心脏毒素和磷脂酶A在眼镜蛇毒诱导的神经传导阻滞和骨骼肌去极化中的作用。
Role of cardiotoxin and phospholipase A in the blockade of nerve conduction and depolarization of skeletal muscle induced by cobra venom.
作者信息
Chang C C, Chuang S T, Lee C Y, Wei J W
出版信息
Br J Pharmacol. 1972 Apr;44(4):752-64. doi: 10.1111/j.1476-5381.1972.tb07313.x.
Abstract
- The effects of phospholipase A (PhA), cardiotoxin (CTX) and neurotoxin (cobrotoxin) isolated from Formosan cobra (Naja naja atra) venom on conduction of the rat phrenic nerve and membrane potential of the rat diaphragm were studied.2. Phospholipase A, lysolecithin and cobrotoxin were without effect on the axonal conduction. Cardiotoxin was the only active agent in cobra venom, but it was less potent than the crude venom.3. The blocking action of cardiotoxin was markedly accelerated by the simultaneous administration of phospholipase A. However, the minimum effective concentration of cardiotoxin (100 mug/ml), was not decreased by phospholipase A. Pretreatment of the nerve with phospholipase A, followed by washout, did not alter the activity of cardiotoxin.4. Cardiotoxin (3 mug/ml) completely depolarized the membrane of superficial muscle fibres within 60 min, being 3 times more potent than the crude venom. Phospholipase A, on the other hand, needed a dose 30 times higher and a prolonged period of incubation to induce depolarization of similar extent. Cobrotoxin was without effect on membrane potentials.5. CaCl(2) (10 mM) effectively antagonized the nerve blocking as well as the depolarizing effect of the crude venom, cardiotoxin or cardiotoxin plus phospholipase A. By contrast, the slow depolarizing effect of phospholipase A was enhanced by high concentrations of calcium.6. Cardiotoxic fractions of Indian cobra venom affected both nerve conduction and diaphragm membrane potential in exactly the same way as cardiotoxin. Toxin A of the same venom was without effect.7. It is concluded that the active agent in cobra venoms either on axonal conduction or on muscle membrane is cardiotoxin. The synergistic effect of phospholipase A on cardiotoxin appears to be due to acceleration rather than potentiation of its action. The mechanism of action of cardiotoxin and its synergism by phospholipase A are discussed.
摘要
研究了从台湾眼镜蛇（眼镜蛇）毒液中分离出的磷脂酶A（PhA）、心脏毒素（CTX）和神经毒素（眼镜蛇毒素）对大鼠膈神经传导和大鼠膈肌膜电位的影响。
磷脂酶A、溶血卵磷脂和眼镜蛇毒素对轴突传导无影响。心脏毒素是眼镜蛇毒液中的唯一活性剂，但效力低于粗毒液。
同时给予磷脂酶A可显著加速心脏毒素的阻断作用。然而，磷脂酶A并未降低心脏毒素的最小有效浓度（100微克/毫升）。用磷脂酶A预处理神经，然后冲洗，并未改变心脏毒素的活性。
心脏毒素（3微克/毫升）在60分钟内使表层肌纤维膜完全去极化，效力是粗毒液的3倍。另一方面，磷脂酶A需要高30倍的剂量和延长的孵育时间才能诱导相似程度的去极化。眼镜蛇毒素对膜电位无影响。
CaCl₂（10毫摩尔）有效地拮抗了粗毒液、心脏毒素或心脏毒素加磷脂酶A的神经阻断和去极化作用。相比之下，高浓度钙增强了磷脂酶A的缓慢去极化作用。
印度眼镜蛇毒液的心脏毒性部分对神经传导和膈肌膜电位的影响与心脏毒素完全相同。同一毒液的毒素A无影响。
得出结论，眼镜蛇毒液中对轴突传导或肌肉膜起作用的活性剂是心脏毒素。磷脂酶A对心脏毒素的协同作用似乎是由于其作用的加速而非增强。讨论了心脏毒素的作用机制及其与磷脂酶A的协同作用。
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