短暂高压氧状态对新生儿是一种安全有效的治疗方法——实验证据
加利福尼亚罗马林达大学健康科学中心神经外科学科
介绍：因多数患者在脑卒中发病后3-6 h内无法就诊，使得临床应用高压氧治疗急性大脑低氧性缺血损伤在一定程度上受到了治疗时间窗的阻碍。例外情况是对于早期卒中或新生儿低氧，如果能在分娩室里放置一个高压氧箱，则能挽救更多的生命或减少新生儿的神经缺损。
实验观察：采用大鼠低氧幼鼠模型，在低氧损伤1 h后，给予1 h的高压氧(1.5-3 个大气压，100% O2) 治疗，6周后结果证实，高压氧治疗对试验幼鼠脑体积发育及形态结构具有极大的保护作用，并且显著提高损伤鼠脑的神经功能。
高压氧机制：高压氧的一个主要机能是抗细胞凋亡，从而挽救正在死亡的细胞并恢复其生理功能。其机制是通过抑制一种死亡信息因子-caspase-3及其下流的一些调节细胞凋亡因子来发挥作用。高压氧可以降低caspase-3表达及活性，减少PARP 的分裂，防止DNA链断裂。
, http://www.100md.com
高压氧治疗后视网膜病变的可能性：应用高压氧的一个主要隐患是有可能导致新生儿视网膜病变。上述方案跟踪评价视网膜对高压氧的反应，根据血管新生水平，视网膜结构改变，低氧-高氧敏感性蛋白，包括低氧诱导因子1a (HIF-1a)及血管上皮生长因子(VEGF)的变化等等来评价视网膜病变。结果显示，高氧情况下无血管新生征象，无视网膜结构改变，HIF-1a 和VEGF蛋白的表达水平也没有发生改变。
结论：短暂高压氧治疗可以抑制细胞凋亡，防止脑损伤。这种治疗不会导致新生儿视网膜病变。
Transient Exposure to HBO is a Safe and Effective Therapy for Neonates: Experimental Evidences
John H. Zhang. Department of Neurosurgery, Loma Linda University Health Science Center, Loma Linda, California
, 百拇医药
Introduction: Clinical application of HBO to acute cerebral hypoxia-ischemia is retarded partially by the limitation of the therapeutic window that most patients are not available to HBO within the first 3-6 hrs after the onset of stroke. An exception is the young stroke or neonatal hypoxia that a HBO chamber placed in the delivery room could save lives or reduce the neurological deficits of newborns.
Experimental observation: we have shown using an established neonatal hypoxia rat pup model that application of HBO (1.5-3 ATA, 100% O2) for one hr, at one hr after hypoxia insult, preserved tremendously brain weight and morphology up to 6 weeks and improved neurological function [Calvert et al. 2002].
, 百拇医药
Mechanisms of hbo: One of the major effects of HBO at the molecular level is its anti-apoptotic action which saves the dying cells and restores their physiological functions. Using the same treatment protocol which preserved brain weight, we have found that HBO inhibited a death signaling factor – caspase-3 and its downstream effectors that mediated programmed cell death (apoptosis). HBO reduced the expression and activity of caspase-3, decreased cleavage of PARP, and prevented DNA fragmentation [Calvert et al. 2003].
, 百拇医药
Chances of retinopathy after hbo: A major concern of using HBO in neonates is the possibility of retinopathy of prematurity. Using the same treatment protocol at 1.5-3.0 ATA for one hour, we evaluated the retinal response to HBO from 24 hrs to 10 weeks. Retinopathy was evaluated by the degree of neovascularization (measuring retinal vascular density), by the structural abnormalities (histology) in the retina, and by the expression of hypoxia-hyperoxia sensitive proteins including hypoxia-inducible factor-1a (HIF-1a) and Vascular Endothelial Growth Factor (VEGF).
, http://www.100md.com
We found no signs of neovascularization, no abnormalities in the structure of the retina and no changes in the protein expression of HIF-1a and VEGF after hyperoxia exposure [Calvert et al., Submitted to Experimental Neurology].
Conclusions: Transient exposure to hyperoxia at hyperbaric pressures prevented brain injury by inhibition of apoptosis. This effective treatment does not cause retinopathy of prematurity., http://www.100md.com
介绍：因多数患者在脑卒中发病后3-6 h内无法就诊，使得临床应用高压氧治疗急性大脑低氧性缺血损伤在一定程度上受到了治疗时间窗的阻碍。例外情况是对于早期卒中或新生儿低氧，如果能在分娩室里放置一个高压氧箱，则能挽救更多的生命或减少新生儿的神经缺损。
实验观察：采用大鼠低氧幼鼠模型，在低氧损伤1 h后，给予1 h的高压氧(1.5-3 个大气压，100% O2) 治疗，6周后结果证实，高压氧治疗对试验幼鼠脑体积发育及形态结构具有极大的保护作用，并且显著提高损伤鼠脑的神经功能。
高压氧机制：高压氧的一个主要机能是抗细胞凋亡，从而挽救正在死亡的细胞并恢复其生理功能。其机制是通过抑制一种死亡信息因子-caspase-3及其下流的一些调节细胞凋亡因子来发挥作用。高压氧可以降低caspase-3表达及活性，减少PARP 的分裂，防止DNA链断裂。
, http://www.100md.com
高压氧治疗后视网膜病变的可能性：应用高压氧的一个主要隐患是有可能导致新生儿视网膜病变。上述方案跟踪评价视网膜对高压氧的反应，根据血管新生水平，视网膜结构改变，低氧-高氧敏感性蛋白，包括低氧诱导因子1a (HIF-1a)及血管上皮生长因子(VEGF)的变化等等来评价视网膜病变。结果显示，高氧情况下无血管新生征象，无视网膜结构改变，HIF-1a 和VEGF蛋白的表达水平也没有发生改变。
结论：短暂高压氧治疗可以抑制细胞凋亡，防止脑损伤。这种治疗不会导致新生儿视网膜病变。
Transient Exposure to HBO is a Safe and Effective Therapy for Neonates: Experimental Evidences
John H. Zhang. Department of Neurosurgery, Loma Linda University Health Science Center, Loma Linda, California
, 百拇医药
Introduction: Clinical application of HBO to acute cerebral hypoxia-ischemia is retarded partially by the limitation of the therapeutic window that most patients are not available to HBO within the first 3-6 hrs after the onset of stroke. An exception is the young stroke or neonatal hypoxia that a HBO chamber placed in the delivery room could save lives or reduce the neurological deficits of newborns.
Experimental observation: we have shown using an established neonatal hypoxia rat pup model that application of HBO (1.5-3 ATA, 100% O2) for one hr, at one hr after hypoxia insult, preserved tremendously brain weight and morphology up to 6 weeks and improved neurological function [Calvert et al. 2002].
, 百拇医药
Mechanisms of hbo: One of the major effects of HBO at the molecular level is its anti-apoptotic action which saves the dying cells and restores their physiological functions. Using the same treatment protocol which preserved brain weight, we have found that HBO inhibited a death signaling factor – caspase-3 and its downstream effectors that mediated programmed cell death (apoptosis). HBO reduced the expression and activity of caspase-3, decreased cleavage of PARP, and prevented DNA fragmentation [Calvert et al. 2003].
, 百拇医药
Chances of retinopathy after hbo: A major concern of using HBO in neonates is the possibility of retinopathy of prematurity. Using the same treatment protocol at 1.5-3.0 ATA for one hour, we evaluated the retinal response to HBO from 24 hrs to 10 weeks. Retinopathy was evaluated by the degree of neovascularization (measuring retinal vascular density), by the structural abnormalities (histology) in the retina, and by the expression of hypoxia-hyperoxia sensitive proteins including hypoxia-inducible factor-1a (HIF-1a) and Vascular Endothelial Growth Factor (VEGF).
, http://www.100md.com
We found no signs of neovascularization, no abnormalities in the structure of the retina and no changes in the protein expression of HIF-1a and VEGF after hyperoxia exposure [Calvert et al., Submitted to Experimental Neurology].
Conclusions: Transient exposure to hyperoxia at hyperbaric pressures prevented brain injury by inhibition of apoptosis. This effective treatment does not cause retinopathy of prematurity., http://www.100md.com