The Natural Repertory of Prof. William Nelson

In 1854, Brainard found that venom in blood taken from animals
bitten by crotalidae did not cause coagulation. In 1860, Mitchell found
that the toxic secretion of the Crotalus adamanteus prevented blood from
clotting in vitro. In 1893, Martin cited that the venom of elapidae (an
example of which is the Pseudechis porphyriacus and the Notechis
scutatus) coagulated blood in the vessels when injected at high doses;
but at low doses it rendered the blood unable to coagulate. The venom of
an Indian cobra when tested at any dose was found to inhibit blood
coagulation in vivo and in vitro. This was found to be true in 1895, by D.
D. Cunningham, in 1898, by Stephens and Meyers, in 1904, by Rogers.
In 1901, George Lamb classified a dissertation of venoms according to
their action on plasma. He noted in his article that Russell’s pit viper
venom coagulated citrated plasma. This plasma does not in itself
spontaneously coagulate. F. Noc confirmed these findings, and
discovered that the venom of Asian and African elepidae prevented the
coagulation of citrated plasma to which calcium chloride had been added
for protection.
In 1904, Paul Morawitz proposed that there was an essential element
of the transformation of fibrinogen to fibrin which allows for the
formation of different blood clots. The serozyme of serum acting on the
cytozyme from the platelets caused thrombin to form. Thrombin was
found to be the factor reacting on fibrinogen.
In 1910, Noc presumed that some venom induced coagulation by the
contribution of active thrombin to the blood. J. Mellanby found that
coagulation of these venoms was increased by the addition of calcium.
In 1912, Maurice Arthus put forth the idea that crotalidae acted as if it
contained thrombin, whereas Russell’s pit viper venom accelerated the
transformation of prothrombin to thrombin.
In 1905, C. J. Martin was able to demonstrate that the coagulating
factors of venoms did not pass through dialysis membranes.
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