硬通道穿刺术与显微小骨窗治疗中等量高血压脑出血患者神经功能恢复的比较

目的 评价微创穿刺血肿引流术与显微小骨窗开颅血肿清除术治疗中等量高血压脑出血的效果. 方法 选择65例中等量（30～70ml）高血压脑出血患者,随机分为微创穿刺血肿引流术（穿刺组,35例）和显微小骨窗开颅血肿清除术（开颅组,30例）,评价两组患者术后3月神经功能缺损程度、日常生活活动能力（ADL）、住院期间的死亡率及并发症. 结果 患者住院期间的并发症发生率差异显著（P＜0.05）,穿刺组少于开颅组.治疗3个月后随访,ADL达自理水平的良好状态者,两组有显著性差异（P＜0.01）,穿刺组优于开颅组.两组的死亡率无显著性差异. 结论 微创血肿冲洗引流术有助于患者神经功能的恢复,提高患者日常生活能力,值得推广和借鉴.     

高血压脑出血时间与颅内血肿微创清除术预后的关联分析

目的探讨高血压脑出血时间与颅内血肿微创清除术预后的关联性。方法回顾性分析本院就诊并接受手术治疗的高血压脑出血患者60例,根据出血时间分为超早期组(出血时间6小时)、早期组(6小时≤出血时间24小时)和延期组(24小时≤出血时间),通过行颅内血肿微创清除术后,观察各组治疗前后颅内血肿、血肿周围水肿变化,NIHSS评分和各组患者的临床疗效比。结果脑血肿和脑水肿情况治疗7天、14天后血肿均有减少,并且差异具有统计学意义(P0.05);治疗前两组NIHSS评分比较,差异无统计学意义(P0.05),治疗14天后各组治疗前和治疗后比较差异具有统计学意义(P0.05);各组高血压脑出血患者的临床疗效对比,超早期优良率为86.7%,早期组为60%,延期组为20%,差异具有统计学意义(P0.05)。结论早期微创颅内血肿清除术可以有效地清除高血压出血的颅内病灶,出血时间和患者的预后关联密切,越早越及时行微创颅内血肿清除术,能够有效提高神经功能恢复状态。     

微创颅内血肿清除术治疗高血压脑出血效果分析

目的观察微创颅内血肿清除术治疗高血压脑出血的效果。方法根据不同治疗方法将92例高血压脑出血患者分为2组。微创组(50例)实施微创颅内血肿清除术,保守组(42例)给予药物治疗。比较2组的疗效。结果微创组血肿清除时间、并发症发生率及治疗后3个月的总有效率均优于保守组,差异均有统计学意义(P0.05)。结论微创颅内血肿清除术治疗高血压脑出血,创伤小、并发症发生率低、有效率高,有利于改善患者的预后。     

双靶点微创清除术治疗大量高血压性脑出血临床研究

目的 对双靶点微创清除术治疗大量高血压性脑出血的疗效进行临床观察与对照研究。方法 将63例出血量＞60ml的高血压性脑出血患者分为治疗组和对照组。治疗组(3l例)采取双靶点微创清除术治疗；对照组(32例)采用单靶点微创清除术治疗。两组分别在入院初始和3周进行中国卒中量表(CSS)评分，3个月后随访，进行Barthel指数日常生活能力量表(ADL）评分。结果 治疗组死亡率及3周时CSS评分明显低于对照组，血肿清除率明显高于对照组。3个月后随访Barthel指数ADL评分明显高于对照组。结论 双靶点微创清除术治疗大量高血压性脑出血的病死率和致残率，疗效好于单靶点微创清除术。     

通过运动诱发电位比较微创穿刺术与小骨窗开颅术治疗高血压性脑出血的疗效

目的比较微创穿刺血肿粉碎清除术和小骨窗开颅血肿清除术治疗高血压脑出血运动诱发电位的影响。方法将60例患者分为微创穿刺血肿粉碎清除术36例和小骨窗开颅手术24例,治疗后第1、2周行运动诱发电位（MEP）检测并进行比较。结果治疗后1周,微创组患者中有29例可引出MEP波形,小骨窗组只有9例可引出肯定波形;治疗后2周,微创组全部病例均能引出MEP波形,小骨窗组有24例患者能引出MEP波形,但潜伏期明显长于微创组。结论微创穿刺引流不但可清除血肿．而且对脑组织损伤小,较小骨窗开颅血肿清除术有利于神经功能的恢复。     

微创颅内血肿清除术治疗高血压脑出血效果观察

目的探讨微创颅内血肿清除术治疗高血压脑出血的效果。方法根据不同治疗方案将104例高血压脑出血患者分为2组,各52例。对照组行开颅血肿清除术,观察组行微创颅内血肿清除术。比较2组治疗效果。结果观察组总有效率高于对照组;术中出血量、手术时间、住院时间及术后3个月NIHSS评分低于对照组,差异均有统计学意义(P0.05)。结论微创颅内血肿清除术治疗高血压脑出血,效果显著,可有效减少术中出血量和改善患者的神经功能。     

开颅血肿清除和硬通道穿刺治疗基底节区高血压脑出血的疗效对比

目的：对比开颅血肿清除和硬通道穿刺治疗高血压基底节区脑出血的效果及预后。方法回顾性分析2005年1月～2013年12月我科192例高血压脑出血的临床资料,其中开颅血肿清除术（开颅组）和穿刺引流术（微创组）各96例。2组年龄、性别、血肿侧别及Glasgow昏迷评分差异无显著性（P＞0．05）。对比2组术中出血量、术后残余血肿量、手术时间、住院时间和术后3周及6个月的临床疗效。结果与开颅组比较,微创组手术时间短[中位数31（24～39） min vs．152（131～170）min,Z＝-11．975,P＝0．000],术中出血少[30例0 ml、66例＜5 ml vs．（332．4±20．2）ml],术后住院时间短[中位数14（10～17）d vs．64（44～75）d,Z＝-44．217,P＝0．000],但术后残余血肿量多[中位数13（8～17）ml vs．7（4～12）ml, Z＝-11．573,P＝0．000]。治疗3周后,微创组Glasgow 预后评分高[中位数4（2～4）分 vs．3（1～4）分,Z＝-8．215,P＝0.000],Barthel指数高[（59．9±4．5） vs．（54．9±4．9）,t＝7．370,P＝0．000]。治疗6个月,微创组Glasgow预后评分高[中位数3（2～4）分vs．2（1～4）分,Z＝-7．448,P＝0．000],Barthel指数高[（64．3±8．4） vs．（59．7±6．8）,t＝4．156,P＝0．000],2组病死率差异无显著性（P＞0．05）。结论微创颅内血肿硬通道穿刺引流术在一定程度上明显优于开颅血肿清除术,值得临床推广应用。     

微创穿刺术治疗中等量高血压脑出血的疗效分析

目的 评价微创穿刺清除术与传统保守治疗中等量基底节区高血压脑出血的效果。方法：回顾性分析84例中等量（30~60 ml）高血压基底节区脑出血患者临床资料,分为微创穿刺血肿清除术（微创组,45例）和传统保守治疗（保守组39例）,评价两组患者1周时的意识恢复情况、治疗1个月时神经功能缺损程度(NID)和3个月时日常生活活动能力(ADL)。结果 治疗第7天时微创组的意识恢复率（75.6%）明显高于保守组（46.0%）;1个月后微创组患者的NID明显低于保守组（P<0.05）;治疗3个月后随访,患者ADL达自理水平的较好状态者（Barthel指数≥80）,两组有显著性差异（P<0.05）,微创组优于保守组。结论：与保守组相比,微创穿刺术可明显改善中等量基底节区脑出血患者早期的意识状况,改善神经功能缺失程度、提高患者日常生活活动能力,降低病残率。     

高血压脑出血开颅血肿清除与微创清除对比分析

目的 探讨微创与开颅血肿清除术对高血压脑出血治疗的可行性和有效性，为临床提供适宜的治疗措施。方法应用开颅血肿清除治疗高血压脑出血12例，应用微创血肿清除治疗高血压脑出血16例。结果 开颅血肿清除抢救成功8例，抢救成功率66．6％，微创血肿清除抢救成功8例，抢救成功率50．0％，但出血8h内12例手术，仅抢救成功4例，而出血3天后手术4例均获成功。结论高血压脑出血早期，血肿量大，中线移位明显，特别是伴有脑疝时，应开颅血肿清除。出血早期因微创术有引起再出血的危险，要慎用。出血3天后的患者，这时出血已停止，血肿已液化，适宜微创血肿清除。     

微创穿刺颅内血肿清除术治疗高血压脑出血21例

目的探讨微创穿刺引流术治疗高血压脑出血的临床效果。方法回顾分析微创穿刺颅内血肿清除术治疗高血压脑出血21例患者的临床资料。结果无1例发生颅内感染。初步清除率40.8%～75.2%,平均56.5%。术后1周复查CT,血肿消失达90%,其余均在手术后2周消失。出院后随访1～3个月,生存19例,占90.5%,死亡2例。结论微创穿刺颅内血肿清除术治疗高血压脑出血,效果显著,值得推广。     

Brain oedema and blood-brain barrier permeability in pulsatile and nonpulsatile cardiopulmonary bypass

In pigs subjected to pulsatile or nonpulsatile cardiopulmonary bypass (CPB) at normothermia for 3 hours, evaluation was made of water content in brain tissue (specific gravity measurements), blood-brain permeability to serum proteins (immunocytochemical demonstration of extravasated proteins, using peroxidase-antiperoxidase technique) and histopathology (paraffin sections). The specific gravity in parietal cortex was higher after pulsatile than after nonpulsatile CPB or in control pigs, the change corresponding to a 6.3% water increase. The tissue water content was unchanged in the internal capsule, basal ganglia and nucleus accumbens after CPB. The vascular permeability to serum proteins was unchanged after nonpulsatile CPB, but after pulsatile CPB minute foci of extravasated serum proteins appeared. All the animals showed dark neurons in cortical and subcortical regions, but these could have been artefacts in immersion-fixed tissue. There were no other signs of ischaemic tissue damage. The study indicated that cortical oedema may follow pulsatile CPB, the cause being altered permeability of the blood-brain barrier to serum proteins.     

Electrophoretographic analysis of blood-brain barrier function

Intracerebral serum proteins were measured in rats with altered blood-brain barrier (BBB) function. The rats were divided into seven groups of five to 10 each and subjected to the following procedures: controls (NOR); bilateral common carotid artery ligation (BLCL), evaluated after 6 hours; three-vessel occlusion (bilateral common carotid and right vertebral arteries) (TVO), evaluated after 6 hours; cold injury (BE6 and BE24), evaluated after 6 and 24 hours; and intracarotid injection of a hypertonic solution (BBB6 and BBB24), evaluated after 6 and 24 hours. The protein components of concentrated, water-soluble extracts of each rat's brain were analyzed by cellulose acetate membrane electrophoresis. Serum proteins of each rat were also analyzed. The intracerebral albumin fraction was increased in groups BE24, BBB6, and some TVO rats. The intracerebral alpha-1 fraction was increased in group BBB24. No difference was found in the electrophoretographic patterns of groups NOR and BLCL. These findings demonstrate that serum albumin is increased in TVO, and suggest that the BBB is damaged as in cold injury, which is thought to cause edema. The predominant intracerebral serum protein appeared to change from the alpha-1 fraction to the albumin fraction in cold-injured animals, which suggests that under this circumstance the BBB becomes progressively permeable to larger molecules. However, following injection of the hypertonic solution, the predominant intracerebral serum protein pattern changed from albumin to alpha-1, indicating recovery of BBB function. These differences in the intracerebral protein profiles may reflect differences between BBB disruption without edema and vasogenic brain edema. Disruption of the BBB may play as important a role in ischemic brain edema as it does in vasogenic edema.     

Breakdown of the blood-brain barrier after fluid percussion brain injury in the rat: Part 2: Effect of hypoxia on permeability to plasma proteins.

Clinical studies have demonstrated that hypoxia after severe brain injury is common and significantly worsens neurologic outcome. We have, therefore, developed a rat model of posttraumatic hypoxic injury in order to identify the pathophysiologic responses after head injury that are worsened by this secondary insult. We examined the effect of hypoxia after brain injury on permeability of the blood-brain barrier to plasma proteins. Animals were divided into two experimental groups: group I (impact alone) and group IH (impact plus hypoxia). Rats were subjected to a lateral fluid percussive brain injury (4.8-5.2 atm). Animals in group IH were exposed to hypoxic conditions (10% O2) for 45 min immediately after injury. In each group, vascular permeability to endogenous immunoglobulins (IgG) and to horseradish peroxidase (HRP) was examined at the light microscopic level. IgG was immunolocalized in brain sections at 1-24 h after injury. In other studies, HRP was given i.v. either before impact or 10 min before killing. Permeability to this protein was assessed at 1-72 h after injury. The distribution of extravasated proteins was similar between the experimental groups at 1 h postinjury. Pronounced abnormal permeability to IgG and HRP (given before impact) occurred in discrete regions throughout both the ipsilateral and contralateral hemispheres. By 6 h after injury, a differential response of the blood-brain barrier was noted between groups I and IH. Widespread leakage of proteins was observed in the injured hemisphere in group IH. This finding was in sharp contrast to group I, in which extravasated proteins remained more localized in the injured hemisphere. The time course for reestablishment of the blood-brain barrier to HRP (given before killing) was determined. The impact site remained permeable to HRP up to at least 72 h postinjury within groups I and IH. In group I, the blood-brain barrier was reestablished in the parasagittal cortex and deep cortical layer by 6 h postinjury. In contrast, the blood-brain barrier in group IH was not restored in similar brain regions until 24 h postinjury. These studies demonstrate that (1) hypoxia after brain injury exacerbates the regional breakdown of the blood-brain barrier to circulating proteins, (2) this influence of hypoxia on permeability is not apparent immediately after injury but rather is expressed at 6 h after injury, and (3) hypoxia after traumatic brain injury delays recovery of the blood-brain barrier. These findings suggest that secondary posttraumatic hypoxia contributes to the vascular pathogenesis of brain injury.     

Breakdown of the blood-brain barrier after fluid percussive brain injury in the rat. Part 1: Distribution and time course of protein extravasation.

Experimental brain injury is associated with marked vasogenic edema, as evidenced by an increase in brain water content. This prominent and widespread response raises questions about the vulnerability of microvasculature in the brain to injury. In the present report we further characterize the vascular response by evaluating the integrity of the blood-brain barrier to circulating proteins. Vascular permeability to endogenous immunoglobulins (IgG) and to the protein horseradish peroxidase (HRP) was examined after a lateral, fluid percussive brain injury in the rat. In study 1 IgG was immunolocalized in brain sections 1-24 hr after injury. In studies 2 and 3 HRP was given intravenously either before impact (study 2) or 10 min before sacrifice (study 3). Permeability to this protein was assessed at 1-6 hr (study 2) or at 1-72 hr (study 3) after injury. In studies 1 and 2 the extravascular accumulation of proteins was evaluated. Pronounced abnormal permeability to IgG and HRP occurred within the first hour after injury and was widespread throughout both hemispheres. The intensity of immunostaining for IgG increased with time up to 24 hr after injury. In contrast, maximal extravascular accumulation of HRP occurred within the first hour after injury. In study 3 the time course for re-establishment of the blood-brain barrier to HRP was determined. Maximal permeability occurred at 1 hr after injury. At 24 hr abnormal permeability was restricted to the impact site and this area remained permeable up to 72 hr after injury. In summary this study demonstrates that breakdown of the blood-brain barrier to plasma proteins is a prominent feature of experimental brain injury. This abnormal permeability is characterized by its transient expression and widespread distribution. The time course for re-establishment of the blood-brain barrier to circulating proteins is most delayed at the impact site.     

Electroencephalographic consequences of sodium dehydrocholate-induced blood-brain barrier disruption: Part 1. Acute and chronic effects of intracarotid sodium dehydrocholate

Prior work has shown that the intracarotid infusion of sodium dehydrocholate can produce prolonged reversible blood-brain barrier (BBB) disruption. Associated with barrier disruption is the occasional presence of behavioral seizure activity. Electroencephalographic changes were monitored in 32 rats after BBB disruption by the left internal carotid artery infusion of sodium dehydrocholate. The electroencephalogram (EEG) was monitored for 3 hours after disruption in 20 animals, and the remaining 12 animals were followed for 24 hours. The EEG was also monitored in 8 additional control animals: 4 had undergone carotid artery infusion with normal saline, and 4 had received sodium dehydrocholate intravenously. The 20 rats monitored for up to 3 hours postinfusion were found to have varying grades of BBB disruption as measured by the presence of Evans blue staining of the brain. EEG alterations in this group included decreased amplitude and slowing as well as the presence of spike activity over the disrupted and the nondisrupted hemispheres. The more extensive the disruption, the more severe the EEG changes. In animals with minimal to moderate disruption, the EEG usually returned to base line levels within 3 hours after infusion. Animals with marked disruption usually had bilaterally flat EEGs before the end of the observation period. The remaining 12 animals were followed for 24 hours postinfusion. Of 9 animals surviving 24 hours, 1 animal had a decrease in amplitude over the disrupted hemisphere; in the remaining 8 animals, the spontaneous EEG was unchanged from predisruption levels except for occasional spikes in 2 animals. Animals infused with intracarotid saline or intravenous sodium dehydrocholate demonstrated no EEG changes or Evans blue staining.(ABSTRACT TRUNCATED AT 250 WORDS)     

大鼠周围神经移植修复马尾神经损伤的早期形态学观察

目的：探讨坐骨神经移植修复马尾神经损伤的可行性,观察马尾神经再生情况。方法：将30只雌性Wistar大鼠分为三组,实验组：将20只大鼠马尾在L2水平行半侧切除,将对侧坐骨神经移植到马尾切除侧,近端接马民行断端,移植的坐骨神经远端与马尾切除侧坐骨神经吻合,分别于术后4、6、8周在光镜及电镜下观察马尾再生情况。实验对照组：5只大鼠,仅切除部分马尾。正常对照组：5只大鼠,不做处理。结果：实验对照组坐骨神经的轴突及髓鞘均崩解,无再生轴突形成。实验组术后4周HE及固蓝染色偶见髓鞘及轴突形成,雪旺细胞数目少,有世噬细胞吞噬现象;术后6周较4周再生髓鞘及神经轴突数目增多,雪旺细胞大量增生,巨噬细胞吞噬现象减少;术后8周高倍镜下可见再生的典型形式,即胶质基质中的退变纤维中有大量簇状细小的有髓神经纤维,电镜下可见含较多细的有髓和无髓神经纤维,内含较多线粒体等管状结构,雪旺细胞核大而明显,胞浆丰富,粗面内质网及高尔基体、线粒体增加明显。结论：周围神经移植修复马尾神经是可能的,马尾神经损伤后有再生的可能性。     

周围神经移植修复脊髓损伤的实验研究

目的：探讨自体坐骨神经移植修复脊髓损伤的可行性。方法：将58只雌性Wistar大鼠分为二组，实验组：采用显微外科技术，将50只大鼠于T13水平切除左半侧脊髓10mm，再取右侧坐骨神经10mm移植到脊髓缺损处，近端接脊髓，远端接马尾，分别于术后2、4、6、8、12、22周在光镜和电镜下观察移植处坐骨神经、吻合口远端马尾神经、左后肢坐骨神经再生情况，并用摄像机记录患肢功能恢复情况。对照组：8只大鼠，于13水平切除左半侧脊髓10mm，不移植坐骨神经，观察脊髓缺损远端马尾神经和左右肢坐骨神经再生情况。结果：对照组坐骨神经的轴突及髓鞘部分崩解，密度降低，无再生轴突形成。实验组术后4周电镜下偶见移植处坐骨神经髓鞘及轴突形成，术后8周光镜及电镜下可见较多细的有髓神经纤维，22周时接近正常；同时观察到左后肢坐骨神经再生；大鼠后肢功能部分恢复，肌力达3级。结论：大鼠脊髓损伤后有再生能力，周围神经移植修复脊髓损伤是可行的。     

Penetration of recombinant interleukin-2 across the blood-cerebrospinal fluid barrier

Recombinant interleukin-2 (rIL-2) is an immunotherapeutic agent with efficacy against certain advanced cancers. The penetration of rIL-2 across the blood-cerebrospinal fluid (CSF) barrier was studied in 12 cancer patients who had no evidence of tumor involvement of the central nervous system. At different times during treatment with intravenous rIL-2, CSF was withdrawn either continuously for 8 to 26 hours via a lumbar subarachnoid catheter (in eight patients) or by a single lumbar puncture (in four). Bioassay showed the appearance of rIL-2 in lumbar CSF 4 to 6 hours after the first intravenous dose, a rise over 2 to 4 hours to a plateau of 3 to 9 U/ml, and clearance to less than 0.1 U/ml by 10 hours after the last dose. An abnormally elevated CSF albumin level in two of the twelve patients indicated alteration of the blood-brain barrier. There were no abnormalities in the CSF glucose level or white blood cell count. The CSF pharmacokinetics contrast with the rapid elimination of rIL-2 from plasma and demonstrate significant blood-CSF barrier penetration. These data support the possibility of achieving CSF levels of rIL-2 that are adequate to maintain activity of lymphokine-activated killer cells after parenteral administration, and argue for rIL-2-associated disruption of the human blood-brain barrier in some patients.     

Penetration of cephaloridine and cephalothin into the cerebrospinal fluid-clinical study (author's transl)]

There were 35 cases, treated with Cephaloridine or Cephalothin after neurosurgical operation. Neurological surgeon always troubled with passage of blood-brain barrier when drug was given. Antibiotics was not exceptionally, therefore we, neurological surgeon, must select the effective drug to bacterium, that which penetrated enough to the intracranial organ through the blood-brain barrier. In this paper, we measured the concentration of Cephaloridine and Cephalothin into cerebrospinal fluid in the cases with non inflammatory meninges. We collected the cerebrospinal fluid from continued ventricle tap and serum, then measured the concentration of the drug with bioassay. Cephaloridie treated cases. 22 cases. 1) 1 g intramuscular injection. 4 cases. Serum level got to highest value, 64 mug/ml (mean value) 1 hour after injection. CSF level got to maximum concentration 46.8 mug/ml. (mean value) serum mean level 21.5 mug/ml. CSF mean level 0.73 mug/ml. 2) 1 g 3 minutes-intravenous injection 5 cases. Serum level got to highest value 67.5 mug/ml. CSF maximum level was 5.25 mug/ml. Serum mean level 19.74 mug/ml. CSF mean level 0.61 mug/ml. 3) 1 g 1 hour-intravenous drip. 9 cases. Serum maximum level 121.0 mug/ml. CSF maximum level 2.30 mug/ml. Serum mean level 20.08 mug/ml. CSF mean level 0.67 mug/ml. 4) 1 g 8 hours-intravenous drip. 3 cases. Serum maximum level 61.0 mug/ml. CSF maximum level 1.36 mug/ml. Serum mean level 14.78 mug/ml. CSF mean level 0.47 mug/ml. Cephalothin treated cases, 12 cases. 1) 1 g 8 hours-intravenous drip, 4 cases. In fact we could detect the drug only in one case, in CSF, and we could not in other three cases. In KF - 4 case, serum maximum concentration was 26.0 mug/ml, CSF maximum concentration was 0.07 mug/ml. Serum mean level 16.97 mug/ml. CSF mean level 0.01 mug/ml 2) 2 g 1 hour-intravenous drip, 9 cases. Serum maximum level 690.0 mug/ml. CSF maximum level 2.03 mug/ml. Serum mean level 29.59 mug/ml. CSF mean level 0.06 mug/ml. In cephaloridine cases, the tendency was observed, that which, as concentration of the drug in CSF increased, cell count and protein decreased, and, as concentration of the drug decreased, cell count and protein increased. CSF/serum concentration ratio of Cephaloridine increased, when time passed, in intramuscular, 3 minutes intravenous, and 1 hour-intravenous drip group. Then only in 8-hours-intravenous prip group. Then only in 8-hours-intravenous drip group, concentration ratio decreased. In Cephaloridine group, mean value of CSF/serum ratio showed. 1 g i.m. 0.084 1 g 3 minutes-i.v. 0.098 1 g 1 hour-i.v. 0.194 1 g 8 hours-i.v. 0.044.     

Relationship between blood flow and blood-brain barrier permeability of sodium and albumin in focal ischaemia of rats: A triple tracer autoradiographic study

Summary Local cerebral blood flow, the permeability of the blood-brain barrier to sodium and serum albumin, and the content of electrolytes were investigated in rats before and at 4 h and 24 h following permanent occlusion of the middle cerebral artery (MCA). Measurements were carried out by triple tracer autoradiography, using¹³¹Iiodoantipyrin,²²NaCl and¹²⁵I-iodinated bovine serum albumin, respectively. Regional sodium and albumin transfer coefficients were calculated by multiple time point analysis, and correlated with the corresponding flow and tissue electrolyte values. In sham operated controls regional sodium and albumin transfer coefficients ranged between 2.16–2.30·10^–3 and 0.22–0.48·10^–3 ml/min per g, respectively. Four hours after MCA occlusion sodium and albumin transfer coefficients were unchanged although tissue sodium content was already increased. After 24 h the sodium — but not albumin — transfer coefficient increased 2–3 fold but the rise in tissue sodium content was slower than after 4 h. At both ischaemia times the unidirectional sodium influx was substantially higher than the actual changes of tissue sodium content. The development of stroke oedema is, therefore, not limited by the alterations of barrier permeability.A preliminary account of this study had been presented at the Symposium Brain Oedema VII, which took place at Bern in June 1990, and has been published in: Reulenet al (eds) (1990) Acta Neurochirurgica [Suppl] 51: 216–219