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HANDBOOK OF PHYSIOLOGY 



CIRCULATION I 



LVED and myocardial segment length remain 

 increased until ventricular systole begins. 



The ability to induce or abolish closure of the 

 mitral valve by varying the activity of the atrium is 

 strong evidence in support of Little's position (io6a) 

 that the atrium may be of importance to valve closure. 

 We believe that the matter can be more simply 

 expressed in terms of the rate of development of a 

 ventriculo-atrial pressure gradient. Increasing the 

 vigor of contraction of atrial systole not only increases 

 the rate of the pressure buildup in the ventricle, but 

 the atrium, like the ventricle, also relaxes more 

 rapidly under sympathetic stimulation, thereby 

 increasing the rate of decline of the pressure in it. 

 These two factors combine to increase the rate of 

 development of the VA pressure gradient and thus 

 promote mitral valve closure. 



G. Summary of Effects of Cardiac Autonomic 

 Nerve Stimulation 



The central nervous system has available direct 

 efferent pathways to the heart over which it can, at 

 any given heart rate, systematically regulate the 

 ventricle's contraction bv either of two means: /) It 

 can control the atrial contraction over a wide range, 

 augmenting tlie atrial contraction by sympathetic 

 stimulation and diminishing it with vagal stimulation. 

 The ventricle is thereby presented with more or less 

 blood at the end of diastole, its end diastolic pressure 

 and fiber length are modified, and a consequent 

 alteration is made in the vigor of its contraction. This 

 can occur in the absence of any change in the con- 

 tractile characteristics of the ventricle. 2) The central 

 nervous system, by way of cardiac sympathetic 

 efferents, can directly cause the ventricle to contract 

 more or less forcefully from whatever end diastolic 

 pressure and fiber length has been obtained. The 

 magnitude of the observed changes is noteworthy. 



A more precise appreciation of the net eff^ect of 

 sympathetic impulses on the heart beating at any 

 given rate is as follows: the more forceful ventricular 

 contraction resulting from .sympathetic stimulation 

 produces more complete systolic emptying and, conse- 

 quently, a lower diastolic impedance to ventricular 

 inflow, i.e., the more complete systolic emptying 

 places the ventricle on a more sensitive portion of its 

 ventricular pressure-length and pressure-volume 

 curve. It is in this circumstance, in which even a small 

 increase in pressure produces a larger fiber length 

 increase, that a more vigorous atrial systole propels 

 blood and elevates ventricular end diastolic pressure. 



It remains to consider the altered timing of events 



which accompanies these phenomena. Reference is 

 made to table i in which it can be seen that sympa- 

 thetic stimulation substantially reduced the total 

 period of the heart's active state (from the beginning 

 of atrial systole to the "relaxation" point, i.e., lowest 

 pressure in diastole). The shortening of the duration 

 of each of the components of the heart's activity during 

 sympathetic stimulation resulted in a longer ventricu- 

 lar diastole, thus allowing both a longer period for 

 inflow and a longer interval during which ventricular 

 relaxation can become complete. The cardiac sympa- 

 thetic nerves may thus be construed, in an important 

 sense, as the guardian of diastole, a view implicit in 

 the experiments of Wiggers in 1927 (128). 



The shorter the diastolic interval, the more im- 

 portant it is for blood to enter the ventricle at an 

 increased rate, thus, not only does the contribution 

 of atrial systole become most important at high heart 

 rates, but it may in addition be expected that the 

 extent to which the atrial systole becomes shorter as 

 well as more forceful will also help to determine the 

 extent to which it can contribute to ventricular filling 

 under these circumstances. 



The alteration of the mechanical events of the 

 cardiac cycle consequent to sympathetic stimulation 

 correlates well with observed electrical phenomena; 

 that is, the increased conduction velocity observed in 

 the atrium, at the atrioventricular node, and in the 

 ventricle (16, 50). There is also a shortening of the 

 total refractory period and, with administered 

 catecholamines, an increased excitability (16). Since 

 increasing the svnchronicity of the ventricle's con- 

 traction results in the production of more stroke work 

 and stroke power from any given LVED pressure 

 (fig. 18), it would appear unwise to attribute the in- 

 creased ventricular work and power produced under 

 sympathetic stimulation solely to a direct effect of 

 the catecholamines on the myocardial fibers without 

 making allowance for the obvious increase in tiie 

 synchronicity with which they contract. This aspect 

 of ventricular performance is construed to be a matter 

 of importance (42a, 105). 



The net eff"ect of efferent vagal impulses, at least 

 with the intensities of vagal stimulation tised in these 

 experiments, was to diminish the \'igor of atrial con- 

 traction; llic\ did not dircctlv modify \-cntricular 

 contractilit\ . 



H. The Xervous Control of l/ir i'rank-Starling Mechanism: 

 Principles of the InncrvatctI Heart 



As a formal means of broadening the basic Frank- 

 Starling relationship and of integrating it with the 



I 



