脑缺氧或缺血能造成脑组织损伤,通常认为这是由于脑的能量代谢衰竭、继发性局部血流失调,或某些自由基团的毒性所致。最近的研究表明,兴奋性氨基酸(谷氨酸和门冬氨酸)在脑缺氧或缺血导致脑损伤中可能起决定性的作用,从而为研究中风、围产期窒息和心脏手术后并发症等缺氧或缺血性脑损伤的预防和治疗,提供了一条重要的新途径。海马神经元受到缺血或经过一次癫痫发作,都能引起相似的神经元损伤。Rothman 通过对胚胎鼠的海马神经元的研究,认为缺血或癫痫都可引起兴奋性氨基酸释放。在离体海马组织的培养中,在起初48小时内,神经元对氰化物或缺氧不敏感。两周后,神经元之间出现了突触联系,并呈现自发电活动。这时,接触氰化物1小时,培养的神经细胞就出现较大的空泡,以后,多数神经元发生退变。如果预先用高浓度的 Cerebral hypoxia or ischemia can cause brain tissue damage, which is generally thought to be due to metabolic energy failure in the brain, secondary regional blood flow disorders, or toxicity of certain free radicals. Recent studies have shown that excitatory amino acids (glutamic acid and aspartic acid) may play a decisive role in brain damage caused by hypoxia or ischemia in the brain, and thus to study stroke, perinatal asphyxia and post-cardiac surgery complications Such as hypoxia or ischemic brain injury prevention and treatment, provides an important new way. Hippocampal neurons are either ischemic or after a seizure can cause similar neuronal damage. Rothman through the embryonic rat hippocampal neurons, that ischemia or epilepsy can cause excitatory amino acid release. In cultured hippocampus tissue, neurons are not sensitive to cyanide or hypoxia within the first 48 hours. Two weeks later, synapses appeared between neurons and showed spontaneous activity. At this point, contact with cyanide 1 hour, cultured neurons appear larger vacuoles, after which most neurons degenerate. If used in advance with high concentrations