EFFECTS OF SNAKE VENOM ON COAGULABILITY OF THE BLOOD 135 



quantity of daboia venom in vitro. This finding threw an entirely different 

 hght on the mechanism of coagulation of the blood plasma in venom toxica- 

 tion. The mere decalcification of the blood or blood plasma by means of 

 sodium citrate brings about, as has been long known, a condition of non- 

 coagulability of the blood so treated, and coagulation can easily be eft'ected 

 by simply adding a sufficient amount of calcium chloride to such fluid. 

 Now, Lamb found that the addition of a small amount of daboia venom, in lieu 

 of CaClj, to such decalcified fluid plasma or blood suffices to produce coagu- 

 lation. Here neither fibrinogen nor paraglobulin is lacking, but an active 

 fibrin ferment is not present on account of the absence of activating salt, 

 calcium chloride, in the mixture. Thus, the function performed by the 

 venom in bringing about such mixture is that of a preformed fibrin ferment. 

 In just what relation this fibrin ferment stands to that of the blood or proto- 

 thrombins or thrombogens is not cleared up. But that it is not supplying 

 these proto-enzymes with calcium chloride is evident from the minute quan- 

 tity required to produce coagulation of the citrate plasmas. In fact, as 

 Martin ^ found later, no relation to the amount of anticoagulating salts con- 

 tained in the blood exists. 



Lamb's extensive paper appeared in 1903, in which this particular phe- 

 nomenon has been dealt with on the ground of further experiments. 



Lamb and Hanna ^ found that the rapid death which follows an injection 

 of daboia venom is invariably caused by extensive intravascular thrombosis, 

 but if the amount of the venom injected is not sufficient to effect this change 

 a negative phase of diminished coagulabihty results, sometimes amounting 

 to complete inhibition of clotting, and that this diminished coagulability is 

 probably an important factor in the production of some of the symptoms 

 which are observed in these cases. 0.000 1 gm. of daboia venom per kilo 

 injected intravenously into a rabbit causes extensive intravascular thrombosis, 

 where 0.0004 grn- is required for a pigeon, when injected subcutaneously. 

 This thrombosis may be confined, if the quantity of venom injected has not 

 been excessive, to the portal veins, the right heart, and the pulmonary arteries; 

 in these cases the blood collected from the other veins, especially from the 

 left heart, remains unclotted, or clots only after a long interval of time, when 

 the clot is very loose and gelatinous. That it is impossible to produce in- 

 creased coagulability and thrombosis by injecting any second quantity of the 

 venom after the negative phase of diminished coagulability had once set in 

 agrees with the observations made by Martin on the Australian snake venoms. 



Lamb ^ next tested the coagulating effect of daboia venom upon the citrated 

 whole blood. While i c.c. of the citrate blood i : 100 required 0.0005 gm., 

 the same quantity of the citrate blood i : 50 required 0.002 gm. of daboia 

 venom to produce coagulation in less than half an hour. 0.0000312 gm. was 



' C. J. Martin. Observations upon fibrin-ferments in the venoms of snakes and the time-relations 



of their action. Jour, of Physiol., igoj, XXXII, 207. 

 2 Lamb and Hanna. Journ. of Path, and Bact., 1902, VIII, i. 

 2 Lamb. On the action of the venoms of the cobra (Naja tripudians) and of the daboia {Daboia russellii) 



on the red blood corpuscles and on the blood plasma. Sci. Mem. Officers, Med. and San. 



Depts. Gov. of India, 1903, new series, No. 4. 



