Gidö G, Katsura K, Kristian T, Siesjö B K
Laboratory for Experimental Brain Research, University Hospital, Lund, Sweden.
J Cereb Blood Flow Metab. 1993 Jan;13(1):179-82. doi: 10.1038/jcbfm.1993.21.
The objective of this study was to establish whether tissues that are energy compromised, but not energy depleted, demonstrate exaggerated calcium transients when subjected to membrane depolarizations of the spreading depression (SD) type. Anesthetized and artificially ventilated rats were given insulin in order to induce progressively lower plasma glucose concentrations. Spreading depression was elicited by local application of KCl; extracellular calcium concentration (Ca2+e) as well as direct current (DC) potential were recorded. When plasma glucose concentration fell below approximately 3 mM, the duration of the Ca2+e transient gradually increased to values exceeding 500% of control. The increase was associated with a corresponding increase in the duration of the DC potential shift, but the amplitude of the Ca2+e transient did not change. It is concluded that a restriction of glucose (or oxygen) supply, as occurs in hypoglycemia (or hypoxia), prolongs the calcium transient associated with depolarization of the SD type, even though tissue phosphocreatinine and ATP concentrations are normal. The results support the contention that repeated depolarizations, occurring in the penumbral zone of a focal ischemic lesion, could lead to calcium-related damage.
本研究的目的是确定能量受损但未耗尽的组织在受到扩散性抑制（SD）类型的膜去极化作用时，是否会表现出夸张的钙瞬变。对麻醉并进行人工通气的大鼠注射胰岛素，以逐步降低血浆葡萄糖浓度。通过局部应用氯化钾引发扩散性抑制；记录细胞外钙浓度（Ca2+e）以及直流（DC）电位。当血浆葡萄糖浓度降至约3 mM以下时，Ca2+e瞬变的持续时间逐渐增加至超过对照值的500%。这种增加与DC电位偏移持续时间的相应增加相关，但Ca2+e瞬变的幅度没有变化。得出的结论是，低血糖（或低氧）时发生的葡萄糖（或氧气）供应受限，会延长与SD型去极化相关的钙瞬变，即使组织磷酸肌酸和ATP浓度正常。这些结果支持了这样的观点，即在局灶性缺血性病变的半暗带中反复发生的去极化可能导致与钙相关的损伤。
