酶屏障抑制剂951治疗血管源性脑水肿

目的观察酶屏障抑制剂951治疗血管源性脑水肿的效果.方法Wistar大鼠腹腔注射苯肾上腺素.制成血管源性脑水肿模型,分注射951和甘露醇组,用远红外线水分分析仪分别测量脑灰、白质水分含量.结果951对脑水肿有显著脱水作用.尤对脑白质的脱水作用比用甘露醇更明显.结论951对脑白质水肿为特征的血管源性脑水肿有选择性治疗作用,是治疗血管源性脑水肿的有效新方法.     

酶屏障抑制剂LB治疗血管生脑水肿的实验研究

目的 观察酶屏障抑制剂ＬＢ对血管源性脑水肿（ＶＢＥ）的治疗作用。方法 Ｗｉｓｔａｒ大鼠腹腔注射苯肾上腺素制成ＶＢＥ模型,分别注射ＬＢ和甘锭药外线水份分析仪分别测量灰、白质水份含量,结果 ＬＢ对脑水肿有显著脱水作用,与甘露醇比较有显著差异,尤其对白质的脱水作用更显著,结论酶屏障抑制剂ＬＢ对脑水肿,尤其对脑白质水肿有选择性治疗作用,是治疗ＶＥＢ的新方法。     

肿瘤血管源性脑水肿研究进展

临床上脑肿瘤周围水肿较为常见，过多的液体在脑肿瘤周围组织间隙积聚即细胞外液体最增多称为肿瘤源性脑水肿。其发生与肿瘤存存或生长有关，常沿脑白质内的神经纤维呈放射状（或指状）分布，通常被归类于血管源性脑水肿，并常致血脑屏障的异常，本文对脑瘤周罔水肿的发生机理、特点、影响州素及其治疗的研究进展作一综述。     

碱性磷酸酶单克隆抗体对大鼠血管源性脑水肿的治疗作用

目的 观察碱性磷酸酶单克隆抗体（AAP）对大鼠血管源性脑水肿（ VCE）的治疗作用。方法 60只大鼠随机分为正常组、VCE组与AAP组。用AAP注射到已制成的VCE模型的Wistar大鼠腹腔,通过远红外线水分分析仪分别测定各组脑灰、白质水分含量百分比。用Evan's blue(EB）测定血脑屏障（BBB）的通透性。结果 AAP组对减少VCE大鼠脑灰、白质水分含量,降低BBB通透性均有显著效果（均P＜0．01）,而与正常组比较无显著差异（P＞0．05）。结论 AAP具有治疗VCE的作用,VCE的发病机制与碱性磷酸酶活性有关。     

一种新型血管源性脑水肿模型的建立

目的　建立简便易行、重复性好、无创伤、符合人类发病条件的ＶＢＥ 新模型。方法　Ｗｉｓｔａｒ鼠腹腔注射苯肾上腺素,测定微血管通透性,测量脑灰、白质水分含量,组织病理证实脑水肿。结果　血脑屏障通透性增高,脑水分增加（Ｐ＜ ０．０１）,灰质水分增加１１．６１％ ,白质水分增加１４．６４％ ,白质比灰质水分增加明显（Ｐ＜ ０．０５）。结论　注射苯肾上腺素制成ＶＢＥ动物模型,操作简便、无创伤、重复性好。     

加味四逆汤治疗脑出血伴血管源性脑水肿23例

四逆汤为<伤寒论>名方,由附子、干姜、炙干草组成,中医理论认为它具有温中祛寒、回阳救逆的功效.临床常用于心肌梗死、心衰、急慢性胃肠炎吐泻过多、各种高热大汗所致之虚脱,各种因素所致的休克等阳衰阴盛者,药理研究已证实其具有显著的升压、强心、抗休克等作用.     

加味四逆汤治疗脑出血伴血管源性脑水肿23例

四逆汤为<伤寒论>名方,由附子、干姜、炙干草组成,中医理论认为它具有温中祛寒、回阳救逆的功效.临床常用于心肌梗死、心衰、急慢性胃肠炎吐泻过多、各种高热大汗所致之虚脱,各种因素所致的休克等阳衰阴盛者,药理研究已证实其具有显著的升压、强心、抗休克等作用.     

加味四逆汤治疗脑出血伴血管源性脑水肿23例

四逆汤为<伤寒论>名方,由附子、干姜、炙干草组成,中医理论认为它具有温中祛寒、回阳救逆的功效.临床常用于心肌梗死、心衰、急慢性胃肠炎吐泻过多、各种高热大汗所致之虚脱,各种因素所致的休克等阳衰阴盛者,药理研究已证实其具有显著的升压、强心、抗休克等作用.     

加味四逆汤治疗脑出血伴血管源性脑水肿23例

四逆汤为<伤寒论>名方,由附子、干姜、炙干草组成,中医理论认为它具有温中祛寒、回阳救逆的功效.临床常用于心肌梗死、心衰、急慢性胃肠炎吐泻过多、各种高热大汗所致之虚脱,各种因素所致的休克等阳衰阴盛者,药理研究已证实其具有显著的升压、强心、抗休克等作用.     

加味四逆汤治疗脑出血伴血管源性脑水肿23例

四逆汤为<伤寒论>名方,由附子、干姜、炙干草组成,中医理论认为它具有温中祛寒、回阳救逆的功效.临床常用于心肌梗死、心衰、急慢性胃肠炎吐泻过多、各种高热大汗所致之虚脱,各种因素所致的休克等阳衰阴盛者,药理研究已证实其具有显著的升压、强心、抗休克等作用.     

Role of extracellular proteins in the dynamics of vasogenic brain edema

Summary The relationship between extravasation of protein into extracellular spaces of brain parenchyma and the water content of such regions were evaluated in an experimental model. In this model, a temporary opening of the blood-brain barrier (BBB) to proteins was produced without significant injury to the cellular elements of brain tissue. Rabbits were subjected to bolus injection of their own blood under 360–400 mm Hg pressure via the internal carotid artery. The opening of the barrier and its duration were evaluated with Evans blue (EB), horseradish peroxidase (HRP), and sodium fluorescein (NaFl) tracers. The water content of brain tissue was assessed by specific gravity (SG) measurements in 1-mm-diameter tissue samples. Quantitative evaluation of protein penetration into brain tissue was carried out using¹²⁵I bovine serum albumin (BSA). The opening of the BBB to proteins persisted up to 9 h, whereas the barrier remained permeable to small molecular NaFl for 24 h. The SG measurements indicated in the areas of EB extravasation a progressive increment in water content up to 9 h, i.e., the duration of BBB opening to proteins. Following this, there was a progressive clearance of edema in spite of the BBB remaining open for NaFl for 24 h. Quantitative evaluations of¹²⁵I-BSA and SG in the same tissue samples, supported by statistical analysis, indicated approximately linear relationship between albumin and water, implying a strong correlation between the development of vasogenic edema and extravasation of proteins into extracellular spaces.     

Distribution of exudated FITC-dextrans in experimental vasogenic brain edema produced by a focal cryogenic injury

Summary Mice were subjected to cortical cryogenic brain injury, and FITC-dextrans (mol. wt. 20,000 or 150,000) were injected intravenously (i.v.). After a survival period of 4 h the distribution of the FITC-dextrans was determined by a histotechnical procedure described recently (Hultström et al. 1982a). This technique is based on freeze-drying and vapor fixation to immobilize the tracer and to provide tissue fixation.In and around the cryogenic injury both tracers leaked out of the cortical and the leptomeningeal vessels and spread into the brain parenchyma. They were seen as multiple, closely apposed droplets of fluorescent material best recognized by fluorescence microscopy under high magnification. The tracers were also taken up by neuronal perikarya and in glial cell nuclei of, presumably, astrocytic origin.Our study shows that the FITC-dextran technique can be used for experimental studies on the vasogenic form of brain edema. The patterns formed by the extravasated tracers have qualitative similarities to those produced by other more commonly used tracers, such as fluorochrome-labeled serum proteins and peroxidase.Supported by grants from the Swedish Medical Research Council, project no. 12X-03030, Trygg Hansa, Svenska läkarsällskapet, and Söderbergs stiftelser     

Uptake of macromolecules into neurons from a focal vasogenic cerebral edema and subsequent axonal spread to other brain regions

Summary Intravenously (i.v.) injected horseradish peroxidase (HRP) which has leaked out of the vessels in a cryogenic cortical injury of adult mice is taken up into a large number of neurons resulting in two different forms of labeling. Diffuse neuronal labeling of, the type previously reported in many conditions with vasogenic brain edema occurred particularly within the primary lesion. The other and more frequent type, here calledgranular neuronal labeling, was present in a wide zone immediately outside the injury. Such neurons contained HRP in numerous cytoplasmic granules and had the same characteristics as normal neurons accumulating HRP after retrograde axonal transport. By using highly sensitive histochemical methods for demonstration of HRP we could also follow bundles of labeled axons out from the primary lesion. Some of them passed the corpus callosum to the fronto-parietal cortex of the contralateral hemisphere.With this report we would like to put emphasize on certain phenomena occurring in neurons which previously have not been particularly recognized in studies on vasogenic brain edema. It can be assumed that in a focal brain lesion components from the edematous fluid and other wound substances can be taken up into nerve cell processes and then be intracellularly transported in different directions. In this way, nerve cell populations located in other brain areas and even in the contralateral hemisphere may be influenced by components from the primary injury.Supported by grants from the Swedish Medical Research Council, project 12X-03020 and Trygg-Hansa, Stokholm     

Relationship between specific gravity,water content,and serum protein extravasation in various types of vasogenic brain edema

Summary Vasogenic brain edema was induced in cats by cold injury (six animals), brain tumors (five animals), and brain abscesses (six animals). Water and electrolyte content, specific gravity, blood volume, and the amount of extravasated serum proteins were determined in small tissue samples taken from gray and white matter at various distances from the lesion. Edema was strictly confined to the white matter of the affected hemisphere and declined from the lesion to the more peripheral regions. It was characterized by the extravasation of serum proteins and an increase of water and sodium content with little or unpredictable changes of potassium and blood volume. The calculated sodium content of edema fluid varied between 129 and 135 eq/ml, and serum protein content between 8.1 and 11.9 mg/ml. In all three types of edema, specific gravity and water content correlated closely with the same slope and intercept of the calculated regression (y=1.119–0.0011x,r=–0.91). The results obtained indicate that the main denominator of specific gravity of edematous white matter is water content and that this relationship is not significantly altered by variations of blood volume or serum protein content.     

Temporal profile of serum albumin extravasation following cerebral ischemia in a newly established reproducible gerbil model for vasogenic brain edema: a combined immunohistochemical and dye tracer analysis

Summary We investigated the temporal profile of the extravasation of serum albumin in a reproducible gerbil model of unilateral cerebral ischemia, using immunohistochemical and dye-tracer techniques to evaluate albumin accumulation and the occurrence of active extravasation, respectively. After 30 min of cerebral ischemia and subsequent reperfusion, immunostaining for albumin became visible in the lateral part of the thalamus during the first 3 h, and then expanded to other brain regions up to 24 h. At both 24 h and 3 days after reperfusion, massive extravasation of albumin was noted in the whole ischemic hemisphere, and this had decreased again by 7 days after reperfusion. The extent and the degree of albumin immunopositivity were almost the same in all animals examined at each period after reperfusion. The extravasation of Evans blue, which was allowed to circulate for 30 min before death, was limited to the lateral part of the thalamus during the first 6 h of reperfusion. In the circumscribed area of massive albumin extravasation, many neurons were immunopositive for albumin; most of these neurons appeared to be intact and also showed immunostaining for microtubule-associated protein 2. The current investigation clearly demonstrated that (1) albumin extravasation was produced with reliable reproducibility in this model, (2) the lateral part of the thalamus was the region most vulnerable to ischemic blood-brain barrier damage, and (3) many apparently intact neurons in the ischemic region were positive for albumin.Supported in part by a Grant-in-aid (01570485) from the Ministry of Education, Science and Culture and by a research grant for cardiovascular diseases (2A-2) from the Ministry of Health and Welfarc in Japan