论文部分内容阅读
用离体孵育的大鼠海马脑片模型，研究了两类钙通道拮抗剂对缺氧海马脑片Ca2+/CaM PKⅡ活性的影响。结果如下：(1)缺氧30min导致大鼠海马脑片Ca2+/CaM PKⅡ活性降至对照组的16.4%；(2)100μmol/L氯胺酮可部分拮抗缺氧导致的酶活性下降，使之恢复至对照组的40.6%；(3)10μmol/L苄丙咯可使缺氧导致的酶活性下降恢复至对照组的35.8%；(4)15μmol/L苄丙咯和50μmol/L氯胺酮联合用药可产生协同作用，使缺氧导致的酶活性下降恢复至对照组的63.8%。由此得出结论：缺氧对海马脑片Ca2+/CaM PKⅡ活性的抑制作用与NMDA受体门控的钙通道和Na+/Ca2+交换通道异常开放有关。
The effects of two types of calcium channel blockers on the Ca2 + / CaM PKⅡ activity in hippocampal slices of hippocampus were studied using rat hippocampal slices incubated in vitro. The results were as follows: (1) 30 min hypoxia resulted in a decrease of Ca2 + / CaM PKⅡ activity in rat hippocampal slices to 16.4% of the control group; (2) 100 μmol / L ketamine partially antagonized the hypoxia-induced decrease of enzyme activity 40.6% of the control group; (3) 10μmol / L Benprofen can reduce the hypoxia-induced enzyme activity to 35.8% of the control group; (4) Combination of 15μmol / L benprofur and 50μmol / L ketamine can produce Synergy, so that hypoxia caused by decreased enzyme activity was restored to 63.8% of the control group. It was concluded that the inhibitory effect of hypoxia on Ca2 + / CaM PKⅡ activity in hippocampal slices was related to the abnormal opening of NMDA receptor-gated calcium channels and Na + / Ca2 + exchange channels.