Wilde A A, Kléber A G
Circ Res. 1986 Feb;58(2):249-56. doi: 10.1161/01.res.58.2.249.
Several reports have shown that electrical and ionic changes occurring in acute myocardial ischemia can be closely mimicked by exposure of tissue to hypoxic, acid-, and glucose-free solutions at elevated [K+]o. In the present work, this approach was chosen to distinguish between the combined effects of hypoxia, substrate withdrawal, and acidosis, and the effects of two different levels of [K+]o (4.7 mM and 11.5 mM) on intracellular sodium activity and resting membrane potential. Measurements were made with microelectrodes in isolated guinea pig papillary muscles. In normoxia at 4.7 mM [K+]o, intracellular sodium activity was 7.5 mM (+/- 1.9 mM, SD) during stimulation at 1 Hz. Combined hypoxia, substrate withdrawal, and acidosis increased intracellular sodium activity significantly, by 3-4 mM in 4.7 mM [K+]o and by approximately 2 mM in 11.5 mM [K+]o, after 9-10 minutes. Increasing [K+]o in normoxic solution decreased intracellular sodium activity by 1.9 mM (+/- 1.3 mM, SD). The transition from normal (4.7 mM [K+]o) Tyrode's solution to "ischemic solution" (hypoxia, acidosis, substrate withdrawal, 11.5 mM [K+]o) was associated with a small initial increase and a subsequent decrease of intracellular sodium activity. The steady state level after 12 minutes was not significantly different from the level in normal Tyrode's solution. The secondary decrease of intracellular sodium activity coincided with the gradual development of inexcitability and was absent in quiescent preparations. Combined hypoxia, acidosis, and glucose-withdrawal produced a depolarization by 7-10 mV at 4.7 mM and at 11.5 mM [K+]o, probably reflecting cellular potassium loss and extracellular potassium accumulation in the restricted extracellular space.(ABSTRACT TRUNCATED AT 250 WORDS)
几份报告表明，在高[K⁺]ₒ条件下，将组织暴露于缺氧、无酸和无糖溶液中，可密切模拟急性心肌缺血时发生的电和离子变化。在本研究中，选用此方法来区分缺氧、底物缺乏和酸中毒的联合作用，以及两种不同水平的[K⁺]ₒ（4.7 mM和11.5 mM）对细胞内钠活性和静息膜电位的影响。使用微电极对分离的豚鼠乳头肌进行测量。在4.7 mM [K⁺]ₒ的常氧条件下，1 Hz刺激时细胞内钠活性为7.5 mM（±1.9 mM，标准差）。联合缺氧、底物缺乏和酸中毒显著增加细胞内钠活性，在4.7 mM [K⁺]ₒ时增加3 - 4 mM，在11.5 mM [K⁺]ₒ时9 - 10分钟后增加约2 mM。在常氧溶液中增加[K⁺]ₒ可使细胞内钠活性降低1.9 mM（±1.3 mM，标准差）。从正常（4.7 mM [K⁺]ₒ）的台氏液转变为“缺血溶液”（缺氧、酸中毒、底物缺乏、11.5 mM [K⁺]ₒ），细胞内钠活性最初有小幅度增加，随后降低。12分钟后的稳态水平与正常台氏液中的水平无显著差异。细胞内钠活性的二次降低与兴奋性逐渐丧失同时出现，在静止标本中未出现。联合缺氧、酸中毒和无糖条件在4.7 mM和11.5 mM [K⁺]ₒ时产生7 - 10 mV的去极化，可能反映了细胞钾流失和细胞外钾在受限细胞外空间的积累。（摘要截短于250字）
