Neonatal hypoxic-ischemic brain injury in Progress.docVIP

 PAGE \* MERGEFORMAT 35 Neonatal hypoxic-ischemic brain injury in Progress Hypoxic-ischemic brain damage (hypoxic-ischemic brain damage, HIBD) is a threat to life and lead to neurological sequelae of neonatal severe disease, prevention and control measures adopted in the current clinical efficacy is unsatisfactory, so HIBD-depth understanding of the pathogenesis and to find more effective control methods, have been perinatal medicine and neuroscience workers attention. 1, HIBD the pathogenesis of (A) acidosis and high-energy phosphate depletion Hypoxic-ischemic brain after rapid depletion of oxygen to mitochondrial respiration and oxidative phosphorylation dysfunction, cell-dependent glucose-limited anaerobic glycolysis produces adenosine triphosphate (ATP), also has resulted in a large number of lactic acid accumulation. PH intracellular ATP shortage and reduce the enzyme to make ATP-dependent loss of function of various ion pumps, leading to cellular ion balance inside and outside the barrier and cell swelling, while inhibiting glycolysis pathway, the activity of key enzymes, further exacerbating the failure of energy metabolism and intracellular edema [1-3]. Acidosis can also reduce the lysosomal membrane stability, to promote the release of lysosomal enzymes to speed up protein, nucleic acid and phospholipid hydrolysis, so that cell degeneration and necrosis. (B) of excitatory amino acid Animal experiments and clinical study confirmed that neonatal hypoxic-ischemic excitatory amino acid release from depolarized nerve endings, brain tissue and cerebrospinal fluid concentrations of excitatory amino acids increased significantly. Glutamate and other excitatory amino acids can activate NMDA receptors, so that ligand-gated calcium channels open and encourage excessive calcium influx; activated non-NMDA receptors to Na flow is increased, increased cellular edema [1-3] . (C) the calcium ion toxi