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Pharmacological studies of the venom from the scorpion Buthus minax (L. Koch)
Toxicon, 1973, Vol. 11, pp. 119-127 . Pergamon Press. Printed in Great Britain
ABSTRACTS FOR CARD INDEXES Fractionation and lethality of venom from the scorpion Buthus minax (L . Koch) : M. F. El-Asmar, O. H. Osman and M. Ismail, Toxicon, 1973, 11, 3. (From Departments of Biochemistry and Pharmacology, Faculty of Medicine, University of Khartoum, Sudan) . Abstract-The venom from the scorpion Buthus »linax was fractionated into seven components by cellulose acetate electrophoresis, using acetate buffer pH 4~2. Two of the electrophoretic fractions were lethal to mice, while the crude venom and one of the lethal fractions increased the amplitude of the twitches of the rat phrenic nerve-diaphragm preparation ; the other lethal fraction produced a blocking effect. 5-Hydroxytryptamine was not demonstrated in thevenom ; however, paper chromatography of the dialysate from, or the acetone extract of the crude venom revealed the presence of 18 ninhydrin stainable spots and two u.v. fluorescent spots. Thirteen of the ninhydrin spotswere identified as amino acids. Immunological studies of scorpion (Buthus minax, L. Koch) venom : M. F. Er.-ÀSIKAR, M. ISMAIL and O. H. OSMAN, Toxicon, 1973, 11, 9. (Departments of Biochemistry and Pharmacology, University of Khartoum, Sudan) . Abstract-An antivenom was prepared for Buthus minax venom by hyper-immunizing rabbits. The antivenom protected the rats against the hypertensive effect of the venom but it did not prevent the respiratory arrest . The antivenom also protected the rats against several times the lethal dose. In mice the antivenom completely protected the animals against doses of the venom equal to the 1n but no such protection was achieved when doses equal to 5 times the >.n were ir>ljected . Using the immunodiffusion and immunoelectrophoresis techniques, four precipitin bands were revealed with B. mirtax venom but only one band was formed with Lelurusquinquestriatus venom and it was not identical with any of the bands formed with B. mlnax. A cross-reaction occurred between the band formed with L. qulrrquestriatus venom and one of the bands formed with B. minax venom. The antivenom did not prevent the hypertensive or the lethal actions of L. quiliquGrtrlatus venom. In view of the abundance of B. minax in the Sudan and other neighbouring countries and the absence of an antivenom for B. minax in the polyvalent antiscorpion venoms, it is suggested that the B, mlnax antivenom ought to be included in the polyvalent scorpion antivenin. Pharmacological studies of the venom from the scorpion Buthus minax (L. Koch) : M. ISIHAU., O. H. OSMAN and M. F. E1.-Asn1Ax, Toxicon, 1973, 11, 15. (Departments of Pharmacology and Biochemistry, University of Khartoum, Sudan) . A6etract-The venom from the scorpion
Buthus minax produced a positive inotropic effect on isolated rabbit and guinea pig hearts but no alteration in rate . The cardiac stimulant action was blocked by propranolol and was absent in reserpinized hearts, indicating the possibility of an indirect action of the venom, probably through the release of catecholamines. In the reserpinized hearts, and in normal hearts after propranolol treatment, the venom produced bradycardia which was blocked by atropine. The venom produced a marked hypertensive effect in cats, dogs, rats and guinea pigs, which was blocked by tolazoline and phenoxybenzamine. In cats and rats the hypertensive effect was preceded by brief hypotension which was partially blocked by atropine . The venom markedly decreased the rate of flow in the perfused hindquarter of the rat and moderately increased capillary permeability . It stimulated the rabbit intestine and guinea pig ileum, an action which was largely blocked by atropine. It increased the size of twitches in the isolated, indirectly stimulated, phrenic hemidiaphragm of the rat and contracted the rectos abdominis muscle of the frog. The latter effect was blocked by tubocurarine. The venom decreased the respiration rate in cats and dogs but caused a slight increase in depth. The decrease in respiration rate was blocked by carotid sinus denervation. It is postulated that the venom stimulates both the sympathetic and parasympathetic systems. TOXICON 1973 VoJ. II .
ABSTRACTS FOR CARD INDEXES Fractionation and lethality of venom from the scorpion Buthus minax (L . Koch) : M. F. El-Asmar, O. H. Osman and M. Ismail, Toxicon, 1973, 11, 3. (From Departments of Biochemistry and Pharmacology, Faculty of Medicine, University of Khartoum, Sudan) . Abstract-The venom from the scorpion Buthus »linax was fractionated into seven components by cellulose acetate electrophoresis, using acetate buffer pH 4~2. Two of the electrophoretic fractions were lethal to mice, while the crude venom and one of the lethal fractions increased the amplitude of the twitches of the rat phrenic nerve-diaphragm preparation ; the other lethal fraction produced a blocking effect. 5-Hydroxytryptamine was not demonstrated in thevenom ; however, paper chromatography of the dialysate from, or the acetone extract of the crude venom revealed the presence of 18 ninhydrin stainable spots and two u.v. fluorescent spots. Thirteen of the ninhydrin spotswere identified as amino acids. Immunological studies of scorpion (Buthus minax, L. Koch) venom : M. F. Er.-ÀSIKAR, M. ISMAIL and O. H. OSMAN, Toxicon, 1973, 11, 9. (Departments of Biochemistry and Pharmacology, University of Khartoum, Sudan) . Abstract-An antivenom was prepared for Buthus minax venom by hyper-immunizing rabbits. The antivenom protected the rats against the hypertensive effect of the venom but it did not prevent the respiratory arrest . The antivenom also protected the rats against several times the lethal dose. In mice the antivenom completely protected the animals against doses of the venom equal to the 1n but no such protection was achieved when doses equal to 5 times the >.n were ir>ljected . Using the immunodiffusion and immunoelectrophoresis techniques, four precipitin bands were revealed with B. mirtax venom but only one band was formed with Lelurusquinquestriatus venom and it was not identical with any of the bands formed with B. mlnax. A cross-reaction occurred between the band formed with L. qulrrquestriatus venom and one of the bands formed with B. minax venom. The antivenom did not prevent the hypertensive or the lethal actions of L. quiliquGrtrlatus venom. In view of the abundance of B. minax in the Sudan and other neighbouring countries and the absence of an antivenom for B. minax in the polyvalent antiscorpion venoms, it is suggested that the B, mlnax antivenom ought to be included in the polyvalent scorpion antivenin. Pharmacological studies of the venom from the scorpion Buthus minax (L. Koch) : M. ISIHAU., O. H. OSMAN and M. F. E1.-Asn1Ax, Toxicon, 1973, 11, 15. (Departments of Pharmacology and Biochemistry, University of Khartoum, Sudan) . A6etract-The venom from the scorpion
Buthus minax produced a positive inotropic effect on isolated rabbit and guinea pig hearts but no alteration in rate . The cardiac stimulant action was blocked by propranolol and was absent in reserpinized hearts, indicating the possibility of an indirect action of the venom, probably through the release of catecholamines. In the reserpinized hearts, and in normal hearts after propranolol treatment, the venom produced bradycardia which was blocked by atropine. The venom produced a marked hypertensive effect in cats, dogs, rats and guinea pigs, which was blocked by tolazoline and phenoxybenzamine. In cats and rats the hypertensive effect was preceded by brief hypotension which was partially blocked by atropine . The venom markedly decreased the rate of flow in the perfused hindquarter of the rat and moderately increased capillary permeability . It stimulated the rabbit intestine and guinea pig ileum, an action which was largely blocked by atropine. It increased the size of twitches in the isolated, indirectly stimulated, phrenic hemidiaphragm of the rat and contracted the rectos abdominis muscle of the frog. The latter effect was blocked by tubocurarine. The venom decreased the respiration rate in cats and dogs but caused a slight increase in depth. The decrease in respiration rate was blocked by carotid sinus denervation. It is postulated that the venom stimulates both the sympathetic and parasympathetic systems. TOXICON 1973 VoJ. II .