大鼠急性局灶性脑缺血动物模型实验研究

脑血管疾病尤其是急性缺血性脑血管疾病的病理生理研究 ,依赖能模拟临床疾病、重复性好的动物模型。本文重点介绍制作大鼠急性局灶性脑缺血动物模型动物的选择、制作方法、各种模型的优缺点及实验影响因素 ,对系统研究急性脑缺血动物模型的选择具有一定的参考价值。     

胎盘源性生长因子在缺血性脑血管病血管再生中的作用

背景：关于胎盘源性生长因子在促血管生长方面的作用还没完全被理解。在胎盘源性生长因子缺陷的模型研究中,胎盘源性生长因子被认为在诱导血管新生中起到关键性的作用。 目的：总结胎盘源性生长因子及其受体在血管再生和缺血性脑血管病中的作用的研究进展。 方法：计算机检索Pubmed和中国知网1990/2009相关文献。中文关键词为“胎盘源性生长因子”;英文关键词为“PLGF,angiogensis”。纳入胎盘源性生长因子的生物特性和在血管再生中的作用相关文献,以及脑缺血后血管再生和脑缺血后胎盘源性生长因子表达的相关文献。排除重复性研究。 结果与结论：文章从胎盘源性生长因子及其受体一般生物学特性,其在血管再生中的作用,胎盘源性生长因子及受体促进血管生成的机制,以及血管内皮生长因子A、胎盘源性生长因子及其受体在脑缺血后的表达和意义等方面进行了叙述。胎盘源性生长因子具有促进病理性血管新生、动脉生成及侧支生成、造血祖细胞动员的功能。胎盘源性生长因子及受体在脑缺血血管再生中有重要的作用,其治疗缺血性脑血管病可能具有很好的临床应用前景。其具体作用和机制还需进一步的研究。     

进程崎岖,前途广阔-颅内外血管搭桥术治疗非烟雾病性慢性脑缺血的研究现状及展望

颅内外血管搭桥术是公认的治疗成人烟雾病患者的主要方法,然而,颅内外血管搭桥术治疗非烟雾病性慢性脑缺血的疗效目前尚未完全阐明,其涉及到脑血流自主调节、脑代谢、认知功能、高级神经活动等一系列脑科学相关领域。因此,本文回顾国内外采用颅内外血管搭桥术治疗非烟雾病性慢性脑缺血的相关研究,以期提高临床工作者的认识,更好地促进颅内外血管搭桥术的应用和推广。     

局灶性脑缺血动物模型制作方法的概述

局灶性脑缺血动物模型在探讨脑血管病的病理生理变化、发病机制及其防治的研究有重要意义。本文概述了开颅物理阻断血流的方法、微栓子栓塞法、线栓法、脑血栓形成动物模型的建立方法、内皮素灌注诱导血管收缩法等模型制作方法等建立局灶性脑缺血动物模型的基本原理及优缺点。     

几种模拟临床发病原因血管性认知功能障碍动物模型的研究进展

血管性认知功能障碍(VCI)是由一系列脑血管疾病,如缺血或出血及急慢性缺氧性脑血管病,导致脑组织损害产生的一种慢性、进行性、持续性智能障碍综合征.本文通过集中介绍能良好模拟临床发病原因的全脑慢性低灌注模型、局灶性低灌注模型、栓塞模型、高血压模型等血管性痴呆动物模型制作方法,并分析各种方法的优缺点,为开展血管性痴呆实验研究者提供参考.     

基质金属蛋白酶-9与脑梗死的研究进展

脑梗死的病理生理过程实质上是在动脉粥样硬化的基础上发生的局部脑组织缺血坏死的过程。脑缺血可引起一系列复杂的导致血管源性水肿的病理变化，包括谷氨酸的释放、白细胞浸润和血一脑屏障的破坏。在实验脑缺血模型中发现，基质金属蛋白酶参与了基底膜和细胞外基质的破坏。     

慢性脑缺血基因表达谱的相关研究

慢性脑缺血是神经系统疾病的一种常见病理状态,可导致持久性或进展性认知与神经功能障碍[1]。利用基因芯片技术可检测慢性脑缺血状态下大鼠海马组织基因表达谱的变化,筛选出候选基因,尤其是与认知功能相关的基因,用于慢性脑缺血分子机制的进一步研究。材料和方法1.动物模型及分     

大鼠脑缺血后诱发学习和记忆障碍模型的研究进展

此文介绍9种脑缺血造成记忆障碍大鼠痴呆模型。血管性痴呆是因脑血管疾病所致的智能及认知功能障碍的临床综合征。脑血管病变是血管性痴呆的基础，在大脑实质可见出血或缺血损害，以缺血性多见。根据血管性痴呆的病理特征此文选取了二血管闭塞法、三血管闭塞法、四血管闭塞法、舌下静脉注射铁粉建立血管性痴呆模型、多发梗死性痴呆动物模型、高血压脑卒中自发大鼠动物模型、高脂血症血管性痴呆大鼠模型、去大脑皮层血管性痴呆动物模型、大脑中动脉闭塞法模型计9种脑缺血模型。并通过对其行为学和形态学筛选，似可模拟血管性痴呆模型．其方法各有所长，适合不同实验方法。     

依达拉奉对慢性脑缺血大鼠一氧化氮及一氧化氮合酶阳性神经元数量的影响

目的观察依达拉奉对脑缺血大鼠脑组织NO含量及NOS阳性神经元数量的影响,为临床上防治慢性脑缺血引发的疾病提供指导。方法 54只Wistar大鼠,分为NO含量组和NOS阳性神经元组,每组再分为模型组、治疗组、假手术组,利用结扎大鼠两侧颈总动脉制作大鼠慢性脑缺血模型,硝酸还原酶法测NO含量,NADPH-d组织化学方法染色NOS阳性神经元,光镜下观察。结果治疗组各时间点NO含量和NOS阳性神经元数量较模型组减少。结论依达拉奉对慢性脑缺血大鼠脑组织具有保护作用。     

局灶性脑缺血再灌注时间窗的病理研究

局灶性脑缺血再灌注时间窗的病理研究刘立，郭玉璞，马中弘局灶性脑缺血的时间窗研究，对脑梗塞的超早期治疗有极大的指导意义。尤其是近年局灶性脑缺血再灌注模型的应用，更为其提供了非常有价值的试验手段。我们采用血管内尼龙线阻断大脑中动脉制成大鼠局灶脑缺血再灌注...     

Course of apparent diffusion coefficient values in cerebral edema of dural arteriovenous fistula before and after treatment

Apparent diffusion coefficient (ADC) values at magnetic resonance imaging (MRI) are useful to distinguish vasogenic and cytotoxic edema due to cerebovascular diseases. Dural arteriovenous fistulas (DAVFs) with retrograde leptomeningeal venous drainage may cause cerebral edema by venous congestion. We report herein the course of ADC values of cerebral edema before and after endovascular treatment in DAVFs. A 65-year-old woman with transverse-sigmoid (T-S) sinus DAVFs with retrograde leptomeningeal venous drainage presented with severe edema in cerebellar hemisphere and brainstem. In preoperative MRI, increased ADC values were observed in the edema area. The isolated sinus was obliterated completely by transvenous embolization. On the following day after treatment, the ADC values in cerebral edema area increased slightly without any new neurological deficits and improved at 1 week later. Rapid resolution of venous congestion due to DAVFs may cause a slight, transient progression of vasogenic edema.     

基质金属蛋白酶-9与脑缺血

脑缺血后基质金属蛋白酶-9(MMP-9)因其表达细胞众多、作用底物广泛而备受医学界重视。脑缺血后表达的MMP-9能降解基底膜而破坏血脑屏障,导致血管源性脑水肿和出血性转化。MMP-9抑制剂有可能成为治疗脑血管病的一条新途径。     

Metabolic encephalopathies

Kinnier Wilson coined the term metabolic encephalopathy to describe a clinical state of global cerebral dysfunction induced by systemic stress that can vary in clinical presentation from mild executive dysfunction to deep coma with decerebrate posturing; the causes are numerous. Some mechanisms by which cerebral dysfunction occurs in metabolic encephalopathies include focal or global cerebral edema, alterations in transmitter function, the accumulation of uncleared toxic metabolites, postcapillary venule vasogenic edema, and energy failure. This article focuses on common causes of metabolic encephalopathy, and reviews common causes, clinical presentations and, where relevant, management.     

Pathogenesis of venous stroke: evaluation with diffusion- and perfusion-weighted MRI

Previous reports have demonstrated the diagnostic usefulness of diffusion- and perfusion-weighted magnetic resonance imaging (MRI) in the evaluation of cerebral venous thrombosis. However, the explanations ascribed for the pathophysiologic mechanisms of venous stroke in these reports were conflicting. Earlier reports supported prominent vasogenic edema associated with mild cytotoxic edema as the potential pathophysiologic mechanism. More recently, a few reports have found cytotoxic edema as the cause for venous stroke. The purpose of this report is to review the pathogenesis of cerebral venous thrombosis after taking into consideration the results of MRI findings. We report two cases of cerebral venous infarction, which had worsening symptoms and signs that resolved after intravenous heparin therapy. In both cases, findings on diffusion-weighted and perfusion-weighted MRI images were compatible with vasogenic edema and viable neuronal tissue. Both the patients recovered without any significant residual sequel. We support the hypothesis that in the pathogenesis of venous stroke vasogenic edema is the initial event, which may or may not be followed by cytotoxic edema eventually evolving to an infarction.     

Relationship between oedema, blood pressure, and blood flow following local brain injury

Vasogenic brain oedema is a concomitant of a wide variety of central nervous system lesions that have in common a disturbance of the blood-brain barrier permeability. Although it is well established that the formation and spread of this extracellular type of oedema is influenced directly by variations of systemic arterial pressure, the consequences of these events on local cerebral blood flow are not known. In the current experiments, vasogenic brain oedema was produced in rats by cold-injury lesions, and local cerebral blood flow measurements were made using a technique of 14C-antipyrine quantitative autoradiography under pharmacologically controlled conditions of hypertension, hypotension, and normotension. Evidence is presented that the formation and spread of vasogenic brain oedema is accompanied by the development of a congruent zone of decreased local cerebral blood flow, and that the magnitude of this field of oedema/ischaemia is a direct function of systemic arterial pressure. These findings may have important clinical implications.     

Posterior reversible encephalopathy syndrome revealing acute post-streptococcal glomerulonephritis

A case of acute encephalopathy with posterior corticosubcortical vasogenic edema on magnetic resonance imaging is reported. Angiography showed cerebral arterial vasospasm. A diagnosis of acute post-streptococcal glomerulonephritis was made 2 days after admission. This report highlights the fact that acute post-streptococcal glomerulonephritis can be revealed by a posterior reversible encephalopathy syndrome and that cerebral vasospasm can concur with vasogenic edema in this condition.     

Relationship between oedema,blood pressure,and blood flow following local brain injury

Abstract

Vasogenic brain oedema is a concomitant of a wide variety of central nervous system lesions that have in common a disturbance of the blood-brain barrier permeability. Although it is well established that the formation and spread of this extracellular type of oedema is influenced directly by variations of systemic arterial pressure. the consequences of these events on local cerebral blood flow are not known. In the current experiments, vasogenic brain oedema was produced in rats by cold-injury lesions, and local cerebral blood flow measurements were made using a technique of ¹⁴C-antipyrine quantitative autoradiography under pharmacologically controlled conditions of hypertension, hypotension, and normotension. Evidence is presented that the formation and spread of vasogenic brain oedema is accompanied by the development of a congruent zone of decreased local cerebral blood flow, and that the magnitude of this field of oedema/ischaemia is a direct function of systemic arterial pressure. These findings may have important clinical implications.     

Genetically determined vascular diseases

Review of literature data concerning genetically determined blood vessel diseases is presented. These disorders are a cause of a process similar to Binswanger's disease but occurring familial. Recurrent TIA, ischemic strokes and other kind of blood supply disturbances lead to numerous and various intensity vasogenic brain tissue damage, particularly in the white matter. Progressive neurological symptoms and dementia form the picture of subcortical leukoencephalopathy in several members of family. Moyamoya disease, fibromuscular dysplasia, hereditary hemorrhagic telangiectasia, hereditary cerebral hemorrhage with amyloidosis, pseudoxanthoma elasticum, two types of subcortical encephalopathy in Japan, HERNS and CADASIL are described.     

Posterior reversible encephalopathy syndrome on computed tomography perfusion in a patient on “triple H” therapy

Introduction: This article reports a case of posterior reversible encephalopathy syndrome on compyted tomography (CT) perfusion in a patient on “Triple H” (hypertension, hypervolemia, and hemodilution) therapy following aneurysmal rupture repair. Case Report: “Triple H” therapy is used in the postoperative course for treatment of vasospasm to prevent stroke and hemorrhage by maintaining cerebral perfusion pressure. Discussion: A potential complication includes vasogenic edema from dysfunction of cerebral blood vessel autoregulation. CT perfusion can detect alterations in cerebral blood flow and volume caused by these hemodynamic changes.     

Vasogenic Edema of the Basal Ganglia after Intra-Arterial Administration of Nimodipine for Treatment of Vasospasm

The intra-arterial administration of nimodipine (IAN) is commonly used for cerebral vasospasm refractory to medical treatments. We report two cases of vasogenic edema after IAN. Our patients with aneurismal subarachnoid hemorrhage presented with vasospasm, which was treated by IAN. Consequently, vasogenic edema developed in the basal ganglia. Reperfusion following IAN for vasospasm may have the potential for inciting vasogenic edema in the ischemic brain.