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  • 1990-1994
  • 1965-1969  (1)
  • Cell membrane-Depolarization  (1)
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  • 1990-1994
  • 1965-1969  (1)
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  • 1
    Electronic Resource
    Electronic Resource
    Springer
    Naunyn-Schmiedeberg's archives of pharmacology 259 (1968), S. 360-374 
    ISSN: 1432-1912
    Keywords: Cobra venom ; Cardiotoxin ; Muscle ; Cell membrane-Depolarization ; Cardiovascular system-ECG ; Kobragift ; Cardiotoxin ; Muskel ; Zellmembran ; Depolarisation ; Zirkulation-EKG
    Source: Springer Online Journal Archives 1860-2000
    Topics: Medicine
    Notes: Summary Lyophilized venom of Naja naja atra was fractionated on column of CM-Sephadex C-50 into 12 fractions by gradient elution with ammonium acetate buffer at pH 5–7. Among them 5 fractions (V–IX) were found to be neurotoxic and 3 (X–XII) to be cardiotoxic. Intraperitoneal LD50 in mice was 0.074 µg/g for the major neurotoxic component (Fr. VIII) and 1.48 µg/g for the major cardiotoxic one (Fr. XII). The latter, named cardiotoxin, caused contracture followed by paralysis of the chick biventer cervicis muscle, the frog sartorius muscle and the rat diaphragm, in consequence of irreversible depolarization of the cell membrane. In the absence of calcium no contracture was produced, although the depolarizing effect remained unchanged. Cardiotoxin caused systolic arrest of the isolated frog heart and the rat atrium, probably by the same mechanism. It also caused a contraction of the guinea-pig ileum, which was largely antagonized by atropine but not by hexamethonium or pyribenzamine. In the presence of cardiotoxin the responses of the ileum to nicotine and to submaximal transmural stimulation were first enhanced and then depressed. Cardiotoxin caused vasoconstriction of the rabbit ear vessels, which was largely antagonized by phenoxybenzamine. It also produced local irritation of the rabbit conjunctiva and the rat hind paw. In cats, cardiotoxin caused a fall in the systolic pressure much more than the diastolic pressure, accompanied by various ECG changes, such as P–R interval prolongation, decreased amplitude of QRS, S–T and T changes, ventricular premature beats, complete A–V block, idioventricular rhythm etc. It is concluded that cardiotoxin acts on various kinds of cells in the animal body, causing irreversible depolarization of the cell membrane and consequently impairing its functions.
    Type of Medium: Electronic Resource
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