1888 - 89 .] Dr T. K. Fraser on Strophanthus hispidus. 
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ventricle very large and full of blood; but yet the interrupting 
systolic contractions were strong, and they completely and deli- 
berately emptied the ventricle of its large accumulation of blood. 
It was found, however, to be extremely difficult, by any adjustment 
of the dose, to produce a standstill of the heart in diastole. The 
heart either recovered altogether, or, in the course of time, the 
diastolic pauses became briefer, and the systole predominated until 
the heart ceased to beat in systolic rigidity. 
The experiments demonstrated that with doses below the mini- 
mum lethal — that is to say, with such doses as would be employed 
in the therapeutic administration of Strophanthus — both the diastole 
and the systole of the heart were rendered more perfect, and that 
the action, therefore, was greatly to increase the working capacity 
of the heart. 
An endeavour was next made to determine upon what structures 
Strophanthus acts in order to produce the changes that follow the 
administration of doses less than lethal. The above experiments 
were repeated after all the nerve connections of the heart with the 
central nervous system had been divided, and also after the vagus 
inhibitory apparatus had been paralysed by atropine; but the action 
that has been described was produced equally well after these 
modifications had been made. It could not, therefore, be explained 
by any action on the central nervous system, nor on the cardio- 
inhibitory influence of the vagus either within or outside the heart. 
As there are several points in the physiology of the heart that yet 
remain unsolved, it would be hazardous to adopt any theoretical 
explanation, without considerable reserve. It, however, appears 
probable that at least two structures are involved in the action of 
Strophanthus on the heart, namely, the muscular fibre itself, and a 
portion of the intra-cardiac nerve apparatus. The action of Stro- 
phanthus upon the muscle of the heart explains the prolonged 
and strengthened systolic contraction, and the ultimate standstill 
in extreme systole, following the administration of lethal and of 
toxic doses. The action upon a part of the intra-cardiac nerve 
apparatus explains the increased amplitude of dilatation and the 
prolonged diastole, which, under nice adjustments of small doses, 
may become permanent, and actually cause a standstill of the heart 
in extreme diastole. The two actions are, in a sense, antagonistic : 
