The foregoing experiments point to certain
definite conclusions which may be summed up in a
(1). The entihaercolytic action of arsenic
is manifested, and is demonstrable, when the
drug is administered in ordinary therapeutic
doses. It occurs after the exhibition of arsenic
by the mouth, by subcutaneous injection, and by
(2) . The antihaemolytic effect is rapidly
produced, but most rapidly when the arsenic is
administered by intravenous injection, being very
pronounced within l5 minutes after the injection.
(3). In every case, there is, following
the chase of increased resistance, e period
in which the resistance of the red blood corpuscles is below normal, the explanation offered
being that the arsenic, during the process of
excretion, takes with it in combination some part
of the cell constituents (lecithin r), thus
rendering the cells less perfect and more easily
destroyed by the haemolytic agent.
(4). The increase of resistance is as
great and as lasting with therapeutic doses as
with large toxic doses; the greatest effect
being obtained by the intravenous injection of
the maximum therapeutic dose.
(5) . After prolonged administration of
arseric, the ree' blood corpuscles lose the pro - rerty of increased resistance, and finally no
longer react, in that respect, to the subsequent
treatment with the drug.
(6) . Sodium Arsenite has a much more
powerful effect in producing the antihaemolytic
action than Salvarsan (No. 606), and in the
minute dose required produces no marked toxic
(7) In the condition of paroxysmal
haemoglobinuria there is no evidence of a lessened resistance of the red blood, corpuscles.
(8) . Arsenic is not capable, even in
solution of 1 in l000, of preventing the lysis
of red blood corpuscles by haemolytic blood sera.
The significance of this fact is in keeping
with the theory that arsenic produces its antihaemolytic action by a chemical combination with
the constituents of the red cells..