832 PROFESSOR E. A. SCHAFER AND DR H. J. SCHARLIEB ON THE 
inhibitory path, there is no conclusive evidence that it acts upon the inhibitory end- 
apparatus in the muscular fibres. According to this view the chloroform-heart— 
provided that the dose is insufficient to kill the contractile tissues generally—is in a 
condition of active inhibition rather than in one of passive paralysis. In support of 
this, it may be stated that although, if the chest be opened immediately after death, 
the heart may be completely irresponsive to all forms of stimuli, after a little while it 
often happens that it begins to respond and even exhibits feeble spontaneous contraction, 
hh ut HM Ha hhblebh hile tls Meh intel bey tn EEL (oy yg fqn ial lala sullay 
il 
aaa any AA 
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AN Luly 
i et 
Fic. 20. —Cardiae inhibition produced during chloroform inhalation by dyspnea resulting from accumulation of mucus in 
air-passages, 
A, blood-pressure ; A}, line 1 centimetre below the zero of blood-pressure ; B, costal respiration: C, diaphragmatic 
respiration. The dyspneic condition is shown by the extreme rapidity of the respiratory movements at the left hand of 
tracing. About the middle of the tracing the obstruction to the passage of air was removed, and with the disappearance 
of the dyspncea the heart resumed its normal rate of rhythm. 
although the chloroform has not been washed away. The phenomenon may be explained 
if we assume that the inhibitory end-apparatus has died before the contractile substance 
of the muscular fibres. | | 
To sum up this part of the subject, the conclusions which it appears justifiable to 
draw regarding the causation of death from the effect of chloroform upon the heart 
are as follows :—(1) Death may be caused in the earliest stage of administration by the 
action of the drug upon the cardio-inhibitory centre, the stimulation being reflex. 
