THE CONTROL OF THE FUNCTION OF THE HEART 52 1 



40 



L.A. 

 cm 



HgO 



T- 1— r-i — ! — r- 



^T n — r~i — r—r-i' n — i — t — i~t r -;- r t -|— ^ --,- -j— , — , . — , — p- 



250 



A.P. 





 40 



L.V.D. 

 or 



O"- 



250 



C.S.R 



mm 



Hg 





 5 



A.F. 3 

 L /min 



V V V V 



\-j 



U V^ 



■■'^J 



FIG. 26 



carotid pressure is higli, the \'FCla is shifted to the 

 riglit; when carotid pressure is low, the V'FCla is 

 shifted to the left. At intermediate carotid pressures, 

 the VFCla is situated correspondingly. The carotid 

 pressures and corresponding symbols are shown at the 

 top (right). Once again, the magnitude of the ob- 

 served changes in stroke work at any given mean 

 atrial pressure is of interest. Figure 255 (right panel) 

 shows similar results for the VFCra- 



As shown above, at any given heart rate, a sympa- 

 thetically induced change in mean left atrial pressure 

 reliably indicates a similar directional change in left 

 ventricular end diastolic pressure. Direct evidence 

 that the ventricle does produce more external work 

 from any given left ventricular end diastolic pressure 

 under the influence of carotid hypotension is shown 

 in figure 26. The tracing at the left was taken during 

 high carotid artery pressure, and that at the right 

 during low carotid artery pressure. Lowering the 

 carotid pressure resulted in a doubling of stroke 

 volume and the production of six times as much 

 stroke work from the same end diastolic pressure. Of 

 particular interest is the observation that during 



carotid hypotension there is a more synchronous tvpe 

 of ventricular contraction and a more rapid rate of 

 relaxation, thus allowing for a longer diastolic interval, 

 changes similar to those observed with stellate stimu- 

 lation. The observed effects of carotid stimulation on 

 the heart are diminished or abolished by sectioning 

 stellate ganglion rami or by ganglionic blockade 

 (106). It might be argued that the increase in ven- 

 tricular contractility observed when carotid pressure 

 is lowered can be attributed to the higher aortic 

 pressure acting through the mechanism of homeo- 

 metric autoregulation (section i). However, it has 

 recently been determined that a marked increase in 

 ventricular contractility is also observed when 

 carotid hypotension is induced and aortic pressure 

 as well as heart rate is kept at the same level (J. 

 P. Gilmore & J. H. Siegel, unpublished observations). 

 Such experiments confirm the suggestion by Sarnoff & 

 Berglund (96), and by Agostoni et al. (i) that carotid 

 sinus stimulation can shift the VFC and are consonant 

 with the observations of Carlsten et al. (22) in man, 

 which led those authors to postulate a refiexly induced 

 cardiac inotropic effect arising from the carotid sinus. 



