Objective: To study the changes of excitatory amino acids (EAAs) and intracellular calcium ([Ca 2+ ]i), and the protective effect of EAAs receptor antagonists in the tissues of rabbit lumbar spinal cord after 40 minue...Objective: To study the changes of excitatory amino acids (EAAs) and intracellular calcium ([Ca 2+ ]i), and the protective effect of EAAs receptor antagonists in the tissues of rabbit lumbar spinal cord after 40 minues ischemia and 4 hours reperfusion. Methods: Thirty healthy rabbits were divided into six groups: sham operation, 40 minues ischemia,4 hour reperfusion, ketamine and MgSO 4 treatment, ketamine treatment, and saline treatment groups. The contents of EAAs (glutamate and aspartate) and [Ca 2+ ] i were measured. Results: The contents of glutamate and aspartate were decreased to 15.18 μmol/g± 2.33 μmol/g and 9.99 μmol/g ± 0.69 μmol/g, respectively; 13.75 μmol/g± 2.58 μmol/g and 6.49 μmol/g± 1.39 umol/g after reperfusion. In the ischemia group, the [Ca 2+ ]i was elevated to 221.2 μg/g ± 4.27 μg/g, and elevated further to 298.3 μg/g± 9.26 μg/g after reperfusion, being significantly higher than that of ischemia and control groups. Ketamine could obviously increase the level of glutamate and aspartate and decrease the level of [Ca 2+ ]i during the ischemia and reperfusion injury. Conclusions: The excitotoxicity of EAAs and the overload of calcium induced by EAAs play a harmful role in ischemia and reperfusion injury. Ketamine has an effective inhibitory effect.展开更多
文摘Objective: To study the changes of excitatory amino acids (EAAs) and intracellular calcium ([Ca 2+ ]i), and the protective effect of EAAs receptor antagonists in the tissues of rabbit lumbar spinal cord after 40 minues ischemia and 4 hours reperfusion. Methods: Thirty healthy rabbits were divided into six groups: sham operation, 40 minues ischemia,4 hour reperfusion, ketamine and MgSO 4 treatment, ketamine treatment, and saline treatment groups. The contents of EAAs (glutamate and aspartate) and [Ca 2+ ] i were measured. Results: The contents of glutamate and aspartate were decreased to 15.18 μmol/g± 2.33 μmol/g and 9.99 μmol/g ± 0.69 μmol/g, respectively; 13.75 μmol/g± 2.58 μmol/g and 6.49 μmol/g± 1.39 umol/g after reperfusion. In the ischemia group, the [Ca 2+ ]i was elevated to 221.2 μg/g ± 4.27 μg/g, and elevated further to 298.3 μg/g± 9.26 μg/g after reperfusion, being significantly higher than that of ischemia and control groups. Ketamine could obviously increase the level of glutamate and aspartate and decrease the level of [Ca 2+ ]i during the ischemia and reperfusion injury. Conclusions: The excitotoxicity of EAAs and the overload of calcium induced by EAAs play a harmful role in ischemia and reperfusion injury. Ketamine has an effective inhibitory effect.
