Alterations in myocardial contractility during stimulation of the cardiac nerves

Abstract

While recording contractile force on base and apical regions of both canine ventricles, together with right atrial force and heart rate, the stellate ganglia and major vagosympathetic trunks distal to the caudal cervical ganglion were electrically stimulated before and after atropine. Augmentor fibers leaving the stellate pass through the ansa, move through the anterior then posterior, enter the caudal cervical ganglion and become intermingled with fibers descending through the vagosympathetic trunk. The recurrent cardiac and stellate cardiac nerves on the right and ventromedial and ventrolateral nerves on the left carry a majority of sympathetic fibers to the heart. The craniovagal, caudovagal nerves, and vagi generally slow or stop the heart and inhibit contractility of all chambers. After atropine these nerves often elicit both accelerator and augmentor responses. The right ventricular conus shows the greatest percent increase in contractile force while the left ventricular base responds strongly to stimulation of either right or left sympathetics. The apical regions of the ventricles concurrently show much less change. The right atrium shows the greatest range in response, varying from complete abolition of contraction to several 100% increase when augmentor fibers were unmasked by atropine. Most cardiac surfaces receive a highly redundant supply from the extrinsic nervous supply.