EFFECT OF STEROIDS ON EDEMA AND SODIUM UPTAKE OF THE BRAIN DURING FOCAL ISCHEMIA IN RATS
EFFECT OF STEROIDS ON EDEMA AND SODIUM UPTAKE OF THE BRAIN DURING FOCAL ISCHEMIA IN RATS
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DOI：
10.1161/01.str.21.8.1199
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发表时间：
1990-08-01
期刊：
影响因子：
8.3
通讯作者：
COESTER, HC
中科院分区：
文献类型：
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作者：
BETZ, AL;COESTER, HC
类固醇降低血脑屏障的通透性并抑制脑毛细血管的主动钠转运。由于缺血早期水肿形成的速率与钠从血液转运至脑的速率有关，因此本研究旨在确定类固醇是否通过抑制血脑屏障钠转运来减少缺血性水肿形成。地塞米松与孕酮进行了比较，因为后者是一种更有效的钠转运抑制剂在孤立的毛细血管。在大脑中动脉闭塞前1小时，用媒介物（n = 22）或2 mg/kg地塞米松（n = 22）或孕酮（n = 17）处理Sprague-Dawley大鼠。缺血4小时后，脑含水量和血脑屏障对[3 H] α-H2O的渗透性降低。测定了氨基异丁酸和钠-22。在对照组中，平均值为±。缺血区中心组织的SEM含水量为82.4 ± 0.01%。百分之零点二在用地塞米松（80.6 ± 0.001）或地塞米松（80.6 ± 0.001）预处理后，脑水肿显著减轻。0.1%，p < 0.001）或孕酮（81.5 . ±. 0.3%，p < 0.05）。血脑屏障对α-半乳糖苷酶的渗透性也显著降低。在任一治疗后正常脑中的氨基异丁酸（例如，2.21 .+-. 0.19和1.37 . ±. 0.10μ l/g/min，p < 0.001，分别用于对照和地塞米松处理），但对钠渗透性没有影响（例如，1.19 .+-. 0.05和1.12 .+-。0.11对照和地塞米松处理分别为μ l/g/min）。此外，类固醇治疗没有降低缺血性脑中钠的血脑渗透性（例如，2.53 .+-. 0.39和2.40 .+-。0.33对照组和地塞米松治疗组分别为μ l/g/min）。我们的结论是，预处理与地塞米松，在较小程度上，孕酮减少脑水肿在缺血的早期阶段，然而，这种效果是不是减少血脑钠转运的结果。
Steroids reduce permeability of the blood-brain barrier and inhibit active sodium transport by brain capillaries in vitro. Since the rate of edema formation during the early stages of ischemia is related to the rate of sodium transport from blood to brain, this study was designed to determine whether steroids reduce ischemic edema formation by inhibiting blood-brain barrier sodium transport. Dexamethasone was compared with progesterone since the latter is a more potent inhibitor of sodium transport in isolated capillaries. Sprague-Dawley rats were treated with vehicle (n = 22) or 2 mg/kg of either dexamethasone (n = 22) or progesterone (n = 17) 1 hour before occlusion of the middle cerebral artery. After 4 hours of ischemia, brain water content and blood-brain barrier permeability to [3H].alpha.-aminoisobutyric acid and sodium-22 were determined. In controls, mean .+-. SEM water content of tissue in the center of the ischemic zone was 82.4 .+-. 0.2%. Brain edema was significantly reduced following pretreatment with either dexamethasone (80.6 .+-. 0.1%, p < 0.001) or progesterone (81.5 .+-. 0.3%, p < 0.05). There was also a significant reduction in blood-brain barrier permeability to .alpha.-aminoisobutyric acid in normal brain following either treatment (e.g., 2.21 .+-. 0.19 and 1.37 .+-. 0.10 .mu.l/g/min, p < 0.001, for control and dexamethasone treatments, respectively), but no effect on the permeability to sodium (e.g., 1.19 .+-. 0.05 and 1.12 .+-. 0.11 .mu.l/g/min for control and dexamethasone treatments, respectively). Furthermore, steroid treatment did not reduce blood-brain permeability to sodium in ischemic brain (e.g., 2.53 .+-. 0.39 and 2.40 .+-. 0.33 .mu.l/g/min for control and dexamethasone treatments, respectively). We conclude that pretreatment with dexamethasone and, to a lesser extent, progesterone reduces brain edema during the early stages of ischemia; however, this effect is not the result of reduced blood-to-brain sodium transport.