40 PHARMACOLOGICAL ACTION OF TETRA-ALKYL-AMMONIUM COMPOUNDS. 



animals the slowing of the frequency of the heart was only 10 per cent, less than 

 before the vagi were divided. The greater vagal effect seen in decerebrate animals as 

 compared with anaesthetised animals is mainly due to greater stimulation of the vagal 

 terminations. 



The fall of blood- pressure in anaesthetised animals is mainly, and the early fall of 

 blood-pressure in decerebrate animals is wholly, vagal in origin, and is due to stimula- 

 tion of the vagus endings in the heart ; but the late fall in decerebrate animals and the 

 fall in anaesthetised animals are partly vascular, and appear, contrary to Iodlbauer's 

 statement, to be peripheral, and not central, in nature. This was shown by observing 

 the effects of stimulating a splanchic nerve on the blood-pressure. Thus in a small 

 etherised rabbit (weight 1600 g.) stimulation of the left splanchnic nerve raised the 

 blood-pressure from 52 mm. Hg to 72 mm. Hg. After the injection of 1 mg. tetra- 

 methyl-ammonium chloride stimulation of the nerve with the same stimulus produced 

 no effect until the blood-pressure commenced to rise. Two minutes after the injection 

 it raised the blood-pressure from 35 mm. Hg to 37 mm. Hg ; four minutes after the 

 injection from 44 mm. Hg to 50 mm. Hg ; and six and a half minutes after the injection 

 from 52 mm. Hg to 65 mm. Hg. Whether the effect is due, as Tillie # maintained for 

 curarin, to a depressant influence on the vasoconstrictor nerve endings or upon the 

 muscle of the vessel walls, has not been determined. The perfusion of the blood-vessels 

 of winter frogs has produced, with concentrations down to 1 in 400,000, only contrac- 

 tion, whereas plethysmographic experiments with the intestines of etherised rabbits 

 have shown only dilatation of the vessels. It seems probable that the dilatation of the 

 blood-vessels is one affecting mainly the splanchnic area and is due to a depressant 

 influence on the terminations of the splanchnic nerves. This is probably the main 

 vascular factor contributing to the fall of blood-pressure, but the diminished resistance 

 associated with the paralysed condition of the voluntary muscles may not be without 

 influence. 



The temporary rise in blood-pressure occurring in atropinised decerebrate animals 

 and the rise following the preliminary fall in non-atropinised decerebrate animals are 

 due to stimulation of the vaso-motor centres. The curve of the rise and fall in non- 

 atropinised animals strongly suggests an asphyxial origin, but while there can be no 

 doubt that the increased carbon dioxide tension in the blood caused by the paralysis 

 of the respiration acting upon an excited vaso-motor centre is partly responsible for 

 the rise, it cannot be wholly due to this cause, since it occurred in similar form in 

 animals with an efficient respiration (see fig. 7, in which, however, the rise is relatively 

 small). Moreover, it only followed the earlier injections of an experiment, and was 

 less marked or absent after moderate or large doses had been given. The rise of blood- 

 pressure may therefore be attributed to stimulation of the vaso-motor centres and the 

 subsequent fall to the increasing preponderance of the peripheral action already 

 referred to. 



* Loc. cit., p. 29. 



