56 THE MECHANISM OF THE CIRCULATION. 



or dividing the spinal cord, the action of the respiratory pump is greatly 

 diminished, the above experiments cannot be accepted as convincing 

 proof of the tonic action of the accelerator nerves. The best proof of 

 such tonicity is the fact that Timofeew l has kept animals for 

 some time after section of these nerves, and has observed in them 

 a persistent decrease in pulse frequency. The tonicity of the accel- 

 erator centre is normally held in check by the stronger tonicity 

 of the vagus centre. 



The influence of the blood pressure on the frequency of the heart 

 has been studied both 011 the isolated heart and on the heart in situ 

 in the normal conditions of life. The results obtained have been 

 contradictory and confusing, because the effects of the two factors 

 of most importance, namely, the venous filling pressure and the 

 arterial or systolic output pressure, have not been in all the researches 

 carefully and separately analysed. If the inflow or venous pressure 

 be kept constant in the excised heart of the frog or tortoise, in wiiich 

 an artificial circulation has been established, then it is said a variation 

 of the arterial pressure, by increasing the resistance to outflow, produces 

 no effect on the frequency. On the other hand, an increase of venous 

 pressure accelerates the heart. 2 Newell Martin drew the same conclu- 

 sion from observations made on the excised heart of the dog maintained 

 in functional activity by a circulation of defibrinated blood at a constant 

 temperature. 



When the normal circulation is maintained with the heart in situ, and 

 all the cardiac nerves are divided, then by compression of the abdominal 

 aorta or excitation of the peripheral end of the spinal cord or of the 

 splanchnic nerves, the arterial tension is raised, and acceleration of the 

 heart is caused, and the more so in proportion to the suddenness of the 

 change of pressure. This result has been obtained by several observers, 

 and, since all the nerves have been divided, the acceleration must be pro- 

 voked by the direct action of the pressure on the heart itself. 3 By all 

 these methods of raising aortic pressure, not only the filling pressure of the 

 heart, but the temperature of the blood may be changed. The variation 

 in frequency cannot therefore be ascribed with certainty to the rise of 

 arterial tension. Since a high intracardiac pressure has been found by all 

 authors to render vagus inhibition more difficult, we must suppose that 

 either the intracardiac centre of this nerve is hindered from action by 

 the rise of diastolic pressure, or that the part of the cardiac musculature 

 at which the contractions originate is rendered thereby hyper-excitable. 4 

 If all the cardiac nerves be intact, a rise of arterial pressure always slows 

 the heart, and a fall accelerates it. This mechanism, first recognised by 

 Marey, 5 is of great importance, for by its means the constancy of the 

 arterial pressure is maintained. So long as the vagi are intact, the arterial 

 pressure cannot be greatly raised. Whether the centres are normally 

 excited by afferent impulses, or directly by the blood pressure, is not 



1 CentralU.f. PhysioL, Leipzig u. Wien, 1889, S. 235. 



2 Howell and Warfield, Johns Hopkins Univ. Stud. biol. lab., Baltimore, 1881, 

 vol. ii. pp. 235-245 ; Tschirjew, Arch. f. PhysioL, Leipzig, 1877, S. 187; J. M. Ludwig and 

 Luchsinger, Arch. f. d. ges. PhysioL, Bonn, 1881, Bd. xxv. S. 228. 



3 Johanssen, Arch. f. PhysioL. Leipzig, 1891, S. 111. 



4 Sustclrinsky, Untersuch. a. d. physiol. Lab. in Wiirzlmrg, 1868, Bd. iii. S. 165 ; 

 Ludwig and Luchsinger, Arch. f. d. ges. PhysioL, Bonn, 1881, Bd. xxv. S. 235 ; Stewart, 

 "Proc. Phys. Soc." Journ. PhysioL, Cambridge and London, 1891, vol. xii. p. xxx. ; Hill 

 and Barnard, ibid., 1897, vol. xxi. p. 338. 



5 "La circulation <\\\ sang," Paris, 1881, p. 334. 



