BLOOD-BRAIN-BARRIER PERMEABILITY AND BRAIN CONCENTRATION OF SODIUM, POTASSIUM, AND CHLORIDE DURING FOCAL ISCHEMIA
BLOOD-BRAIN-BARRIER PERMEABILITY AND BRAIN CONCENTRATION OF SODIUM, POTASSIUM, AND CHLORIDE DURING FOCAL ISCHEMIA
复制标题
DOI：
10.1038/jcbfm.1994.5
复制
发表时间：
1994-01-01
影响因子：
6.3
通讯作者：
REN, XD
中科院分区：
文献类型：
--
作者：
BETZ, AL;KEEP, RF;REN, XD
局灶性脑缺血早期脑水肿的形成与钠含量和血脑屏障(BBB)钠转运增加有关。这项研究的目的是确定氯是否是在缺血脑中积聚的主要阴离子，氯的血脑屏障转运速率与其积累速率的比较，以及血脑屏障钠转运的刺激是否也见于其他阳离子。采用阻断大鼠大脑中动脉(MCAO)的方法制作局灶性脑缺血模型。在MCAO后6h内，缺血皮质中央的脑组织含水量以0.15+/-0.02(SE)g/g干重/h的速度递增，同时伴有脑钠(48+/-12mU/g干重/小时)和钾(34+/-7mU/g干重/小时)的净增加。氯的净积累速率(16+/-1µmol/g干湿重/小时)接近于阳离子的净增加速率。MCAO后3h，测定血脑屏障对三种离子(Na-22、Cl-36和Rb-86)和两种被动通透性示踪剂[[H-3]α-氨基异丁酸(H-3]AIB)和[C-14]尿素的通透性。对任何一种被动示踪剂的通透性都没有增加，表明血脑屏障是完整的。氯-36的内流速率是缺血脑组织净蓄积速率的3倍，Na-22的内流速率是各自净蓄积速率的1.8倍。与[H-3]AIB相比，缺血皮质对Na-22的血脑屏障通透性显著增加，对Rb-86的相对通透性显著降低，对Cl-36的相对通透性无明显变化。这些结果表明，血脑屏障钠转运的刺激是钠的专一性的。此外，在缺血的早期阶段，氯化物与钠一起在大脑中积累；然而，与其从血液到大脑的运输速度相比，其积累速度较低。因此，抑制血脑屏障钠转运比抑制血脑屏障氯化物转运更有可能减少水肿的形成。
Brain edema formation during the early stages of focal cerebral ischemia is associated with an increase in both sodium content and blood-brain barrier (BBB) sodium transport. The goals of this study were to determine whether chloride is the principal anion that accumulates in ischemic brain, how the rate of BBB transport of chloride compares with its rate of accumulation, and whether the stimulation seen in BBB sodium transport is also seen with other cations. Focal ischemia was produced by occlusion of the middle cerebral artery (MCAO) in anesthetized rats. Over the first 6 h after MCAO, the amount of brain water in the center of the ischemic cortex increased progressively at a rate of 0.15 +/- 0.02 (SE) g/g dry wt/h. This was accompanied by a net increase in brain sodium (48 +/- 12 mu mol/g dry wt/h) and a loss of potassium (34 +/- 7 mu mol/g dry wt/h). The net rate of chloride accumulation (16 +/- 1 mu mol/g dry wt/h) approximated the net rate of increase of cations. Three hours after MCAO, the BBB permeability to three ions (Na-22, Cl-36, and Rb-86) and two passive permeability tracers {[H-3]alpha-aminoisobutyric acid (H-3]AIB) and [C-14]urea} was determined. Permeability to either passive tracer was not increased, indicating that the BBB was intact. The rate of Cl-36 influx was 3 times greater and the rate of Na-22 influx 1.8 times greater than their respective net rates of accumulation in ischemic brain. The BBB permeability to Na-22 relative to that of [H-3]AIB was significantly increased in the ischemic cortex, the relative permeability to Rb-86 was significantly decreased, and the relative permeability to Cl-36 was unchanged. These results indicate that the stimulation in BBB sodium transport is specific for sodium. Further, chloride accumulates with sodium in brain during the early stages of ischemia; however, its rate of accumulation is low compared with its rate of transport from blood to brain. Therefore, inhibition of BBB sodium transport is more likely to reduce edema formation than is inhibition of BBB chloride transport.