脑出血患者血浆及脑脊液内皮素—1含量对照研究

本文对照研究了脑出血患者血浆及脑脊液（ＣＳＦ）内皮素－１（ＥＴ－１）含量改变及其临床意义。发现脑出血患者血浆与ＣＳＦ、ＥＴ－１含量均增高；单纯脑血肿者以血浆含量增高为主；脑实质出血伴有脑室系统或蛛网膜下腔出血（ＳＡＨ）者血浆及ＣＳＦ含量均显著升高；小量出血与中大量出血比较血浆含量无显著性，而大量出血者ＣＳＦ、ＥＴ－１含量增高。提示脑出血者血浆ＥＴ－１增高可能与机体应激有关，而ＣＳＦ、ＥＴ－１升高可     

小儿病毒性脑炎患者内皮素—1含量的研究

采用放射免疫均相竟争法，测定５６例急性病毒性脑炎（ＡＶＥ）患儿的血浆和脑脊液（ＣＳＦ）中内皮素－１（ＥＴ－１）含量。结果发现，ＡＶＥ急性期患儿血浆ＥＴ－１含量明显高于疾病对照组和正常对照组（Ｐ＜０．０１），急性期血浆和ＣＳＦ中ＥＴ－１含量高于恢复期（Ｐ＜０．０１），血浆与ＣＳＦ中ＥＴ－１含量呈正相关（ｒ＝０．８５８，Ｐ＜０．００１），病情严重、抽搐频繁、ＥＥＧ和脑ＣＴ或ＭＲＩ显示病变部位广泛者，血浆和ＣＳＦ中ＥＴ－１含量增高更为显著。认为ＥＴ－１是一种新的内源性致病因子，在ＡＶＥ病程发展与转归中起重要作用。     

中枢神经系统感染患者血浆与脑脊液中内皮素变化的研究

目的探讨中枢神经系统感染（ＣＮＳＩ）时血浆与脑脊液（ＣＳＦ）中内皮素（ＥＴ）的变化。方法采用放射免疫法测定６６例ＣＮＳＩ患者血浆和ＣＳＦ中的ＥＴ－１水平。结果ＣＮＳＩ患者ＣＳＦ中的水平较对照组高，对照组与病毒脑、结脑组相比有显著性差异（Ｐ分别＜０．００１、０．０５），与化脑组相比无显著性差异（Ｐ＞０．０５），血浆中的水平与ＣＮＳＩ关系不明显（Ｐ＞０．０５）；ＣＮＳＩ伴重度脑功能障碍者ＣＳＦ和血浆中ＥＴ－１水平明显高于伴轻中度脑功能障碍者（Ｐ＜０．００１）或无脑功能障碍者（Ｐ＜０．００１），轻中度脑功能障碍又明显高于无脑功能障碍者（Ｐ＜０．００１）。结论ＣＳＦ和血浆中ＥＴ－１水平与ＣＮＳＩ的病种无关，而与脑损伤的程度有关，其含量增高可作脑实质损伤的重要指标，ＥＴ－１可能是脑实质损伤的重要因素     

内皮素一氧化氮在蛛网膜下腔出血后脑血管痉挛中的动态变化

目的：探讨内皮素（ＥＴ－１）和一氧化氮（ＮＯ）代谢产物在蛛网膜下腔出血（ＳＡＨ）后症状性脑血管痉挛（ＳＣＶＳ）发生机制中的作用。方法：建立兔的症状性脑血管痉挛模型,观察ＳＡＨ后不同时间血浆和脑脊液（ＣＳＦ）中ＥＴ－１和ＮＯ代谢产物含量变化。结果：ＳＡＨ后第４天和第７天血浆和ＣＳＦ中ＥＴ－１含量均显著升高（Ｐ〈０．０１）。且以ＳＡＨ后第４天为著。ＳＡＨ后第４天和第７天血浆和ＣＳＦ中ＮＯ代谢产物含量也明显升高（Ｐ〈０．０１）,但二者之间无显著性差异（Ｐ〉０．０５）。结论：ＳＡＨ后血浆和ＣＳＦ中ＥＴ－１和ＮＯ代谢产物含量增加在ＳＣＶＳ发生机制中起重要作用。     

脑出血患者血浆中ET—1,SP含量变化及临床意义

目的动态观察３０例脑出血患者血浆内皮素－１（ＥＴ－１）、Ｐ物质（ＳＰ）含量变化。方法应用放射免疫分析法（ＲＩＡ）。结果（１）急性期血浆ＥＴ－１、ＳＰ含量显著高于对照组。（２）急性期血浆ＥＴ－１、ＳＰ含量显著高于恢复期。（３）急性期血浆ＥＴ－１含量与ＳＰ含量呈正相关。结论ＥＴ－１、ＳＰ共同参与和影响脑出血的病理生理过程，血浆ＥＴ－１、ＳＰ含量的增高在一定程度上反映了脑出血的严重程度     

自发性脑出血后神经功能与脑血流动态变化的相关研究

研究６６例自发性脑出血（ＳＩＣＨ）患者急性期、亚急性期、恢复期的ＳＰＥＣＴ脑血流显像和神经功能的关系，发现：（１）临床神经功能与ｒＣＢＦ的变化密切相关；（２）失语组与无失语组者Ｂｒｏｃａ区和Ｗｅｒｎｉｃｋｅ区ｒＣＢＦ亦存在显著差异，失语的恢复与ｒＣＢＦ的恢复相一致；（３）交叉性小脑失联络（ＣＤＤ）现象与出血量及出血部位有关，出血量大和／或优势半球出血易引起ＣＤＤ。提示积极改善脑出血患者亚急性期和恢复期的脑血流量，有助于临床神经功能的恢复。     

脑梗塞患者血浆中内皮素和P物质的含量变化及临床意义

应用放射免疫分析法（ＲＩＡ）动态观察３０例脑梗塞患者血浆内皮素－１（ＥＴ－１）、Ｐ物质（ＳＰ）含量，其结果表明：（１）急性期血浆ＥＴ－１、ＳＰ含量显著高于对照组。（２）急性期血浆ＥＴ－１含量显著高于恢复期，ＳＰ含量显著低于恢复期。（３）急性期血浆ＥＴ－１含量与ＳＰ含量呈正相关。结果提示ＥＴ－１、ＳＰ共同参与和影响脑梗塞的病理生理过程，血浆ＥＴ－１、ＳＰ含量的增高在一定程度上反映了脑梗塞的严重程度。     

实验性犬SAH后CVS血浆、CSF中ET、CGRP含量动态变化及巴曲酶的保护作用研究

采用放免法动态观察了２５只实验性犬ＳＡＨ后ＣＶＳ动物模型的血浆、ＣＳＦ中ＥＴ及ＣＧＲＰ含量变化及巴曲酶的保护作用。结果：单纯注血组及巴曲酶治疗组的血浆、ＣＳＦ中ＥＴ含量较对照组明显增高（Ｐ＜０．０１），ＣＧＲＰ含量明显降低（Ｐ＜０．０１）。单纯注血组在注血后３０ｍｉｎ血浆、ＣＳＦ中ＥＴ含量开始升高，ＣＧＲＰ含量开始下降，至第７ｄＥＴ达最高值，ＣＧＲＰ达最低值。经蛛网膜下腔及静脉注入巴曲酶０．４ＢＵ／ｋｇ／ｄ组，血浆及ＣＳＦ中ＥＴ含量均较同期单纯注血组明显降低（Ｐ＜０．０１），而ＣＧＲＰ则明显升高（Ｐ＜０．０１）。提示血浆、ＣＳＦ中ＥＴ、ＣＧＲＰ失衡是ＳＡＨ后ＣＶＳ的原因之一。巴曲酶可防止ＥＴ升高和ＣＧＲＰ降低。     

实验性犬SAH后CVS血浆、CSF中NPY、ANP含量动态变化及巴曲酶的保护作用研究

目的探讨蛛网膜下腔出血（ＳＡＨ）后脑血管痉挛（ＣＶＳ）的发病机理和防治方法。方法采用放免法动态观察了犬ＳＡＨ后血浆、ＣＳＦ中神经肽Ｙ（ＮＰＹ）、心钠素（ＡＮＰ）含量动态变化及巴曲酶的保护作用。结果单纯注血组及巴曲酶治疗组血浆、ＣＳＦ中ＮＰＹ、ＡＮＰ含量较注血前及同期正常对照组明显增高（Ｐ＜０．０１）；单纯注血组在注血后３０ｍｉｎ血浆、ＣＳＦ中ＮＰＹ含量开始升高，ＣＳＦ中ＡＮＰ含量亦在注血后３０ｍｉｎ升高，血浆ＡＮＰ含量则在第２ｄ开始升高，至第７ｄ最高。蛛网膜下腔给药组和静脉注入巴曲酶０．４ＢＵｋｇ－１ｄ－１组血浆、ＣＳＦ中ＮＰＹ、ＡＮＰ含量均明显低于同期单纯注血组（Ｐ＜０．０１）。结论血浆、ＣＳＦ中ＮＰＹ、ＡＮＰ的异常增高是ＳＡＨ后ＣＶＳ的原因之一，巴曲酶可以防止ＮＰＹ和ＡＮＰ的异常增高。     

帕金森病和多系统萎缩患者脑脊液阿片肽含量变化的研究

采用放射免疫法检测８例帕金森病（ＰＤ）和１３例具帕金森综合征的多系统萎缩（ＭＳＤ）患者脑脊液（ＣＳＦ）中β－内啡肽（β－ＥＰ）、亮脑啡肽（ＬＥＫ）、强啡肽Ａ_（１－１３）（ＤｙｎＡ_（１－１３））含量。发现患者组ＣＳＦ中β－ＥＰ和ＬＥＫ含量显著高于对照组，ＤｙｎＡ_（１－１３）含量变化不显著。帕金森病和多系统萎缩两组间ＣＳＦ中三种阿片肽含量相差不明显。提示且ＥＰ、ＬＥＫ含量增高可能与ＰＤ和ＭＳＤ患者所共有的肌张力增高和肌强直等锥体外系症状产生有关。     

颅底肿瘤术后脑脊液中ET-1的动态变化与脑血管痉挛的相关性研究

目的探讨颅底肿瘤术后脑脊液中内皮素-1（ET-1）的动态变化规律及其与脑血管痉挛（CVS）的相关性。方法颅底肿瘤病人33例，在术后第3、5、7、10和14天用放免法测定脑脊液中ET-1的含量；手术前1天和术后第1、3、5、7、10和14天用经颅多普勒超声动态监测双侧颈内动脉、双侧大脑前动脉和中动脉的血流速度。结果术后发生CVS的患者第3天脑脊液中ET-1水平即升高，第7天达到高峰，而后逐渐下降；术后第5、7和10天，中、重度CVS组ET-1水平明显高于对照组（P〈0.05），术后第7和10天，重度CVS组ET-1水平高于轻、中度CVS组和无CVS组（P〈0.05）；术后脑脊液中ET-1的水平与大脑中动脉平均血流速度呈正相关（r=0.635，P〈0.01）。结论颅底肿瘤术后患者脑脊液中ET-1水平的升高参与了术后CVS的发生，且其变化与术后CVS呈正相关，提示其含量可预测颅底肿瘤病人术后CVS的严重程度和预后。     

脑梗死患者血液和脑脊液ET_1及VEGF的同步检测及与病变关系

目的 探讨内皮素（ＥＴ１）和血管内皮细胞生长因子（ＶＥ ＧＦ）在脑梗死发病中的意义及其相互关系。方法 分别应用放免法测定脑梗死患者血浆和脑脊液中ＥＴ１及ＥＬＩＳＡ法测定血清和脑脊液中ＶＥＧＦ。结果 脑梗死组血浆和脑脊液中ＥＴＩ含量明显高于对照组,急性期更高,而且脑脊液中ＥＴ１的增加（Ｐ＜０．０１）比血浆中的ＥＴ１增加（Ｐ＜０．０５）更显著;血清和脑脊液中ＶＥＧＦ含量在急性期均明显高于对照组,恢复期下降。脑脊液中ＶＥＧＦ含量与病情轻重有关,而血浆ＥＴ１含量与梗死灶大小有关。以梗死灶大小为参照、急性期血浆ＥＴ１与血清ＶＥＧＦ两者呈正相关;以病情轻重为参照,急性期脑脊液中ＥＴ１与ＶＥＧＦ两者呈正相关。结论 脑梗死患者血液和脑脊液中ＥＴ１及ＶＥＧＦ的不同变化表明,两者都参与了脑梗死的发病过程,且具有相关性,ＥＴ１和ＶＥＧＦ均与脑梗死的发生发展密切相关。     

Increased plasma endothelin-1 levels in patients with intracerebral hemorrhage

Endothelins (ETs) are discovered peptides that are widely distributed in neurons and nonneuronal cells of the human nervous system. Previous studies showed that ischemic stroke may be associated with increased plasma ET-1 levels. There are no studies to show plasma ET-1 levels in intracerebral hemorrhage. Plasma ET-1 levels in 30 patients with cerebral hemorrhage within 72 hours after the onset of focal neurological deficit were measured by a microplate enzyme immunoassay. Thirty sex- and age-matched healthy subjects were accepted as a control group. The clinical neurological status in the patients was evaluated according to the modified Matthew Scale. The mean plasma ET-1 level in hemorrhagic stroke patients was significantly higher than in control subjects (2.39±2.08 v 0.65±0.32 fmol/mL, (P < .05). There was a significant difference in ET levels between patients who died in the hospital and patients who survived (P < .05). The mean ET-1 concentration in patients with severe neurologic deficit was significantly higher than in patients with mild neurologic deficit (P < .05). There was a correlation between hematoma volumes and plasma ET-1 levels in the patients (r = 0.66, Pt < .001). The mean plasma ET-1 concentration was found to be significantly higher in patients with intraventricular hemorrhage than in patients without intraventricular hemorrhage (P < 0.05). There were no significant differences in ET-1 levels between supratentorial and infratentorial subgroups or among supratentorial subgroups (P > .05). It was concluded that plasma ET-1 levels were increased in the acute period of hemorrhagic stroke. Plasma ET-1 levels may be associated with hematoma volume, which is related to a poor prognosis of the cerebral hematoma. We suggest that increased plasma ET-1 levels may be a consequence of local cerebral hemorrhage or the acute stress condition of the disease.     

脑出血应激性高血糖患者血浆内皮素—1变化规律的临床研究

目的 通过对脑出血应激状态下血浆内皮素-1（ET-1）变化规律的研究,为脑出血的治疗提供新方法。方法 对30例脑出血应激性高血糖患者血浆ET-1水平在发病24h、48h、72h及第7d、14d的含量进行测定并与脑出血非高血糖组及正常人组比较。结果 应激性高血糖组血浆ET-1水平明显升高,急性期1-3d维持在较高水平,以后随时间呈下降趋势;ET-1与血糖、血压呈直线正相关;ET-1水平越高,则预后越差。结论 脑出血患者血浆ET-1水平升高与应激反应有关,且对预后产生不利影响。     

Effect of endothelin receptor antagonists on non-muscle matrix compaction in a cell culture vasospasm model

Endothelin-1 (ET-1), a potent vascular smooth muscle constrictor, is one of the possible spasmogens in cerebral vasospasm. However, the role of ET-1 in non-muscle compaction (another aspect of the pathogenesis of cerebral vasospasm) has not been reported. This study was undertaken to demonstrate the effect of ET-1, as well as erythrocyte lysate and bloody cerebrospinal fluid (CSF), on fibroblast populated collagen lattice (FPCL) compaction. Human dermal fibroblasts were used to form FPCL. The concentration-dependent effect of ET-1 was examined in the absence and presence of an ETA receptor antagonist (BQ-485), or an ETB receptor antagonist (BQ-788), or both. FPCL compaction was determined by measuring reduction of areas over five days following treatment. To compare the effect of ET-1 on lattice compaction, erythrocyte lysate and bloody CSF obtained from a cerebral vasospasm patient were also tested. We found that ET-1 increased FPCL compaction in a concentration-dependent (but not time-dependent) manner. Erythrocyte lysate produced the strongest compaction, however, without time-dependence. Bloody CSF promoted FPCL compaction in a time-dependent fashion. Compaction induced by ET-1 was inhibited by BQ-485 but not by BQ-788. We concluded that ET-1 promotes FPCL compaction by activation of ETA receptors. Other components in bloody CSF or erythrocytes may also contribute to FPCL compaction.     

脑缺血后脑组织和血浆中内皮素的变化

建立兔大脑中动脉阻断(MCAO)脑缺血模型。将48只兔随机分为四组:C(正常对照和假手术对照组)和脑缺血 I_2、I_4、I_(24)组,每组12只,测脑 H_2O、Na~+、K~+、Ca~(2+)、内皮素(ET)和血浆 ET。结果示脑缺血侧脑皮质和血浆中 ET 含量显著高于对照组(P<0.001),且随时相递增(P<0.01),ET与脑 H_2O 含量之间呈显著正相关(P<0.05),提示 ET 可能参与脑缺血、脑水肿的发生发展。     

Hypoxic modulation of striatal lesions induced by administration of endothelin-1

Levels of endothelin-1 (ET-1), a potent endogenous vasoconstrictor, are elevated in plasma and cerebrospinal fluid (CSF) following cerebral ischemia and reperfusion injury. The present study sought insight into the potential differential vasoactive effects on the cerebral vasculature and resultant neural damage of ET-1 during normoxic vs. ischemic conditions and upon reperfusion. Under normoxic conditions, intrastriatal stereotaxic injection of exogenous ET-1 (40 pmol) induced a significant (P<0.05) reduction (相似文献   

Endothelin and aneurysmal subarachnoid haemorrhage: a study of subarachnoid cisternal cerebrospinal fluid.

Endothelin (ET) is considered one of the most potent vasoconstrictor polypeptides; several experimental studies have suggested its possible role in the pathogenesis of arterial vasospasm after subarachnoid haemorrhage (SAH). Previously reported data on plasma and CSF levels of endothelin in patients with a diagnosis of SAH have been controversial. Cisternal endothelin CSF levels and the possibility that they could be related to vasospasm and other clinical patterns of SAH were investigated. CSF samples were obtained from 55 patients admitted after angiographic diagnosis of intracranial aneurysm. Levels of ET-1 and ET-3 were measured through radio-immunoassay technique. Twelve patients who had operations for unruptured aneurysms were considered control cases; 43 patients with SAH were classified according to: Hunt and Hess grading at admission, vasospasm grading, CT classification and timing of surgery. In all 55 patients ET-1 was measured, while positive levels of ET-3 were found only in 17 cases of 48. No linear correlation was found between cisternal CSF ET-1 levels when considering time of surgery, CT classification, Hunt and Hess grading at admission, and vasospasm grading. The results of ET-3 assay should be considered with great caution because of the low percentage of positive cases. Cisternal CSF levels of ET-1 and ET-3 are not directly related to the occurrence of arterial vasospasm after the aneurysm rupture, or to other major clinical patterns of SAH; however, ET-1 expression occurs either in paraphysiological (unruptured aneurysm) or in pathological conditions (SAH). It is suggested that ET may potentiate, or may be potentiated by, other factors playing a consistent pathophysiological role in the development of vasospasm.     

Endothelin-1 levels in plasma and cerebrospinal fluidfollowing subarachnoid haemorrhage

A serial measurement of endothelin-1(ET-1) levels in plasma, cisternal and ventricular cerebrospinal fluid(CSF) was performed in 16 patients with subarachnoid haemorrhage (SAH). The patients were classified as grade III or IV according to the clinical grade of Hunt and Hess, and computerised tomography(CT) was classified as Fisher's CT group 3. Cisternal and ventricular CSF and plasma were obtained from the patients on the day of operation days 0-3, days 5-8 and days 14-18 after SAH. ET-I concentration in each sample was quantified by sandwich-enzyme immunoassay. ET-I levels in plasma and CSF were the highest between days 0-3 and then decreased. The ET-I levels in the cisternal CSF were significantly higher during days 0-3(p<0. 01) and days 5-8(p<0. 01) than those in the ventricular CSF It is suggested that ET-I could play an important role in the early stages of the cerebral vasospasm.     

Intrathecal complement activation in neurological diseases evaluated by analysis of the terminal complement complex

The terminal complement complex (TCC) was determined in plasma and cerebrospinal fluid (CSF) from 208 neurological patients. Elevated CSF TCC levels were observed in higher frequencies in patients with infectious diseases (80%), radiculoneuritis (62%), multiple sclerosis (30%), and miscellaneous autoimmune diseases (27%) than in patients with miscellaneous non-inflammatory diseases (2-13%). The plasma level of TCC was significantly increased only in the infectious group. No positive correlation was observed between the plasma and the CSF TCC concentration in the whole patient population nor in subgroups divided according to blood-brain barrier function. Furthermore, the CSF TCC concentration did not correlate with the serum/CSF albumin ratio or with CSF total protein concentration when this was below 1.0 g/l. It is concluded that an elevated TCC concentration in CSF reflects intrathecal complement activation and that quantification of TCC in CSF may be a valuable supplement in the examination of neurological diseases.