Influence of hyperglycemia and of hypercapnia on cellular calcium transients during reversible brain ischemia
Influence of hyperglycemia and of hypercapnia on cellular calcium transients during reversible brain ischemia
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DOI：
10.1007/bf00231980
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发表时间：
2004
影响因子：
2
通讯作者：
A. Ekholm;T. Kristian;B. Siesjö
中科院分区：
文献类型：
--
作者：
A. Ekholm;T. Kristian;B. Siesjö
本研究的目的是找出缺血前高血糖（在正常血糖动物中）或过度高碳酸血症（在正常血糖动物中）如何影响缺血期间的钙瞬态，因为这可以通过测量细胞外钙浓度（[Ca2+]e）来评估。在此范围内，将正肌酸-正常血糖控制动物与诱导高血糖或高碳酸血症动物进行比较，所有动物都受到10分钟的前脑缺血，用离子敏感玻璃微电极测量[Ca2+]电位和直流电位。高血糖和高碳酸血症延缓了诱导缺血后离子稳态的丧失。此外，高血糖和高碳酸血症都减少了再循环时Ca2+挤压的延迟。结果，高血糖和高碳酸血症都显著降低了缺血钙瞬态，这是通过计算细胞最大钙负荷持续时间来评估的。结果表明，由高血糖或过度高碳酸血症引起的脑损伤的加重不太可能与细胞钙稳态的进一步紊乱有关。
The object of the study was to find out how preischemic hyperglycemia (in normocapnic animals) or excessive hypercapnia (in normoglycemic animals) affect the calcium transient during ischemia, as this can be assessed by measurements of the extracellular calcium concentration ([Ca2+]e). To that extent, normocapnic-normoglycemic control animals were compared with animals with induced hyperglycemia or hypercapnia, all being subjected to 10 min of forebrain ischemia, the [Ca2+]eand d.c. potential being measured with ion-sensitive glass microelectrodes. Hyperglycemia and hypercapnia delayed the loss of ion homeostasis following induction of ischemia. Furthermore, both hyperglycemia and hypercapnia reduced the delay of Ca2+extrusion upon recirculation. As a result, both hyperglycemia and hypercapnia significantly reduced the ischemic calcium transient, as this was assessed by calculating the duration of maximal calcium load of cells. The results make it less likely that aggravation of brain damage by hyperglycemia or excessive hypercapnia is related to a further derangement of cell calcium homeostasis.