THE CIRCULATION OF THE BLOOD. 



Seat of action 

 of 



Modifications of the Nerve Mechanism of the Heart due to the 

 Physiologic Action of Drugs. The functions of different parts of the 

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

 effects which 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 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- 

 muscle. Fig. 147. In consequence of this, the 

 influence of 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. 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 

 this primary decrease is not so marked and the inference is that the alkaloid 

 primarily stimulates the cardio-inhibitor center and increases its normal 

 function and perhaps the terminal branches of the vagus fibers, the pre-gangli- 



Uqgws nerve . 



Seatofaction 

 of Atropin. 



FIG. 147. DIAGRAM SHOWING 

 THE RELATION OF THE VAGUS TO 

 THE HEART MUSCLE-CELL. 



