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用蛙胫前肌小束为材料，研究了提高胞外钾［Ｋ＋］Ｏ对咖啡因挛缩的作用。［Ｋ＋］Ｏ从２ｍｍｏｌ／Ｌ提高到１０或２５ｍｍｏｌ／Ｌ，由３ｍｍｏｌ／Ｌ咖啡因引起的挛缩明显增强。以ＰＫＣ／ＰＣ（ＰＫＣ和ＰＣ分别为在高钾和正常钾条件下的咖啡因挛缩）表示的咖啡因挛缩增强，依赖［Ｋ＋］Ｏ和高钾作用时间。随着１０ｍｍｏｌ／Ｌ［Ｋ＋］Ｏ作用时间延长，直至１０ｍｉｎ，增强逐渐增加。但是，２５ｍｍｏｌ／Ｌ［Ｋ＋］Ｏ作用１ｍｉｎ时增强达到最大，然后下降到对照。ＰＫＣ／ＰＣ变化时程不能用高钾引起的去极化解释，而与由相似［Ｋ＋］Ｏ引起的胞浆自由钙变化时程相符。提示，至少在蛙骨骼肌，高钾引起的咖啡因挛缩增强主要是由胞浆自由钙升高引起的。
Using the frog anterior tibial muscle bundle as a material, the effect of increasing extracellular potassium [K +] O on caffeine contracture was studied. The increase in [K +] O from 2 mmol / L to 10 or 25 mmol / L markedly increased contractures caused by 3 mmol / L caffeine. Increased caffeine contracture, expressed as PKC / PC (PKC and PC, respectively, caffeine contractures under high potassium and normal potassium conditions, respectively), is dependent on [K +] O and high potassium duration of action. With 10mmol / L [K +] O prolonged action, until 10min, the increase gradually increased. However, 25 mmol / L [K +] O increased maximally at 1 min and then decreased to the control. The time course of PKC / PC changes can not be explained by the depolarization caused by high potassium, but consistent with the time course of free calcium change of cytoplasm caused by similar [K +] O. Tip, at least in the frog skeletal muscle, elevated potassium caffeine contracture enhancement is mainly caused by free cytoplasmic free calcium.