本文阐述了围产期缺氧缺血性脑损害的病理生理变化,主要表现为脑血流障碍、能量代谢衰竭、自由基产生增多,兴奋性氨基酸及相应受体活性改变、钙离子自稳机制紊乱及某些基因和蛋白质表达异常。缺氧缺血后的低灌注及脑损害加重,可能与脑组织中自由基产生增多、细胞内游离钙离子增多和兴奋性氨基酸作用有关。围产期脑缺氧缺血性损害有其一定自身特点,高血糖对该病无害,甚至有益。 This article describes the pathophysiological changes of perinatal hypoxic-ischemic brain damage, mainly manifested as cerebral blood flow disorders, energy metabolism failure, increased production of free radicals, excitatory amino acids and corresponding receptor activity, calcium self-stabilizing mechanism Disorders and abnormal gene and protein expression. Hypoxic-ischemic hypoperfusion and increased brain damage may be related to increased production of free radicals in brain tissue, increased intracellular free calcium and the role of excitatory amino acids. Perinatal cerebral hypoxic-ischemic damage has its own characteristics, hyperglycemia harmless to the disease, and even beneficial.