26 THE MECHANISM OF THE CIRCULATION. 



equal to - 20 mm. Hg. Evidence of negative pressure is found at the 

 end of systole in the intraventricular pressure curves taken by the 

 sphygmoscope and by the Hii'rthle manometer, or by the method em- 

 ployed by Bayliss and Starling. 



The origin of the negative pressure has received many explanations. 

 It has been supposed that by shortening the long diameter of the heart 

 certain longitudinal muscle bands enlarge its cavity, and produce the 

 diastole. 1 It has also been suggested that if the circular fibres con- 

 tinue to contract after the longitudinal fibres have ceased to shorten the 

 ventricle, these fibres will help to extend and dilate the ventricles. 2 

 When the output of blood takes place the aortic orifice is distended, 

 and this distension must be shared by the adjacent portions of the 

 ventricle (conus arteriosus). 3 Many of the spiral ventricular fibres 

 take origin thence, and it is conceivable that the dilatation of the aorta 

 by the undoing of the spiral of these muscle bands may contribute to 

 the production of diastole. 4 



From the arrangement of the musculature of the heart, it is 

 obvious that a great part of the muscle must be strongly compressed 

 by the contraction of the remainder. The columnar carneee will, 

 for example, be driven like so many elastic cushions against one 

 another. So soon as contraction ceases this will lead to an elastic 

 rebound of the walls. Again, in diastole, the walls of the heart 

 become like those of a flaccid bag, and under the influence of gravity 

 fall apart. Thus, if an excised heart be placed in a vessel of water, 

 and be rhythmically squeezed, the fluid can be pumped out from the 

 aorta and pulmonary orifices, for, after each compression, the heart, in 

 consequence of the elastic rebound and the force of gravity, relaxes. 

 Goltz and Gaule obtained, after sudden compression, a negative 

 pressure in the empty heart. This must have been entirely brought 

 about by the elastic rebound, following on the removal of the com- 

 pressing agent. 



The flow of blood in the coronary arteries may be another cause of 

 diastole. Chauveau and Iiebatel 5 have proved that the blood is driven 

 back towards the aorta and out of the coronary system during systole, 

 while the current once more sets into those vessels at the end of 

 systole. It has been demonstrated by Donders 6 that a high-pressure 

 injection of these arteries in the excised heart produces a negative 

 pressure in the ventricular cavity, and that this pressure by expand- 

 ing the wall aids in the causation of diastole. In the same way 

 as the distension of a hollow curved and elastic tube opens out the 

 curvature, so the injection of the coronary arteries dilates the heart. 

 If this be the true cause of the negative pressure, some relationship 

 should be found between its amount and the height of the aortic 

 pressure. 



Moens urged that the negative pressure is systolic, and not diastolic in 

 time, and endeavoured to explain its origin by the following experiment : 7 — 



1 Spring, Mem. Acad. roy. de mid. dc Belg., Bruxelles, 1861, tome xxxiii. p. 78. 



2 v. Frey, "Die Untersuch. des Pulses." Berlin, 1892, S. 94. 



3 Mink, Oentralbl.f. Physiol., Leipzig u. Wien, 1890, S. 568. 



4 Gaule, ibid., S. 617. 



5 Rebate], " Keen, expt'r. snr la circ. dans les art. coronaires," These de Paris, 1872. 



6 "Physiol, des Mensch.," 1859, Bd. ii. S. 42. 



7 Arch./, d. gcs. Physiol., Bonn, 1879, Bd. xx. S. 529. 



