• 作者： 蕭水銀；符文美；李鎮源
• 作者服務機構： 國立臺灣大學醫學院藥理學研究所
• 中文摘要： 心?毒素可使蛙心的心縮力增?，高濃度的毒素使心跳停止於收縮期，本研究的目的擬改變陽離子濃度或藥物如Verapamil及河豚毒素對心?毒素之作用所產生的影響，並與其對毛地?素及原藜蘆素之作用之影響加以比較研究，以期闡明心 ?毒素之作用機構。結果發現心?毒素之作用受離子或藥物之影響與毛地?素或原藜蘆素完全不同，如低鈣增?心臟毒素之作用，但對毛地?素及原藜蘆素有抑制作用；而高鈣對這三種?心劑作用之影響恰與低鈣相反；高鉀只輕微抑制心臟毒素及 原藜蘆素之作用，但明顯的抑制毛地?素的作用；低鈉及河豚毒素對心?毒素之作用稍增或不影響，但對原藜蘆素有抑制作用，Verapamil本身是一種心舒劑，選擇性的抑制鈣離子進入細胞內，因而抑制心縮力。當Verapamil存在時，心臟毒素的作用變得更明顯。由此結果以及鈣離子對心?毒素具有選擇性的對抗作用，推論心?毒素對蛙心的作用可能與其對骨骼肌的作用一樣，先經由釋放細胞膜之鈣離子的結果，而與毛地黃素抑制Na+-K+-ATPase活性及原藜蘆素增加細胞膜鈉離子 滲透性的結果才增加心縮力的作用機構迥然不同。
• 英文摘要： The action of cardiotoxin, ouabain and protoveratrine A on the isolated perfused frog heart was comparatively studied and their interactions with cations, verapamil and tetrodotoxin were carried out in order to shed light on the mechanism of action of cardiotoxin. Similar to ouabain and protoveratrine A, cardiotoxin can induce a positive inotropic effect as well as contracture and cardiac arrest. At concentrations lower than 3 μM, cardiotoxin was more potent than ouabain in inducing a positive inotropic effect. At higher concentrations, cardiotoxin induced contracture and cardiac arrest. Although changes of cation concentrations (low or high Ca++, low Na+ and high K+) reduced the contractile force and heart rate, a new steady state reached within 5 min. Exceptionally, tetro-dotoxin did not affect the contractile force but induced cardiac arrhythmia. Treatment of the heart with low Ca++ for 20 min potentiated cardiotoxin and ouabain while verapamil potentiated cardiotoxin and protoveratrine A in inducing a positive inotropic effect. Interactions of cardiotoxin with cations, verapamil and tetrodotoxin in the frog heart in terms of inducing cardiac arrest were different from those of ouabain and protoveratrine A. Low Ca++ potentiated cardiotoxin but antagonized ouabain and protoveratrine A. On the contrary, high Ca++ antagonized cardiotoxin but potentiated ouabain. Low Na+ potentiated cardiotoxin moderately. High K+ antagonized ouabain markedly. Both verapamil and tetrodotoxin inhibited protoveratrine A only. All of these findings suggest that cardiotoxin exerted its effect on the heart by a mechanism different from that of ouabain and protoveratrine A. In view of the specific antagonism by Ca++, cardiotoxin probably exerted its cardiac action by releasing membrane-bound Ca++ as it was postulated in the skeletal muscle.
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