purgative on the intestinal canal.

Pilcher and Sollmann [Footnote: Pilcher and Sollmann: Jour.
Pharmacol. and Exper. Therap., 1913, vi, 323.] have shown that the
fall of blood pressure after the administration of nitrites is
mostly due to the action of these drugs on the peripheral vessels.
Chloroform, of course, depressed the vasomotor center, but ether had
no effect on this center, or slightly stimulated it. Such
stimulation, however, Pilcher and Sollmann believe may be secondary
to asphyxia. Nicotin they found to cause intense stimulation of the
vasomotor center. Ergot and hydrastis and its alkaloids seem to have
no effect on the vasomotor center. Strophanthus acted on this center
only moderately, and digitalis very slightly, if at all. Camphor in
doses large enough to cause convulsions stimulated the vasomotor
center. In smaller doses it generally stimulated the center
moderately, but not always. Even when this center was stimulated,
however, the camphor did not necessarily increase the blood
pressure. The rise in blood pressure from epinephrin is due entirely
to its action on the peripheral blood vessels and the heart. It has
no action on the vasomotor center. They found that strychnin in
large doses may stimulate the vasomotor center moderately, but
usually it did not act on this center unless the patient was
asphyxiated; then it acted intensely. The conclusion to be drawn
from their experiments is that when there is asphyxia, increased
venous pressure, and also a rising blood pressure from the
stimulation of carbon dioxid, strychnin is contraindicated.

It should be recognized that digitalis very frequently not only does
not raise blood pressure, but also may lower it; especially in
aortic insufficiency and when there is cyanosis. Even with some