1. 本實驗的目的擬以白兔肌漿網膜為模型，研究心臟毒素對細胞膜的作用，並希望藉此探討心臟毒素的作用機構。
2. 心臟毒素抑制白兔骨骼肌肌漿網膜儲存鈣離子的作用，此抑制作用可為外加卵磷脂和鈣離子所對抗。
3. 心臟毒素促進白兔骨骼肌肌漿網膜的Ca++－Mg++－ATPase的活性，此促進作用亦可為鈣離子，鎂離子，卵磷脂和神經苷脂類所對抗。
4. 魚精蛋白及聚離胺酸對肌漿網儲存鈣離子，Ca++－Mg++－ATPase活性的作用與心臟毒素的結果相同。
5. 以上結果顯示，心臟毒素、魚精蛋白及聚離胺酸非直接抑制肌漿網攝取鈣離子，可能是經由其帶正電的鹼性基與膜上磷脂質的負電結合，改變肌漿網膜的構造，降低肌漿網儲存鈣離子的能力，此作用可為鈣離子所對抗；此結果與心臟毒素之許多藥理作用可為鈣離子對抗相符合，至於心臟毒素在肌漿網膜上這些作用與引起骨骼肌攣縮作用的關係，討論之。 1.The purpose of this study is to use sarcoplasmic reticulum (SR) as a model of the biological membrane for the exploration of action of cardiotoxin (CTX).
2.CTX inhibits 45 Ca++ uptake of SR of the rabbit skeletal muscle. The inhibition by CTX can be antagonized by both lecithin and Ca++
3.CTX activiate Ca++-Mg ++-ATPase activity of SR. Ca++, Mg++, lecithin and ganglioside antagonize the activation by CTX of Ca++-Mg++-ATPase.
4.The effects of protamine and polylysine on 45 Ca++ uptake and Ca++-Mg++-ATPase are similar with those of CTX.
5. These results indicate that CTX, protamine and polylysine inhibit Ca++ accumulation by SR rather than inhibit Ca++ uptake of SR by interacting their positive charges with phospholipids of the SR membrane. These ionic interactions result in the change of conformation of the SR membrane and can be interrupted by Ca++. The implication of this result in the relation with CTX-induced contracture of the skeletal muscle is discussed.
