• 作者： 何純郎; 李鎮源
• 作者服務機構： 中央研究院生化研究所; 國立臺灣大學醫學院藥理科
• 中文摘要： 蛇毒磷脂?甲對天竺鼠及大花鼠之輸精管所引起之收縮產生初期短暫及末期持久之抑制。此抑制作用可用增加鈣離子
  濃度或增加電刺激頻率來對抗。在初期抑制期間平滑肌本身對某些假定之神經傳遞物質之敏感度沒有改變，但在末期抑制
  期間有顯著降低。抑制前列腺素合成，使用交感神經拮抗藥物或使用嗎啡拮抗劑均不能改變磷脂?甲引起之抑制效果，但
  膽素脂?抑制劑可對抗而阿多平可加強磷脂?甲產生之抑制作用。由以上結果推論磷脂?甲對輸精管運動傳遞之初期抑制
  作用為腱前作用而末期抑制作用則包括腱前作用及肌毒性作用二種；?活性雖為兩種抑制作用所必需但其他作用機轉，如
  抑制乙醯膽鹼釋放等作用應存在於具腱前神經毒性之?之作用中以引起較強之初期抑制作用。
  卵
• 英文摘要： β-Bungarotoxin, notexin and other phospholipases A purified from Naja nigricollis and Naja najaatra venoms caused an initial transient and a late progressive inhibition of the neurogenic twitch-likeresponse evoked by transmural stimulation of guinea-pig and rat vasa deferentia. Increase of the calciumconcentration in the bathing solution, or of the number of pulses per train of stimulation antagonizedthe inhibitory actions. The sensitivity of the muscle to some putative neurotransmitters such as nore-pinephrine, acetylcholine and ATP was not changed during maximal initial inhibition, while a decreasein response of the muscle to these transmitters was found during maximal late inhibition. By comparison,presynaptically active phospholipases A such as β-bungrotoxin and notexin were more potent in inducinginitial inhibition than non-neurotoxic phospholipases A from Naja nigricollis and Naja naja atra venoms.Release of prostaglandins, endogenous morphine-like substances and the adrenergic neurotransmitter wasnot involved as evidenced by the failure of indomethacin, naloxone and adrenergic blockers to inhibit theaction of β-bungarotoxin. However, the inhibition by β-bungarotoxin was antagonized by eserine andenhanced by atropine. It is concluded that the initial inhibition by phospholipases A of the twitch-likeresponse of the vas deferens is due to a presynaptic action, while the late inhibition may include bothpresynaptic and musculotropic actions. Although enzyme activity is essential for both phases of inhibition,other mechanisms, including inhibition of the cholinergic release mechanism, may also be involved in theinitial inhibitory action of presynaptically active phospholipases A .
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