Helps S C, Parsons D W, Reilly P L, Gorman D F
Department of Anaesthesia, Royal Adelaide Hospital, South Australia.
Stroke. 1990 Jan;21(1):94-9. doi: 10.1161/01.str.21.1.94.
Many bubbles that enter the brain circulation pass through the arterioles and capillary beds and do not obstruct blood flow. Nevertheless, such bubbles could still disrupt brain function. An open-brain model in five anesthetized rabbits used the minimum dose of air (25 microliters) necessary to cause embolism of the exposed vessels, and these bubbles passed through the vessels without any trapping. Despite their rapid transit, the bubbles provoked a marked dilatation of the affected pial arterioles (mean increase after 15 minutes of 27%) that persisted for 90 minutes after the bubbles had disappeared. The changes in vessel diameter were associated with a delayed, but significant and progressive, reduction in both cerebral blood flow measured by hydrogen clearance and neural function measured by cortical somatosensory evoked response. The decrease in blood flow correlated well with the depression of neural function (r = 0.67). Because both cerebral blood flow and neural function temporarily returned to normal after air embolism, the subsequent changes seen in this model cannot be explained simply by the mechanical obstruction of blood flow by bubbles.
许多进入脑循环的气泡会通过小动脉和毛细血管床，不会阻碍血流。然而，这些气泡仍可能扰乱脑功能。在五只麻醉兔身上建立的开颅模型中，使用了导致暴露血管栓塞所需的最小空气剂量（25微升），这些气泡穿过血管而未被截留。尽管气泡快速通过，但它们引发了受影响软脑膜小动脉的明显扩张（15分钟后平均增加27%），并且在气泡消失后持续90分钟。血管直径的变化与通过氢清除法测量的脑血流量和通过皮层体感诱发电位测量的神经功能的延迟但显著且渐进的降低有关。血流减少与神经功能抑制密切相关（r = 0.67）。由于空气栓塞后脑血流量和神经功能会暂时恢复正常，因此该模型中随后出现的变化不能简单地用气泡对血流的机械阻塞来解释。
