320 THE NERVOUS REGULATION OF THE HEART 



potassium which, on being set free, temporarily inhibits the systolic 

 processes. Several facts might be cited in support of this view. Thus 

 it has been shown that this salt, when added in certain amounts to the 

 perfusion fluid, gives rise to a diastolic arrest of the heart which closely 

 resembles that resulting from the excitation of the vagus. Under 

 these conditions, the inhibitor power of the vagus may be restored at 

 any time by simply removing the excess of the potassium. Use is 

 also made of the observation that this salt exists in large quantities 

 in cardiac muscle and that a heart gives off unusual amounts of dif- 

 fusible potassium whenever it is inhibited with the aid of the vagus. 

 In accordance with the aforesaid theory, it is held that the vagus 

 impulses incite a cleavage of some kind of the combined tissue-potas- 

 sium so that some of it is set free in a soluble form. The subsequent 

 interaction between the potassium thus rendered available and the 

 cells of the heart, occurs chiefly in that region in which the beat origi- 

 nates. The latter amplification of this theory serves to explain the 

 fact that an inhibited . heart retains its irritability toward direct 

 stimulation. Hemmeter 1 has attempted to test this theory experi- 

 mentally by analysis of the ash of the blood contained in inhibited 

 hearts, as well as by arresting the activity of a normally beating heart 

 by supplying it directly with the blood of an inhibited organ. The 

 results of these experiments, however, have failed to substantiate 

 the preceding contentions so that they cannot be regarded as h'aving 

 been removed from the realm of a mere hypothesis. 



The Result of the Inhibition. It may be inferred from the above 

 discussion that the inhibitor mechanism does not cease its activity at 

 any time. Impulses are discharged by the cardiac center with rhythmic 

 regularity. They are then conducted to the heart, where they tend 

 to hold this organ in check. In this way, the automatic activity 

 of this organ is subjected to a constant restraint with the result that a 

 normal frequency and amplitude of contraction is obtained. But 

 whenever this check is removed, the accelerator influences gain the upper 

 hand and finally produce an augmentor effect. In an experimental 

 way these inhibitor impulses may be prevented from reaching the 

 periphery by simply dividing the conducting path (Fig. 169). Obvi- 

 ously, therefore, the section of the vagi nerves must lead to an in- 

 crease in the rate of the heart, and naturally, this increase must be- 

 come the more evident, the less the original frequency of contraction. 



These constant discharges from the inhibitor center may also be 

 blocked by cooling the vagi nerves at any point of their course, or by 

 moistening them with an agent which diminishes their conductivity, 

 for example, with magnesium sulphate. In this connection it should 

 be emphasized again that the inhibitor power of these nerves is not 

 equal and hence, their division is usually followed by varying degrees 

 of acceleration. Thus, it may happen that the section of only one of 

 the vagi nerves produces scarcely any acceleration, while the division 



1 Biochem. Zeitschr., 1914, 63. 



