缺氧和/或缺糖对大鼠突触体游离钙浓度和氨基酸释放的影响

目的：研究缺氧和/或缺糖对大鼠突触体游离钙浓度和氨基酸释放的影响。方法：营养液中去除糖和/或氧，建立大鼠脑突触体缺氧、缺糖和缺血模型。检测静息及高钾去极化状态下，各种模型突触体游离钙浓度及兴奋性氨基酸(EAA)和抑制性氨基酸(IAA)释放量的变化。结果：与正常突触体相比，缺氧60min后，静息和KCl除极突触体的游离钙浓度无明显改变，而缺糖导致静息和KCl除极突触体游离钙浓度显著升高。糖和氧同时去除影响更为明显。缺氧和/或缺糖对大鼠突触体氨基酸释放的影响与此相似，缺糖对突触体氨基酸释放的影响比缺氧更明显。其中EAA门冬氨酸和IAA甘氨酸、牛磺酸、γ-氨基丁酸释放量明显增加。而谷氨酸亦有增加趋势。结论：缺糖和缺氧在缺血致脑损伤中的机制可能不同，其中缺糖有更为重要的作用。缺糖和/或缺氧致脑损伤过程中IAA的增加可能是机体的一个自我保护机制。

Effects of anoxia and/or aglycaemia on the release of free calcium and amino acids from rat brain synaptosomes

Objective:To study the effects of anoxia and/or aglycaemia on the release of free calcium concentrations([Ca 2+ ]i)and amino acids from rat brain synaptosomes.Methods:Anoxic and/or aglycaemic synaptosome models were established by substration of glucose and/or oxygen from synaptosome suspension.The release of excitatory amino acids(EAA)and inhibitory amino acids(IAA),and[Ca 2+ ]i from every synaptosomes model was determined under the conditions of either resting or stimulation of50mmol/L KCl.Results:After anoxia60min,there were no significant differences in[Ca 2+ ]i in resting and KCl-depolarized synaptosomes,compared with normoxia.But a lack of glucose in the incubation medium led to significant increase of[Ca 2+ ]i in same conditions.Both lack of glucose and oxygen caused further increase of[Ca 2+ ]i.The effects of anoxia and/or aglycaemia on release of amino acid were similar to these results,the ef-fects of aglycaemia were greater than that of anoxia.Thereinto,the release of EAA(aspartate)and IAA(glycine,taurine,GABA)were in-creased significantly,but glutamate lightly.Conclusion:These results suggest that the relative contributions of anoxia and aglycaemia to ischemic cerebral damage may be different.The effects of aglycaemia were greater than that of anoxia.The increase of IAA may be a self-protective mechanism during the cerebral damage caused by anoxia and/or aglycaemia.