Brain disturbances due to rapid decompression-induced air bubbles, and effects of hyperbaric oxygenation

1.为了观察大鼠在减压后0.25 ~ 72小时血脑屏障（BBB）、脑微循环和组织学的变化，将大鼠暴露于6大气压空气中90分钟后快速减压。在减压后立即观察到的Evans蓝染色的宽区域和印度墨填充的缺陷区域随着时间的推移而缩小，在减压后3 ~ 24小时内无法检测到。减压后立即观察到的脑组织水肿，血管周围空间增大，神经细胞染色深，减压1 ~ 24小时后也减少。然而，这些可逆的失压变化在减压后48至72小时再次出现。这些早期可逆的紊乱被解释为血管内形成的微泡的物理化学效应。另一方面，缺血72 h后血脑屏障和微循环障碍的再次出现提示了失压微泡所致颞叶脑缺血后的成熟现象。高压氧（HBO）快速减压后即刻效果高压氧（HBO）快速减压后未见埃文斯蓝染色区，但仍观察到印墨填充缺损区及组织学改变。因此，快速减压后的微循环紊乱即使在hbo后仍然存在。缺血再灌注及一氧化氮合酶（NOS）抑制对大鼠前脑缺血再灌注模型脑血流和谷氨酸释放的影响。在低流量脑缺血模型中，NOS抑制后，尽管全身MAP增加导致脑灌注压升高，但仍出现血管收缩作用，谷氨酸水平低于对照组。然而，在完全脑缺血模型中，皮质CBF下降到初始对照水平的一半左右，脑灌注压未增加。谷氨酸水平显著高于对照组。少

1.Effect of rapid decompressionTo examine the changes in blood-brain barrier (BBB), cerebral microcirculation and histology from 0.25 to 72 hrs after decompression, rats were exposed to experimental compression to 6 atm abs air for 90 min and subsequent rapid decompression. The wide area stained with Evans blue and the regions of defective filling with Indian ink observed immediately after decompression decreased in size with time and were undetectable during 3 to 24 hrs after decompression. The edematous brain tissue with enlarged perivascular space and darkly stained nerve cells observed immediately after decompression also decreased after one to 24 hrs from decompression. These reversible dysbaric changes, however, were reappeared at 48 to 72 hrs after decompression. These early reversible derangements were interpreted to be the physico-chemical effects of intravascularly formed microbubbles. On the other hand, the reappearance of BBB and microcirculatory disturbances at 72 hrs afte … More r decompression suggested the maturation phenomenon after temporal brain ischemia induced by dysbaric microbubbles.2.Effect of hyperbaric oxygenation (HBO) immediately after rapid decompressionThe area stained with Evans blue was not seen after HBO,but the regions of defective filling with Indian ink and histological changes were still observed. Thus microcirculatory disturbances after rapid decompression remain even after HBO.3.Effect of ischemia-reperfusion and nitric oxide synthase (NOS) inhibition on CBF and glutamate releaseThe effects was studied in the rat forebrain ischemia-reperfusion model.In low flow cerebral ischemic model, after NOS inhibition, the vasoconstrictive effects occurred despite an increase in cerebral perfusion pressure by increased systemic MAP,and glutamate levels were lower than control Group. In complete cerebral ischemic model, however, cortical CBF decreased to about half of the initial control level, without an increase in cerebral perfusion pressure. In addition, glutamate levels was higher than control Group. Less