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

1.快速减压的影响为观察减压后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6atm绝对压力空气中90分钟，随后快速减压。减压后立即观察到的伊文思蓝染色的宽区域和印度墨水填充缺陷区域的大小随着时间的推移而减小，并且在减压后3至24小时内无法检测到。减压后立即观察到的水肿脑组织、血管周围间隙扩大和神经细胞深染也在减压后1 ~ 24小时减少。然而，这些可逆的减压变化在减压后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，BBB和微循环障碍在72小时后再次出现， 关于我们 2.减压后即刻高压氧（HBO）的作用：高压氧后Evans蓝染色区消失，但仍可见墨汁灌注缺损区及组织学改变。因此，即使在HBO后，快速减压后的微循环障碍仍然存在。3.缺血-再灌注和一氧化氮合酶（NOS）抑制对CBF和谷氨酸释放的影响在大鼠前脑缺血-再灌注模型中研究了这种影响。在低流量脑缺血模型中，在NOS抑制后，尽管通过增加全身MAP增加脑灌注压，谷氨酸水平低于对照组。而在完全性脑缺血模型中，皮质CBF下降至初始对照水平的一半左右，脑灌注压没有增加。此外，谷氨酸水平高于对照组。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