Tiger Snake Venom Research Articles

Coagulant activity of tiger snake (Notechis scutatus scutatus) venom.

TIGER snake venom has the ability to clot blood. Holden1 and Blomback2 have presented evidence that prothrombin, Factor V and calcium ions are required for the venom to convert fibrinogen to fibrin. We have studied the action of this venom on several purified clotting factors. As the crude venom was used in these experiments, the results obtained may arise from more than one active constituent present in the venom.

Effects of venoms on the squid giant axon

Tiger snake venom was the most potent of 9 venoms tested in its ability to render the squid giant axon reactive to d-tubocurarine (curare); its potency in this regard is about equal to that of cottonmouth moccasin venom which was the most potent venom previously found. Timber rattlesnake, sea snake, scorpion, and yellow hornet venom and a component from cobra venom referred to as neurotoxin were completely inactive. These results are in agreement with the hypothesis that phospholipase A is the component of venoms responsible for reducing the permeability barriers, surrounding the excitable membrane of squid axons, to acetylcholine (ACh) and curare, thereby allowing them to interact with the ACh receptors in the conducting membrane and block electrical activity. Neuraminidase, saponin, arsenite, veratridine, NN-dimethylformamide, dimethyl sulfoxide and histamine failed to render the axon responsive to the action of curare. Venoms and the cationic detergent cetyltrimethylammonium remain as the only compounds found so far which are effective in altering the structural permeability barriers surrounding the excitable membrane of the squid giant axon.

BIOLOGIC RELATIONSHIP OF ENDOTOXIN AND OTHER TOXIC PROTEINS. IV. EFFECT OF HEPARIN ON ENDOTOXIN-INDUCED HYPERSUSCEPTIBILITY TO SNAKE VENOMS.

Summary1. Heparin in intravenous doses of 10 to 100 mg counteracted the immediate lethal effects of Russell's viper venom and tiger snake venom in rabbits, but did not prevent the deaths of the animals from the delayed toxic effects of the venom. 2. Heparin in the same intravenous doses did not interfere with the early death that occurs in endotoxin-treated rabbits given Russell's viper venom or tiger snake venom. 3. Heparin neither increased nor decreased the toxicity of moccasin venom in rabbits. 4. Finally, heparin did not affect the EIHS to Agkistrodon piscivorus venom when it was administered before endotoxin, shortly after endotoxin, or just before venom challenge.The authors are greatly indebted to Miss Ann E. Gabrielsen for valuable criticism and advice in the preparation and editing of this work. They also appreciate the technical assistance of Messrs. Nils Rune Forsen, Thomas K. Norrie and Gene Monson.

Tiger-Snake Venom in Treatment of Accessible Hemorrhage

Tiger-Snake Venom in Treatment of Accessible Hemorrhage

Antagonism between the actions of staphylococcal toxin and tiger snake venom.

EARLY work on the mode of action of staphylococcal toxin showed that in rabbits it constricts the pulmonary and coronary blood vessels1. More recently it was found that vascular spasm and alteration in capillary permeability are factors largely responsible for such characteristic toxic lesions as renal cortical necrosis and dermonecrosis in rabbits2. Such effects are readily demonstrated when staphylococcal alpha toxin is injected subcutaneously into the mouse, and the animal is killed after an appropriate interval, if a solution of the dye, pontamine sky blue, has been injected intravenously a few minutes beforehand. In the centre of the lesion is seen an area, 10 mm. or more in diameter, which, although hyper-aemic, completely fails to stain; surrounding this central area which does not take the dye is a narrow zone stained an intense blue.

STUDIES ON THE CHEMICAL NATURE OF THE ANTIFERMENTING PRINCIPLE IN BLACK TIGER SNAKE VENOM

The anti‐fermenting principle in black tiger snake venom is destroyed by heat to a large extent, and is almost completely destroyed by precipitation with methyl alcohol, ethyl alcohol, and acetone. It does not dialyse through cellophane membranes. Ammonium sulphate and sodium chloride precipitate it partially from aqueous solutions. It is completely destroyed by alkali, but is relatively stable in acid solutions. Exposure to the air in neutral solution for several days does not appreciably affect the activity. Pepsin destroys it rapidly.These properties in our opinion show conclusively that the active principle is a protein. Granting the correctness of this conclusion, the fact that it acts in very great dilutions suggests that the inhibitory effect on the fermenting enzyme complex is itself of enzymatic nature.

A New Method of Determining Plasma Fibrin

The usual method of estimating the fibrinogen content of the blood is by recalcifying the oxalated plasma in order to convert the fibrinogen into fibrin. The quantity of fibrin precipitated is then determined by the Kjeldahl, the gravimetric, the colorimetric, or the refractometric methods. The method of determining plasma fibrin presented here is based on the coagulant activity of certain types of snake venom. Martin was the first to demonstrate the striking activity of the venoms of certain Australian snakes in causing coagulation of blood both in vivo and in vitro. Lamb found that minute doses of such venoms could also coagulate in vitro blood which had lost the capacity for spontaneous coagulation on account of the addition of citrates, oxalates or fluorides. Among the venoms noted for their coagulating action are those of the following snakes: Notechis scutatis (tiger snake), Pseudechis porphyriacus (black snake), Echis carinata (phoorsa) and Viperi russelli (daboia). The former 2 species are found in Australia and the latter 2 in India. In addition, certain species of the Lachesis group of vipers are known to exhibit this property. In the present investigation, tiger snake venom, which apparently has the most powerful coagulating action, was used. In all probability, the venoms of the other species mentioned can also be used. The actual technique of estimating the concentration of fibrinogen (as fibrin) in the plasma with the aid of tiger snake venom is as follows: One cc. of oxalated plasma is diluted 25 to 30 times with normal saline solution. (The quantity of powdered potassium oxalate used for collecting the blood need not be accurately measured.) To the diluted plasma is added 0.3 cc. of a 1 to 5,000 dilution of dried tiger snake venom in normal saline.