论文部分内容阅读
由于缺血和缺氧的影响,许多神经递质的浓度发生变化,包括升高的内源兴奋性的氨基酸谷氨酸盐引起过度的对突触后N-甲基-D-天氡氨酸(NM-DA)受体的刺激。升高的NMDA使与其相关的钙离子通道开放,过量的钙离子进入细胞内引起细胞死亡,而NMDA的拮抗剂可以抑制谷氨酸盐的活性防止细胞死亡发生。CGS 19755是一种竞争性的NM-DA受体拮抗剂,已在动物试验中证实对缺血性卒中的神经损伤有保护作用。由于过量的CGS 19755还可引起镇静、头晕、恶心、精神不振等副作用,本实验即对CGS在卒中患者的安全剂量和耐受性进行研究。实验在卒中发生12h内进行,不同剂量药物
Due to the effects of ischemia and hypoxia, many concentrations of neurotransmitters are altered, including the elevated endogenous excitatory amino acid glutamate causing excessive inhibition of postsynaptic N-methyl-D-aspartate (NM-DA) receptor stimulation. Elevated NMDA causes its associated calcium channels open, excessive calcium ions into the cell causing cell death, and NMDA antagonists can inhibit the activity of glutamate to prevent cell death. CGS 19755 is a competitive NMDA receptor antagonist that has been shown to have protective effects in nerve injury in ischemic stroke in animal studies. Due to the side effects of excessive CGS 19755, such as sedation, dizziness, nausea, and lack of energy, this study investigated the safe dose and tolerability of CGS in stroke patients. Experiments were performed within 12 h of stroke with different doses of drug