454 AN AMERICAN TEXT-BOOK OF PHYSIOLOGY. 



is lessened, 1 this diminution in force appearing often before any noticeable 

 change in periodicity. 



The diastolic pressure increases, as is shown by the lower level of the curve 

 gradually rising farther and farther above the atmospheric pressure line. 2 



The volume of blood in the ventricle at the close of diastole is increased. So 

 also is the volume at the close of systole (residual blood) sometimes to such 

 a degree that the volume of the heart at the end of systole may be greater than 

 the volume of the organ at the end of diastole before the vagus was excited. 3 



The output and the input of the ventricle, that is, the quantity of blood dis- 

 charged and received, are both diminished by vagus excitation. 4 



The ventricular tonus } or state of constant slight contraction on which the 

 systolic contractions are superimposed, is also diminished, as is well shown by 

 an experiment of Stefani. 5 In this experiment the pericardial sac is filled with 

 normal saline solution under a pressure just sufficient to prevent the expansion 

 of the heart in diastole. On stimulation of the vagus, the heart dilates fur- 

 ther. A considerably higher pressure is necessary to overcome this dilatation. 

 Stefani finds also that the pressure necessary to prevent diastolic expansion is 

 much greater with intact than with cut vagi. Furthermore, the heart is much 

 more easily distended by the rise of arterial pressure through compression of 

 the aorta when the vagi are severed than when they are intact. Franck has 

 noticed that the walls of the empty ventricle become softer when the vagus is 

 stimulated. 6 



The propagation of the cardiac excitation is more difficult during vagus 

 excitation. 7 Bayliss and Starling 8 demonstrate this on mammalian hearts 

 made to contract by exciting the auricle three or four times per second ; the ven- 

 tricle as a rule responds regularly to every auricular beat. If, then, the vagus 

 is stimulated with a weak induced current, the ventricle may drop every other 

 beat, or may for a short time cease to respond at all to the auricular contrac- 

 tions. The defective propagation is not due to changes in the auricular con- 

 traction, for even an almost inappreciable beat of the auricle can cause the 

 ventricle to contract. Nor is it due to lowered excitability of the ventricle, 

 for the effect described is seen with currents too weak to depress the irrita- 

 bility of the ventricle to an appreciable extent. 



The action of the vagus is accompanied by an electrical variation. This 

 has been shown in the muscular tissue of the resting auricle of the tortoise 9 

 (see Fig. 117). The auricle is cut away from the sinus without injuring the 

 coronary nerve, which in the tortoise passes from the sinus to the auricle and 

 contains the cardiac fibres of the vagus. After this operation the auricle and 

 ventricle remain motionless for a time, and this quiescent period is utilized for 



1 Coats, 1869, p. 187 ; Nuel, 1874, p. 87 ; Gaskell, 1882, p. 1011 ; Heidenhain, 1882, p. 388; 

 Mills, 1885, p. 283. Roy and Adami, 1892, p. 224, are of contrary opinion. 



2 Roy and Adami, 1892, p. 227. 



s Roy and Adami, 1892, p. 218; compare Stefani, 1893, p. 136; 1895, p. 175. 



4 Roy and Adami, 1892, pp. 217, 228. 5 Stefani, 1891, p. 182. 



6 Franck, 1891, p. 486. 7 Gaskell, 1883, p. 100 ; McWilliam, 1888, p. 367. 



Bayliss and Starling, 1892, p. 412. 9 Gaskell, 1887, p. 116 ; 1887, p. 404. 



