THE CIRCULATION OF THE BLOOD 



327 



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. The inference, therefore, is 

 that the alkaloid exerts its action upon the re- 

 ceptor substance that intervenes between the 

 nerve endings and the muscle-cells and impairs 

 its power of conducting nerve impulses from 

 the vagus nerve proper to the heart-muscle. 

 Fig. 145. In consequence of this, the influence 

 of the cardio-inhibitor center is cut off and the 

 cardio-accelerator being unopposed in its ac- 

 tivity, 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-accele- 

 rator center. 



Nicotin. After the administration of nicotin in sufficient amounts 

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

 still in diastole for a few seconds, and secondarily increased both in fre- 

 quency and force beyond the normal. If the vagus nerves be first divided 



Seat of action 

 of tficotin 



Vagus nerve. 



FIG. 145. DIAGRAM SHOWING 

 F THE VAGUS TO 



