Kinoshita K, Ehara T
J Mol Cell Cardiol. 1984 May;16(5):405-19. doi: 10.1016/s0022-2828(84)80612-4.
The protective effects of high-K, high-glucose solution (GK solution) on electromechanical activity in the isolated guinea-pig ventricular muscle were studied. The basal test solution (basal GK solution) contained 30 mM KCl, 230 mM glucose and 4 mM NaHCO3, that is nominally Ca-free. Various types of GK solutions were also prepared by modifying the composition of this solution. When the muscle was exposed to the basal GK solution, the resting potential fell to about -40 mV, the muscle lost the excitability, and an irreversible contracture gradually developed. This contracture was prevented by elevating [Na]o above 60 mM. Reduction of [K]o to 20 mM, addition of EGTA (0.4 mM), or lowering the temperature (23 degrees C) also suppressed the above contracture. When the GK solution with high Na (106-115 mM NaCl added to basal GK solution in exchange for glucose) was applied, contractures frequently developed upon reintroduction of Tyrode solution (Ca-paradox-like phenomenon). Thus the Ca-free GK solution with 60 mM Na (56 mM NaCl added to basal GK solution in exchange for glucose) induced no contracture, either during or after the test period. Recovery of the action potential after this application was all but complete. On the other hand, addition of 0.9 to 1.8 mM Ca to this solution produced another type of contracture which was sensitive to verapamil. The cardioplegic effects of the Ca-free GK solution with 60 mM Na persisted under hypoxic conditions, and glucose appeared to play a significant role in preventing the hypoxia-related contracture. In contrast, the high-Na (110 mM Na) GK solution containing 0.2 to 0.5 mM Ca and Tyrode solution, both of which produced no contracture under normoxic conditions, did produce contractures under hypoxic conditions. Therefore, Ca-free GK solution containing an appropriate concentration (around 60 mM) of Na may protect the normoxic and hypoxic myocardium against intracellular Ca overload. The related mechanisms involved were discussed with special reference to membrane functions and intracellular Ca-regulating systems.
研究了高钾高糖溶液(GK溶液)对离体豚鼠心室肌电机械活动的保护作用。基础测试溶液(基础GK溶液)含有30 mM氯化钾、230 mM葡萄糖和4 mM碳酸氢钠,即名义上无钙。还通过改变该溶液的成分制备了各种类型的GK溶液。当肌肉暴露于基础GK溶液时,静息电位降至约-40 mV,肌肉失去兴奋性,并逐渐出现不可逆的挛缩。将[Na]o升高至60 mM以上可防止这种挛缩。将[K]o降至20 mM、添加乙二醇双四乙酸(EGTA,0.4 mM)或降低温度(23摄氏度)也可抑制上述挛缩。当应用高钠GK溶液(向基础GK溶液中添加106 - 115 mM氯化钠以替代葡萄糖)时,重新引入台氏液后经常会出现挛缩(类似钙反常现象)。因此,含60 mM钠(向基础GK溶液中添加56 mM氯化钠以替代葡萄糖)的无钙GK溶液在测试期间或之后均未引起挛缩。应用此溶液后动作电位的恢复几乎完全。另一方面,向该溶液中添加0.9至1.8 mM钙会产生另一种对维拉帕米敏感的挛缩。含60 mM钠的无钙GK溶液在缺氧条件下仍具有心脏停搏作用,葡萄糖似乎在预防缺氧相关挛缩中起重要作用。相比之下,含0.2至0.5 mM钙的高钠(110 mM钠)GK溶液和台氏液在常氧条件下均未引起挛缩,但在缺氧条件下确实会引起挛缩。因此,含有适当浓度(约60 mM)钠的无钙GK溶液可能保护常氧和缺氧心肌免受细胞内钙超载的影响。特别参考膜功能和细胞内钙调节系统讨论了相关机制。