524 



HANDBOOK OF PHYSIOLOGY 



CIRCULATION I 



C. Function of the Carotid Sinus 



During the course of these iiivestigations a pattern 

 of the baroceptor's functional role has been evolved 

 which brings together a variety of observations in a 

 manner that seems to have an appealing unity. This 

 position holds that a dominant physiologic responsi- 

 bilitv of the carotid sinus in circulatory regulation is 

 to augment or diminish the contraction of the 

 ventricle. The basis for this is as follows ; 



/) Carotid hypotension diminishes venous dis- 

 tensibility. The net effect of such a change, if it alone 

 occurs, is an increased ventricular end diastolic pres- 

 sure and fiber length, and thus an augmented 

 ventricular contraction. Splenic contraction would 

 have the same effect. 



.2) Carotid hvpotension augments and shortens the 

 atrial contraction by means of the carotido-vago- 

 atrial and the carotido-sympatho-atrial reflexes. The 

 net effect of such an atrial augmentation, if it alone 

 occurs, is an increased ventricular end diastolic 

 pressure and fiber length and thus an augmented 

 ventricular contraction. 



2) At any given heart rate carotid hypotension 

 directly augments the stroke work and stroke power 

 produced by the ventricle from any given end diastolic 

 pressure or fiber length. 



4) Since carotid hypotension directly augments 

 ventricular stroke power by shortening the systolic 

 time for any given amount of work produced and also 

 produces a more rapid rate of relaxation, it thus pro- 

 vides for a longer interval of diastolic filling than 

 would otherwise occur. This factor becomes espe- 

 cially important at high heart rates. 



5) The more complete systolic emptying conse- 

 quent to carotid hypotension places the ventricle on a 

 lower and more sensitive portion of its diastolic 

 pressure-length curve. As a result there will be more 

 filling and a greater fiber elongation produced by any 

 given atrial systole than if the more complete systolic 

 emptying had not taken place. 



6) The increased peripheral vascular resistance 

 during carotid hypotension maintains a higher aortic 

 pressure at any given stroke volume and heart rate 

 than would otherwise be present. In addition to 

 maintaining an adequate pressure for coronary per- 

 fusion, the higher aortic pressure produces an in- 

 creased ventricular contractility through homeo- 

 metric autoregulation (Anrep effect). 



7) Tachycardia, per se, increases ventricular 

 contractility through homeometric autoregulation 

 (Bowditch effect) in addition to the concomitant 



inotropic influence of the increased sympathetic 

 outflow. 



8) Whatever catecholamines are secreted by the 

 adrenal medulla in response to a lowering of carotid 

 sinus pressure would be expected to reinforce the 

 effects enumerated above. 



The intended purpose of synthesizing the available 

 information in this manner is not to disparage the 

 importance of changes in heart rate per se or to 

 minimize the importance of regional changes in 

 peripheral vascular resistance. Rather, the purpose 

 is to invite a re-evaluation of the proper role of the 

 carotid sinus in circulatory regulation. It seems fair 

 to insist that to view the carotid sinus as a sense organ 

 which acts primarily to safeguard blood flow to the 

 vital organs, such as the brain and heart, is no longer 

 a tenable position. It would seem much more appro- 

 priate to cast it in the role of a sensing element which 

 helps to regulate blood flow to all the tissues of the 

 organism in accordance with their activity and 

 metabolic requirements (44, 78, 101). To a substan- 

 tial extent the baroceptor operates much like a 

 voltage regulating element in an electrical system; 

 i.e., it causes an appropriate variation of input so as 

 to maintain a constant voltage when the current 

 requirements of the system it is supplying are changed. 

 An example of its operation in this manner was ob- 

 tained recently in experiments in which it was demon- 

 strated that local muscular activity effectively pro- 

 duces a functional sympathectomy in the vascular bed 

 of the active area (78a); under such circumstances it 

 can be shown that when carotid pressure is elevated, 

 thus inhibiting the stimulatory action of its reflex 

 autonomic activity, the blood flow through the 

 active muscular area is lower, the \enous p02 and 

 pH from it are decreased, and the arteriovenous O2 

 difference across it is widened, each by substantial 

 amounts relative to what these values are when 

 carotid pressure is lower (78a). 



D. Reflex Changes in Heart Rate and Contractility 



It would almost appear that the medullary centers 

 appreciate the extent to which tachycardia encroaches 

 on the time available for diastole (14, 60, 79, 125) and 

 thus do not have the temerity to impose tachycardia 

 without providing simultaneous inotropic safeguards 

 against a time-limited diastolic ventricular relaxation 

 as well as the restricted period for coronary inflow 

 which would otherwise take place. A simultaneous 

 increase of both heart rate and stroke volume further 

 intensifies the need for a more forceful and svnchro- 



