Sharma Hari Shanker, Johanson Conrad Earl
Laboratory of Cerebrovascular Research, Institute of Surgical Sciences, Department of Anaesthesiology and Intensive Care, University Hospital, Uppsala University, SE-75185 Uppsala, Sweden.
Prog Brain Res. 2007;162:459-78. doi: 10.1016/S0079-6123(06)62023-2.
The blood-CSF barrier (BCSFB) in choroid plexus works with the blood-brain barrier (BBB) in cerebral capillaries to stabilize the fluid environment of neurons. Dysfunction of either transport interface, i.e., BCSFB or BBB, causes augmented fluxes of ions, water and proteins into the CNS. These barrier disruptions lead to problems with edema and other compromised homeostatic mechanisms. Hyperthermic effects on BCSFB permeability and transport are not as well known as for BBB. However, it is becoming increasingly appreciated that elevated prostaglandin synthesis from fever/heat activation of cyclooxygenases (COXs) in the BCSFB promotes water and ion transfer from plasma to the ventricles; this harmful fluid movement into the CSF-brain interior can be attenuated by agents that inhibit the COXs. Moreover, new functional data from our laboratory animal model indicate that the BCSFB (choroidal epithelium) and the CSF-bordering ependymal cells are vulnerable to whole body hyperthermia (WBH). This is evidenced from the fact that rats subjected to 4h of heat stress (38 degrees C) showed a significant increase in the translocation of Evans blue and (131)Iodine from plasma to cisternal CSF, and manifested blue staining of the dorsal surface of the hippocampus and caudate nucleus. Degeneration of choroidal epithelial cells and underlying ependyma, a dilated ventricular space and damage to the underlying neuropil were frequent. A disrupted BCSFB is associated with a marked increase in edema formation in the hippocampus, caudate nucleus, thalamus and hypothalamus. Taken together, these findings suggest that the breaching of the BCSFB in hyperthermia significantly contributes to cell and tissue injuries in the CNS.
脉络丛中的血 - 脑脊液屏障（BCSFB）与脑毛细血管中的血脑屏障（BBB）共同作用，以稳定神经元的液体环境。任何一个转运界面，即BCSFB或BBB功能失调，都会导致离子、水和蛋白质向中枢神经系统（CNS）的通量增加。这些屏障破坏会引发水肿问题以及其他体内稳态机制受损。热对BCSFB通透性和转运的影响不像对BBB那样广为人知。然而，人们越来越认识到，BCSFB中环氧合酶（COXs）因发热/热激活而导致的前列腺素合成增加，会促进水和离子从血浆转移到脑室；抑制COXs的药物可以减弱这种有害的液体向脑脊液 - 脑内部的移动。此外，我们实验室动物模型的新功能数据表明，BCSFB（脉络丛上皮）和与脑脊液相邻的室管膜细胞易受全身热疗（WBH）影响。这一事实证明，遭受4小时热应激（38摄氏度）的大鼠，伊文思蓝和碘（131）从血浆到脑池脑脊液的转运显著增加，并在海马体和尾状核的背表面出现蓝色染色。脉络丛上皮细胞和下层室管膜变性、脑室扩张以及下层神经纤维受损的情况很常见。BCSFB破坏与海马体、尾状核、丘脑和下丘脑水肿形成的显著增加有关。综上所述，这些发现表明，热疗中BCSFB的破坏显著促成了中枢神经系统中的细胞和组织损伤。
