512 



HANDBOOK OF PHYSIOLOGY 



CIRCULATION I 



TABLE I . Changes in Cardiac Cycle Due to Stellate 

 Ganglion Stimulation Heart Rate Constant at 

 ii6/min* {Total cycle time = §20 msec) 



Duration of atrial systole, msec* 

 Duration of ventricular systole, 



msec'' 

 Duration of ventricular diastole, 



msec" 

 A-R interval, msec* 

 Increment in LVED (cm H^O) 



produced by atrial systole 

 Duration of isometric contraction 



msec= 

 Relaxation time, msec' 



* Analysis of tracing shown in fig. 19 (lower). 



» From beginning of increase in atrial pressure until 

 beginning of rise in ventricular pressure. *" From begin- 

 ning of rise in ventricular pressure until aortic incisura. 

 ' From beginning of aortic incisura to the rise in ventricular 

 pressure. "^ A-R interval; from beginning of rise in atrial 

 pressure to lowest point of ventricular diastolic pressure 

 ("relaxation point"). •■ From beginning of rise in ven- 

 tricular pressure until beginning of rise in aortic pressure. 

 ' From aortic incisura until lowest point of ventricular 

 diastolic pressure. 



nephrine. In the tracings shown in figure 19 (lower) 

 mild efferent vagal nerve stimulation was used so as 

 to slow the normally conducting paced heart to a 

 rate approximating that of the unanesthetized resting 

 dog. This mild vagal activity was held as a constant 

 background throughout the course of the experiment. 

 The control tracing is at the left; that during stellate 

 stimulation is at the right. In each tracing the arrows 

 indicate the left atrial "a" wave, the atrially induced 

 increase in left ventricular end diastolic pressure, and 

 myocardial segment length. Table i shows the values 

 for each of the components analyzed. It is clear from 

 these tracings that during stellate stimulation the 

 atrial contraction produces a larger end diastolic 

 increment of both ventricular pressure and segment 

 length. The greater rise in end diastolic ventricular 

 pressure can only be attributed to the more vigorous 

 atrial contraction; the greater elongation of the myo- 

 cardial segment is attributable not only to the more 

 forceful atrial contraction but also to the lower posi- 

 tion on the ventricle's pressure-length curve (fig. 12) 

 brought about by the more complete systolic empty- 

 ing in the previous beat. 



C Influence oj Efferent Vagal Xerve Stimulation 

 on the Ventricle 



Some of the hemodynamic consequences of efferent 

 vagal nerve stimulation, while the heart rate is main- 

 tained constant by atrial pacing, are shown in figure 

 20 (upper left). During periods of stimulation of the 

 distal cut end of the left vagus nerve (signals at A and 

 B) mean right and left atrial pressures rise while 

 aortic pressure, cardiac output, and stroke work fall. 

 That the magnitude of the response is a function of 

 the vagal impulse frequency used is shown in the data 

 in figure 20 (upper right); the observed responses in- 

 crease in a stepwise manner as the stimulation fre- 

 quency is increased from o to 6 per sec. These effects 

 are blocked by the administration of atropine. It 

 should be noted that the carotid sinus pressure was 

 maintained constant throughout the course of this 

 experiment in order to control the reflex sympathetic 

 influences emanating from this area (see section 111). 



These data could be explained in three different 

 ways: /) that despite the lack of available anatomic 

 evidence for vagal innervation of the ventricle (32, 

 70) vagal stimulation can in some way influence the 

 force of ventricular contraction from any given end 

 diastolic pressure; 2) that changes in mean left atrial 

 pressure do not, during vagal stimulation, indicate 

 similar directional changes in left ventricular end 

 diastolic pressure; or ^) that changes in left ventricu- 

 lar myocardial extensibility during vagal stimulation 

 could account for the observed phenomena. The last 

 possibility has been excluded by observations showing 

 that vagal nerve stimulation does not modify the end 

 diastolic pressure-length curve (67). Relevant to 

 number 2, experiments have been done in which data 

 were gathered in such a manner as to relate both 

 mean left atrial pressure and left ventricular end 

 diastolic pressure to the stroke work of the left ventri- 

 cle before and during vagal stimulation (105). The 

 results of one such experiment are shown in figure 20 

 (lower). In panel A, the relation of left ventricular 

 end diastolic pressure and left ventricular stroke 

 work before (solid circles) and during (open circles) 

 stimulation of the distal cut end of the left vagus 

 nerve (6.7 volts, 15 per sec) is shown. No change in 

 left ventricular contractility occurred, i.e., the left 

 ventricle produced as much work from any given end 

 diastolic pressure during vagal stimulation as without 

 it. These observations are in accord with the apparent 

 lack of vagal fiber distribution to the ventricular myo- 

 cardium. Mean aortic pressure ranged from 58 to 165 

 mm Hg when tiie control values were obtained and 



