and peripheral resistance; after chlorisondamine, the larger response to norepinephrine depended on a greater peripheral response. Response to serotonin after either ganglioplegic, or after atropine, was largely due to a greater increase in peripheral resistance. Enhanced responsiveness to angiotensin was due to increase in cardiac output or elimination of the normal decrease. Ganglioplegics increased the peripheral response to tyramine, while atropine increased both the cardiac and peripheral response. Response to vasopressin was enhanced by ganglioplegics due to a larger increase in peripheral resistance and a lesser decrease in cardiac output than normally caused by this hormone.