目的　观察急性中、重度低压缺氧条件下 ,大鼠血脑屏障通透性的变化特点 ,为阐明低压缺氧作用下脑功能障碍的可能机理提供生理学依据。　方法　选择雄性 SD大鼠 18只 ,随机分为对照组、5 0 0 0 m及 80 0 0 m急性低压缺氧暴露组。实验组动物于低压舱内 ,以 2 0 m/ s的速率上升 ,至5 0 0 0 m(或 80 0 0 m) ,停留 5 h,而后以 2 0 m/ s的速率下降至地面。出舱后立即经心脏灌注硝酸镧固定液 ,开颅取脑 ,制成切片 ,置透射电镜下观察。　结果　急性低压缺氧暴露 5 h后即刻 ,即可见镧颗粒通过大鼠脑皮质的毛细血管内皮细胞膜及血管内皮细胞间的紧密连接 ,沉积于毛细血管内皮细胞浆内、细胞核膜上以及血管周围 ,弥漫性地分布于脑间质细胞间隙 ,并附着于神经细胞膜上 ,而对照组大鼠 ,镧颗粒仅滞留于大脑皮质的毛细血管腔内。　结论　 5 0 0 0 m以上低压缺氧连续暴露 5 h,可引起大鼠血脑屏障通透性增加。这可能在低压缺氧导致脑水肿的发生以及脑功能障碍的过程中起重要作用 Objective To observe the changes of the permeability of the blood-brain barrier in acute hypobaric hypoxia and hypobaric hypoxia in rats and provide the physiological basis for elucidating the possible mechanism of hypoglycemia and cerebral dysfunction. Methods Eighteen male Sprague-Dawley rats were randomly divided into the control group, the control group, the control group, the control group and the control group. The experimental animals in the low-pressure cabin, at a rate of 20 m / s, to 5 0 0 0 m (or 80 0 0 m), stay 5 h, and then 20 m / s rate down to the ground. Immediately after exiting the chamber, the heart was infused with lanthanum nitrate fixative solution. The brain was craniotomized to make slices, which were observed under transmission electron microscope. Results Immediate exposure to acute hypobaric hypoxia for 5 h showed that the lanthanum particles were deposited on the capillary endothelial cells, the nuclear membrane and perivascular cells through tight junctions between the capillary endothelial cells and the vascular endothelial cells in the cerebral cortex. Diffusely distributed in the interstitial cells of the brain, and attached to the membrane of nerve cells, while the control group rats, lanthanum particles only remain in the capillary cavity of the cerebral cortex. Conclusion Continuous exposure to hypobaric hypoxia for more than 5 000 h resulted in an increase of blood-brain barrier permeability in rats. This may play an important role in the process of hypobaric hypoxia leading to cerebral edema and brain dysfunction