Harvey A L, Marshall R J, Karlsson E
Toxicon. 1982;20(2):379-96. doi: 10.1016/0041-0101(82)90001-0.
Four polypeptides were isolated by non-exchange chromatography from the crude cardiotoxin fraction of Thailand cobra (Naja naja siamensis) venom. Fraction I and 71 amino acid residues including 1 tryptophan, while fractions, II, III and IV had 60 amino acids and no tryptophan. When tested on isolated skeletal muscle (chick biventer cervicis, chick embryo muscle in culture, guinea pig hemidiaphragm) and cardiac muscle (guinea pig and cat left atria, cat papillary muscle) preparations, fractions II, III and IV, but not fraction I, caused contracture and depolarization. The cardiotoxin-induced contractions could be prevented by pretreatment with raised concentrations of calcium, but were not influenced by a wide range of pharmacological agents which modify nerve-muscle transmission or muscle contractility. The results suggest that cardiotoxins do not act at a specific step in normal excitation-contraction coupling but directly on cell membranes, where they probably cause the formation of pores which result in depolarization and in the influx of calcium.
通过非交换色谱法从泰国眼镜蛇（Naja naja siamensis）毒液的粗制心脏毒素组分中分离出四种多肽。组分I有71个氨基酸残基，包括1个色氨酸，而组分II、III和IV有60个氨基酸且没有色氨酸。当在离体骨骼肌（鸡双头肌、培养的鸡胚肌肉、豚鼠半膈肌）和心肌（豚鼠和猫的左心房、猫乳头肌）标本上进行测试时，组分II、III和IV而非组分I会引起挛缩和去极化。心脏毒素诱导的收缩可通过用升高浓度的钙进行预处理来预防，但不受广泛的改变神经 - 肌肉传递或肌肉收缩性的药理剂的影响。结果表明，心脏毒素并非作用于正常兴奋 - 收缩偶联的特定步骤，而是直接作用于细胞膜，在那里它们可能导致形成孔隙，从而导致去极化和钙内流。
