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TEXT-BOOK OF PHYSIOLOGY 



stimulation of which not only brings about a reflex inhibition of the heart, 

 but also a dilatation of the peripheral arteries and a fall of blood-pressure 

 through a depressive influence on the vaso-motor centers. To this nerve 

 the term depressor has been given. A consideration of the physiologic 

 action of this nerve will be found in the section devoted to the nerve mechan- 

 isms concerned in the maintenance of the blood-pressure. 



Modifications of the Nerve Mechanism of the Heart that Follow 

 Slightly Toxic Doses of Drugs. The functions of different parts of the 

 nerve mechanism of the heart may be demonstrated by an analysis of the 

 effects that follow the administration of slightly toxic doses of the alkaloids 

 of various drugs. The effects can be shown to be due to a stimulation or to 

 a depression of the normal activity of one or more portions of the 

 mechanism. The alkaloid may exert its specific action on the central 

 portions in the medulla, or on the peripheral portions in the heart, or on 

 both simultaneously. The heart-muscle may at the same time be stimu- 

 lated or depressed in its action either in the same or in the opposite 

 direction to that of the nerve mechanism. As a result the heart-beat may 

 be increased or decreased both in rate and force. 



The following examples will illustrate the action of alkaloids in general. 



Atropin. After the administration of atropin in sufficient amounts the 



heart-beat increases in frequency in all animals in which the cardio-inhibitor 



centers exert a steady inhibitor influence over 

 the heart. This is especially true in man and 

 the dog. In animals in which the inhibitor 

 control is slight, as the rabbit and frog, the in- 

 crease in frequency is not very marked. In all 

 animals thus far experimented on after the ad- 

 ministration of atropin, neither stimulation of 

 the trunk of the vagus nor stimulation of the 

 intracardiac ganglia will arrest or even retard 

 the heart-beat. IThe inference, therefore, is 

 that the alkaloid exerts its action upon the gan- 

 glion cells and their terminal branches, impair- 

 ing their chemic integrity and abolishing their 

 normal function, that of conducting nerve im- 

 pulses from the vagus nerve proper to the heart- 



^ F R;A 48 '"~ DlAGRAM V HOWING musd e- Fig. 148. In consequence of this, the 

 THE RELATION OF THE VAGUS TO n c , ,..,.,. . ~. 



THE HEART-MUSCLE CELL. influence or the cardio-inhibitor center is cut off 



and the cardio-accelerator being unopposed in 



its activity, the rate of the beat is increased. After a variable period 

 the heart returns to its normal rate. Stimulation of the vagus is again 

 followed by the usual inhibition. As atropin is partly oxidized, and 

 partly excreted, it is assumed that the nerve terminals have been restored 

 by nutritive forces to their normal condition and their conductivity regained. 

 This having been accomplished the vagus nerve impulses can again reach 

 the heart-muscle and the cardio-inhibitor center is, therefore, enabled to 

 re-establish inhibitor control and antagonize the activity of the cardio- 

 accelerator center. 



Nicotin.Mter the administration of nicotin in sufficient amounts 

 the heart-beat is primarily decreased in frequency even to the point of stand- 



Seat of action 

 of Mcotin 



Sympathetic 



Vagus nerve. 



Seatofactim 

 of Atropin. 



