脉络宁口服液的抗脑缺血作用

目的　观察脉络宁口服液的抗脑缺血作用。方法　结扎大鼠两侧颈总动脉 ,制备急性不完全性脑缺血模型 ;采用麻醉犬在体实验法 ,观察药物对脑循环的影响。结果　口服液对大鼠急性不完全性脑缺血所致的脑血管通透性增加和脑水肿均有一定改善作用。口服液还能降低麻醉犬脑血管阻力 ,增加脑血流量。结论　脉络宁口服液有抗脑缺血作用 ,这一作用与其增加脑循环有关 ,与注射液相比 ,此作用较为缓慢、持久     

脑缺血散治疗脑梗死的临床研究

目的探讨脑缺血散治疗脑梗死的临床效果,为临床治疗脑梗死寻找新的散剂提供参考。方法选择220例脑梗死患者,随机分成对照组和脑缺血散组,对比分析临床治疗效果。结果脑缺血散组治疗脑梗死的临床效果明显优于对照组(P<0.01)。结论脑缺血散治疗脑梗死是有效安全的,可作为脑梗死治疗的辅助用药。     

脉络宁口服液的抗脑缺血作用

目的 观察脉络宁口服液的抗脑缺血作用。方法 结扎大鼠两侧颈总动脉，制备急性不完全性脑缺血模型；采用麻醉犬在体实验法，观察药物对脑循环的影响。结果 口服液对大鼠急性不完全性脑缺血所致的脑血管通透性增加和脑水肿均有一定改善作用。口服液还能降低麻醉犬脑血管阻力，增加脑血流量。结论 脉络宁口服液有抗脑缺血作用，这一作用与其增加脑循环有关，与注射液相比，此作用较为缓慢、持久。     

七氟醚在脑中风疾病中的神经保护作用研究进展

脑中风是一种以脑部缺血和出血性损伤为主要临床表现的疾病。它是全球性死亡的主要原因之一,可以引起患者严重的长期残疾和认知功能障碍。然而,目前可用在脑中风患者身上的有效保护措施非常有限,尤其是针对那些围手术期患者。近年来,包括七氟醚在内的多种吸入麻醉剂的介入为脑缺血中风患者的神经保护开辟了一条新道路。在大脑缺血损伤中,七氟醚可以通过抗氧化、抗凋亡、抑制炎症反应、调节大脑血流量、维持血脑屏障和促进神经再生等来发挥神经保护作用。此文对七氟醚在脑缺血-再灌注损伤中的临床应用及神经保护作用相关机制进行综述,旨在阐明七氟醚在脑中风的神经保护中的重要作用。     

Role of vinpocetine in cerebrovascular diseases

A cerebrovascular accident, or stroke, is defined as the abrupt onset of a neurological deficit, which can be due to ischemia. Cerebral ischemia is caused by a reduction in blood flow that thereby decreases cerebral metabolism. Chronic cerebral hypoperfusion leads to irreversible brain damage and plays an important role in the development of certain types of dementia. Vinpocetine, chemically known as ethyl apovincaminate, is a vinca alkaloid that exhibits cerebral blood-flow enhancing and neuroprotective effects. Non-clinical and clinical studies have suggested multiple mechanisms responsible for the beneficial neuroprotective effects of vinpocetine. As no significant side effects related to vinpocetine treatment have been reported, it is considered to be safe for long-term use. This vasoactive alkaloid is widely marketed as a supplement for vasodilation and as a nootropic for the improvement of memory. The present review focuses on studies investigating the role of vinpocetine in cerebrovascular diseases.     

Protein transduction technology offers novel therapeutic approach for brain ischemia

Transient or permanent reduction in cerebral blood flow following ischemia can lead to severe and irreversible tissue damage to the brain. Emerging biochemical evidence suggests a role for apoptosis in neuronal death following cerebral ischemia. Despite the abundance of studies on the subject, therapeutic interventions for ischemia-related cell injury have so far proved disappointing in clinical trials. Recently, four new, exciting studies reported the use of protein transduction technology to deliver anti-apoptotic molecules to protect neuronal cells following ischemic stroke in vivo. These studies offer new avenues for the treatment and prevention of cell death following brain injuries.     

新型带吻合口动脉夹在急性全脑缺血再灌注模型中的应用

目的评估新型带吻合口动脉夹在急性全脑缺血再灌注模型中的应用价值。方法健康SD大鼠35只,随机分为3组:正常组(n=5):只暴露血管不夹闭;实验组(n=15):使用新型的带吻合口微型动脉夹进行夹闭;对照组(n=15):使用传统的微型动脉夹进行夹闭。采用颈总动脉(CCA)阻断法建立全脑缺血再灌注模型,分离暴露双侧颈总动脉后予以微型动脉夹夹闭,进入缺血期,夹闭20min后移去微型动脉夹去除双侧颈总动脉的夹闭,进入灌注期。实验结束后处死大鼠取全脑大体标本。观察大鼠达到全脑缺血所需的时间、脑组织大体标本、缺血过程中动脉夹的夹闭状况。结果正常组大鼠脑组织大体标本皮层颜色较红润、浅表血管丰富;实验组大鼠脑组织皮层颜色苍白、表面血管塌陷,血流大量少,其中部分出现血液无复流的现象;对照组大鼠脑组织皮层颜色微红、表面血管部分塌陷,血流减少。实验组动脉夹在缺血过程中仅3例出现松动,而对照组动脉夹在缺血过程中有6例出现松动、5例出现滑脱。达到全脑缺血所需的时间实验组较对照组更快。结论新型带吻合口动脉夹可以有效的对血管进行夹闭,使缺血更加彻底,并且在夹闭的过程中有较高的稳定性,可以有效的避免动脉夹的松动、滑脱等现象。     

The Protective Effect of Ischemic Postconditioning Against Ischemic Injury: From the Heart to the Brain

Postconditioning, a series of mechanical interruptions of reperfusion after ischemia, prevents ischemia/reperfusion injury in myocardial infarction. The extensive studies of postconditioning in myocardial infarction have led to clinical trials. This article reviews the protective effects of postconditioning against ischemia from the heart to the brain and provides insights on how studies of postconditioning in the field of heart ischemia have shed light on postconditioning of the brain. Because brain ischemia has many mechanisms in common with heart ischemia, it is logical to test whether postconditioning protects against brain ischemia as well. A few groups have reported that postconditioning reduces infarct size in focal cerebral ischemia and improves deficits of short-term memory and motor coordination after global cerebral ischemia. However, many outstanding issues remain elusive regarding the protective effects of postconditioning against cerebral ischemia. Future studies should further identify parameters that generate the strongest protection for postconditioning against cerebral ischemia and should study whether postconditioning provides long-term protection. In addition, clarification of the underlying protective mechanisms should be pursued. This will certainly enhance our understanding of this novel phenomenon and may provide important clues for developing pharmacological analogues for stroke treatment. An erratum to this article can be found at     

大鼠局灶性脑缺血对自主神经系统的影响

目的：研究心脏自主神经功能在急性局灶性脑缺血及再灌注后的变化情况。方法：通过线栓法建立大鼠局灶性脑缺血再灌注模型，连续记录大鼠局灶性脑缺血再灌注不同时间段的动脉血压、心电图信号以及心率．比较分析缺血组缺血后各时段与假手术组相应时段缺血前后以及再灌注前后的动脉血压、心率以及心率变异性的变化。结果：急性脑缺血组动脉血压、心率较假手术组均显著升高，心率变异性的能量有较大的变化；再灌注后，动脉血压、心率及心率变异性均有不同程度的恢复。而且缺血时间越短，恢复越快。结论：在急性脑缺血后，心脏自主神经活动减弱．而交感神经活动相对增强或者迷走神经活动减弱。     

电刺激小脑顶核治疗脑微循环障碍所致脑缺血缺氧40例

目的观察电刺激小脑顶核(FNS)在人血液中红细胞形态及数目发生改变时引起的脑微循环障碍、脑功能失调、脑缺血、缺氧等症状时的治疗作用及机制。方法选取40例具有脑缺血、缺氧症候群的患者,随机分为两组,分别予以FNS治疗和服用尼莫地平片,共15 d;分别于治疗前,治疗后检查血常规、单光子发射计算机断层显像(single photon emission computed tomography,SPECT)。结果治疗前,血常规中红细胞各参数都有不同程度增高,并伴有SPECT的定性分析显示均有不同程度低灌注区;治疗后,应用FNS组红细胞各项参数均有所下调,并伴SPECT ROI区域计数的改善及SPECT的灌注缺损显著改善,临床症状随之减轻或消失,而尼莫地平组上述各项指标改善不明显,临床症状亦改善不明显。结论FNS能够干预红细胞,使之具有良好的红细胞变形能力(erythrocyte deformability,ED),使脑微循环得到有效灌注,从而纠正脑缺血、缺氧。     

高压氧对围生期缺氧缺血事件新生儿脑血流的影响

目的通过检测围生期缺氧缺血事件新生儿高压氧（HBO）治疗前后的脑血流,了解高压氧治疗对有围生期缺氧缺血事件新生儿脑灌注的影响。方法于2008年12月-2010年12月在我院住院的有围生期缺氧缺血病史的新生儿中,随机选取30例,用彩色超声多普勒检测每次HBO治疗前后通过大脑中动脉（McA）脑血流情况,连续检测其大脑前动脉的收缩期峰值（VS）、舒张末期速度（Vd）、阻力指数（RI）。所得数据采用SPSS13．0统计软件进行统计分析。结果脑血流速度的改变：HBO治疗的第1、2天,治疗前后脑血流速度无明显改变;治疗第3天,Vs、Vd较前降低,其中Vs差异有显著性（P〈0．05）,Vd差异有极显著性（P〈0．01）;治疗第4天,Vs、Vd较前降低,Vs、Vd差异有极显著性（P〈0．01）。血管阻力指数的变化：HBO治疗的第1、2天,无明显改变;治疗第3天,RI较前升高,RI差异有极显著性垆〈0．01）治疗第4天,RI较前升高,RI差异有极显著性（P〈0．01）。结论对围生期缺氧缺血事件新生儿进行HBO治疗,初期脑灌注影响不明显,治疗后期产生明显影响,可使脑血管收缩并致血流速度减慢,从而影响脑灌注。     

左旋氨氯地平对局灶性脑缺血小鼠模型脑梗死体积的影响

目的研究左旋氨氯地平对局灶性脑缺血小鼠模型脑梗死体积的影响,探讨左旋氨氯地平对缺血性脑梗死的神经保护作用。方法制备小鼠大脑中动脉脑缺血再灌模型,根据是否使用左旋氨氯地平随机分为3组：左旋氨氯地平缺血前处理组,缺血生理盐水处理组,假手术对照组;多普勒超声血流仪监测梗死侧脑区的脑血流量;TYC染色检测脑梗死体积。结果与缺血生理盐水处理组相比较,左旋氨氯地平缺血前处理组梗死侧脑区的脑血流量没有明显变化,而脑梗死体积较小,差异有统计学意义（P〈0．05）。结论使用左旋氨氯地平可能有助于减少缺血性脑梗死体积。     

Current state on development of neuroprotective agents for cerebral ischemia

The improvement of decreased cerebral blood flow using thrombolytic agents, anti-thrombin drugs, and antiplatelet drugs has been essential for acute ischemic stroke. Edaravone, a free radical scavenger, has been commercially available as a novel neuroprotective agent for ischemic stroke in Japan from 2001. The appearance of a neuroprotective agent implies that therapeutic strategy can be expanded through a combination with thrombolysis. In the previous development, several cases have reported that neuroprotective compounds failed in clinical trials. However, recent studies have clarified that the cerebral ischemia induced the neuronal cell death by mediating multiple mechanisms with necrosis and/or apoptosis. The cytotoxicity derived from the NO/peroxynitrite/free radical generating system, one of intracellular Ca2+ signaling, is a typical event in ischemic injury, which is protected by edaravone. Furthermore, it is suggested that suppression of excessively activated voltage-dependent Na+ and Ca2+ channels is effective as a strategy for neuroprotection, since abnormal excitatory stimuli in the neuronal network result in the cerebral infarction. The development of several compounds having different mechanisms of action for acute stroke is in progress. It is therefore prospected that the various novel neuroprotective agents will be provided for assuring the option of therapeutic strategy, since the reinforcement of medical stroke care including diagnosis contributes to the prolongation of the therapeutic time window.     

Cerebral ischemia in gerbils: effects of acute and chronic treatment with adenosine A2A receptor agonist and antagonist

Despite significant progress in understanding of the potential of adenosine A₁ receptor-based therapies in treatment of cerebral ischemia and stroke, very little is known about the effect of selective stimulation of adenosine A_2A receptors on the outcome of a cerebrovascular arrest. In view of a major role played by adenosine A₂ receptors in the regulation of cerebral blood flow, we have investigated the effect of both acute and chronic administration of the selective adenosine receptor agonist 2-[(2-aminoethylamino)-carbonylethylphenylethylamino]-5′-N-ethylcarboxoamidoadenosine (APEC) and antagonist 8-(3-chlorostyryl)caffeine (CSC) on the outcome of 10 min ischemia in gerbils. Acute treatment with APEC improved recovery of postischemic blood flow and survival without affecting neuronal preservation in the hippocampus. Acute treatment with CSC had no effect on the cerebral blood flow but resulted in a very significant protection of hippocampal neurons. Significant improvement of survival was present during the initial 10 days postischemia. Due to subsequent deaths of animals treated acutely with CSC, the end-point mortality (14 days postischemia) in this group did not differ statistically from that seen in the controls. It is, however, possible that the late mortality in the acute CSC group was caused by the systemic effects of brain ischemia that are not subject to the treatment with this drug. Chronic treatment with APEC resulted in a statistically significant improvement in all studied measures. Although chronic treatment with CSC improved postischemic blood flow, its effect on neuronal preservation was minimal and statistically insignificant. Mortality remained unaffected. The results indicate that the acute treatment with adenosine A_2A receptor antagonists may have a limited value in treatment of global ischemia. However, since administered CSC has no effect on the reestablishment of postischemic blood flow, treatment of stroke with adenosine A_2A receptor antagonists may not be advisable. Additional studies are necessary to elucidate whether chronically administered drugs acting at adenosine A₂ receptors may be useful in treatment of stroke and other neurodegenerative disorders.     

促红细胞生成素在脑缺血保护机制中的作用与相关中药干预研究进展

缺血性脑卒中是一种严重危害患者身心健康的疾病,除传统药物组织型纤溶酶原激活剂外,该病的治疗药物一直处于积极探索中。现有证据表明促红细胞生成素以协调的方式在多个层面上对脑缺血具有保护作用,如减少谷氨酸产生的兴奋性毒性、逆转血管痉挛、促进脑血管新生、减少细胞凋亡和炎症等。因此本文就目前几种能够促进EPO生成的中药在脑缺血方面的作用及机制展开综述,以期为缺血性脑卒中的药物治疗提供参考。     

褪黑素对大鼠局灶性脑缺血的影响

目的:探讨褪黑素对大鼠局灶性脑缺血保护作用.方法:用线栓法建立大鼠大脑中动脉栓塞(MCAO)模型.大鼠随机分为假手术组、缺血组、褪黑素组(4 mg&#8226;kg 1)、尼莫地平组(0.2 mg&#8226;kg 1).缺血前30 min舌下静脉给药.持续性缺血30 min,6,24 h后处死动物,测定脑梗死体积,脑组织丙二醛(MDA)、一氧化氮(NO)含量和NOS活性(分光光度法);透射电镜观察脑组织超微结构改变.结果:MCAO后,脑梗死体积及MDA含量随时间延长而增大,6 h后基本稳定;缺血30 min NO含量及NOS活性升高,缺血6 h降低,24 h再度升高.与模型组比较,褪黑素组能缩小脑梗死体积、降低脑组织中MDA含量、缺血30 min NO含量及NOS活性升高,6,24 h降低,且显著改善脑组织的超微病变,减少神经细胞的凋亡.结论:褪黑素对大鼠局灶性脑缺血有一定的保护作用,机制可能与降低脑组织中NO含量和NOS活性、减轻脑组织生物膜脂质过氧化损伤及减少神经细胞的凋亡有关.     

CCR2/CCL2对脑缺血再灌注损伤影响的研究进展

CC趋化因子受体2（CCR2）是趋化因子受体中的重要一员,与其配体CC趋化因子配体2（CCL2）在神经炎症中发挥着重要的作用。本文综述了CCR2/CCL2的表达及功能,并探讨抑制CCR2/CCL2对脑缺血再灌注损伤的影响及其机制。抑制CCR2/CCL2可降低血脑屏障通透性,并通过影响单核/巨噬细胞、小胶质细胞和星形胶质细胞抑制炎症反应,进而减轻脑缺血再灌注损伤。因此,抑制CCR2/CCL2可能是治疗脑缺血损伤的潜在靶点,为相关药物研发提供依据。     

牵引配合温针对颈性眩晕患者脑血流状态的影响观察

目的 探讨牵引配合温针治疗颈性眩晕对脑血流状态的改善作用。方法 对53例颈性眩晕患者在牵引配合温针治疗20次前后的经颅多普勒（TCD）检测结果进行对比分析。结果 治疗后与治疗前比较，除左侧大脑前动脉外，双侧大脑中、大脑后及右侧大脑前动脉平均血流速度均显著降低（P〈0．01）；双侧椎动脉均较治疗前的平均血流速度有明显提高（P〈0．01）。结论 牵引配合温针治疗可双向调整颅内动脉异常的血流速度，从而达到改善和治疗颈性眩晕之目的。     

Intranasal Delivery of Exendin-4 Confers Neuroprotective Effect Against Cerebral Ischemia in Mice

Exendin-4 is now considered as a promising drug for the treatment of cerebral ischemia. To determine the neuroprotective effects of intranasal exendin-4, C57BL/6J mice were intranasally administered with exendin-4 daily for 7 days before middle cerebral artery occlusion (MCAO) surgery. Intranasally administered exendin-4 produced higher brain concentrations and lower plasma concentrations when compared to identical doses administered interperitoneally. Neurological deficits and volume of infarcted lesions were analyzed 24 h after ischemia. Intranasal administration of exendin-4 exhibited significant neuroprotection in C57BL/6 mice subjected to MCAO by reducing neurological deficit scores and infarct volume. The neuroprotective effects of exendin-4 were blocked by the knockdown of GLP-1R with shRNA. However, exendin-4 has no impact on glucose and insulin levels which indicated that the neuroprotective effect was mediated by the activation of GLP-1R in the brain. Exendin-4 intranasal administration restored the balance between pro- and anti-apoptotic proteins and decreased the expression of Caspase-3. The anti-apoptotic effect was mediated by the cAMP/PKA and PI3K/Akt pathway. These findings provided evidence that exendin-4 intranasal administration exerted a neuroprotective effect mediated by an anti-apoptotic mechanism in MCAO mice and protected neurons against ischemic injury through the GLP-1R pathway in the brain. Intranasal delivery of exendin-4 might be a promising strategy for the treatment of ischemic stroke.     

依达拉奉对慢性脑缺血大鼠神经功能损伤的保护和MDA、SOD的影响

目的:探讨依达拉奉对慢性脑缺血大鼠神经功能损伤的保护和海马区、额叶皮质区丙二醛(MDA)、超氧化物歧化酶(SOD)的影响。方法:对72只大鼠用结扎离断法制作颈动脉局灶性慢性脑缺血模型。脑缺血3周腹腔注射依达拉奉3 mg.kg-1为依达拉奉组(n=6),另设对照组(n=6)和脑蛋白水解物组(n=6,3 mg.kg-1腹腔注射脑蛋白水解物)。随后用卒中指数评分标准和神经病学症状评分标准评估大鼠神经功能损伤程度,用可见光分光光度计观察不同脑组织匀浆标本,检测脑组织中的MDA、SOD。结果:脑缺血4周后,依达拉奉组大鼠的神经功能障碍明显轻于缺血对照组和脑蛋白水解物组;依达拉奉组MDA明显低于其它两组;SOD明显高于其它两组(P<0.01)。结论:依达拉奉对大鼠脑缺血神经功能损伤有保护的作用,其机制可能是通过清除自由基,上调SOD值,抑制脂质过氧化。