谷氨酸载体在鼠脑缺血神经元死亡中的作用

目的研究谷氨酸载体在脑缺血神经元死亡中的作用。方法用原位杂交和免疫组织化学方法观察大鼠脑缺血后脑内谷氨酸载体ＧＬＡＳＴｍＲＮＡ和胶质纤维酸性蛋白（ＧＦＡＰ）表达的变化，用药理分析手段观察谷氨酸载体摄取抑制剂Ｌ反式吡咯烷２，４二羧酸（ＬｔｒａｎｓＰＤＣ）对脑缺血致神经元损伤的影响。结果脑缺血后２４小时，大脑皮层缺血周边区ＧＬＡＳＴｍＲＮＡ和ＧＦＡＰ表达无显著变化；而缺血后７２小时，缺血周边区ＧＬＡＳＴｍＲＮＡ和ＧＦＡＰ表达都显著增加，脑缺血后２４小时和７２小时，缺血侧海马ＣＡ１区ＧＬＡＳＴｍＲＮＡ表达则无显著变化；与侧脑室注射生理盐水组相比，侧脑室注射１μｇ或２μｇＬｔｒａｎｓＰＤＣ有使脑梗塞体积增大的趋势，但差异无显著意义；侧脑室注射５μｇＬｔｒａｎｓＰＤＣ使脑梗塞体积显著增大。结论脑缺血后谷氨酸载体功能可能呈代偿性增强，提示谷氨酸载体在限制脑缺血时谷氨酸神经毒中起重要作用。     

D1和D2受体拮抗剂对乙灶性脑缺血梗塞体积及脑血流的影响

目的 研究多巴胺（ＤＡ）Ｄ１受体拮抗剂ＳＣＨ－２３３９０和Ｄ２受体拮抗剂Ｅｔｉｃｌｏｐｒｉｄｅ对可逆性乙灶性脑缺血梗塞体积及皮层半暗带脑血流的影响。方法 采用激光多普勒脑血流计测量大鼠可逆性乙灶性脑缺血各时相皮层半暗带脑血流,并于缺血后２４小时断头取脑切片,ＴＴＣ染色,计算机图样分析系统测量脑梗塞体积。结果 Ｄ１受体拮抗剂ＳＣＨ－２３３９０可明显缩小局灶性脑缺血梗塞体积,改善缺血期各时相皮层半暗带     

脑梗塞患者血小板体积改变的观察

目的研究脑梗塞患者血小板体积的变化及其与脑梗塞的因果关系。方法用全自动血细胞分析仪对８１例脑梗塞、５０例短暂性脑缺血发作（ＴＩＡ）患者静脉血平均血小板体积（ＭＰＶ）进行了观察,并与７０例老年人进行了比较。同时,用流式细胞仪对脑梗塞和脑出血患者（各１０例）血小板体积进行了比较。结果脑梗塞、ＴＩＡ患者血小板体积均明显增大,病程中无明显变化。结论脑梗塞患者在卒中之前出现血小板体积增大,是脑梗塞的危险因素之一     

抗肿瘤坏死因子抗体减轻小鼠短暂性脑缺血损伤

脑缺血后肿瘤坏死因子的表达明显增加。本研究将中和性抗肿瘤坏死因子单克隆抗体注入脑室内，以观察阻断内源性肿瘤坏死因子过度表达对小鼠短暂性脑缺血损伤的影响。小鼠随机分为对照组和抗肿瘤坏死因子抗体组，每组８只。脑缺血和再灌流均通过监测脑血流证实。将中和性单克隆Ｈａｍｓｔｅｒ抗小鼠肿瘤坏死因子抗体或对照载体在恢复再灌时立即注入脑室。小鼠大脑中动脉阻塞１ｈ再灌流２３ｈ断头取脑。脑梗塞体积测定用常规ＨＥ染色和计算机图象分析。以血管外内源性白蛋白免疫组化染色检测血脑屏障的损伤。对照组和肿瘤坏死因子抗体治疗组在脑缺血和再灌后脑血流无显著差异（Ｐ＞０．０５）。抗肿瘤坏死因子抗体组脑梗塞体积和血脑屏障损伤体积较对照组明显减小。阻断内源性肿瘤坏死因子能显著减少小鼠暂时性脑缺血脑梗塞体积和血脑屏障损伤体积（Ｐ＜０．０５）。脑梗塞体积的减小和血脑屏障损伤体积的减小相对应。提示内源性肿瘤坏死因子能加重暂时性脑缺血损伤。     

大鼠实验性皮层脑梗塞及其定量研究

本文报告了大鼠皮层脑梗塞模型的制作和梗塞体积定量检测的方法。动物在嗅束外缘外侧１～３ｍｍ范围内电凝并切断右侧大脑中动脉，术后２４小时处死动物，制成等距冠状石腊切片，经Ｈ－Ｅ染色，用图像分析技术测量切片上的梗塞面积，进而算出梗塞体积。该模型有较高的成功率和稳定性。     

脑血管性痴呆的P300研究

脑血管性痴呆的Ｐ_（３００）研究刘凤荣，王晓红，汤洪川近年来，用事件相关电位方法来检测神经心理认知功能，国内外已有不少报道，本文用Ｐ３００检测技术对老年人脑血管性痴呆与脑梗塞及正常老年人各３０名。进行了比较分析，现报道如下：１材料与方法１．１病例选择?..     

介入溶栓方法治疗急性脑缺血性疾病（摘要）

介入溶栓方法治疗急性脑缺血性疾病（摘要）杨树源，高永中，贺能树一、临床资料与方法１９９３年２月至１９９４年２月我们对１１例急性颈内动脉系统脑梗塞病人进行了介入性颈内动脉溶栓治疗。其中男性８例，女性３例。治疗均在发病后１～６天内进行。溶栓前常规全脑血管...     

氧载体透射疗法对脑梗塞患者血清中LPO,SOD水平的影响

脑梗塞的病理生理机制中，自由基对其损害是受到脑缺血损伤后，自由基产生增多，并可造成激烈的自由基连锁反应，使缺血脑细胞的坏死进一步加重，自由基还进一步向周围穿透、延伸，使边缘地带脑细胞进一步损伤、扩展。１对象与方法１．１研究对象（１）８５例脑梗塞患者为...     

人参皂甙Rb1对脑缺血半影区葡萄糖转运体3表达的影响

人参皂甙是从植物根、茎、叶中提取出的主要有效成分，具有多种生物活性。除了有增强机体免疫力、抗肿瘤、抗衰老、降低血糖等作用外，对脑缺血损伤还有保护作用，可减小脑梗塞体积。我们用大鼠脑缺血再灌注模型，观察人参皂甙Rb1对脑缺血再灌注损伤后缺血半影区葡萄糖转运体3（GLUT3）mRNA、蛋白表达以及脑梗塞体积的影响，从能量代谢角度进一步探讨Rb1的神经保护机制。     

降钙素基因相关肽对大鼠局灶性脑缺血保护作用的研究

线栓法建立大鼠局灶脑缺血动物模型，定量研究降钙素基因相关肽（CGRP）对大鼠局灶脑缺血体积的影响。结果：模型建立前1小时使用CGRP预防性治疗可明显减小脑缺血体积，与对照组比较减幅达54％（P＜0．01）；模型建立后2小时CGRP治疗组脑缺血体积仅比对照组减少12％（P＞0．05）。提示：CGRP对缺血神经组织有保护作用，但治疗时间窗较短。     

Quantitative measurement of cerebral blood flow and cerebral blood volume after cerebral ischaemia

CBF obtained by the hydrogen clearance technique and cerebral blood volume (CBV) calculated from the [14C]dextran space were measured in three groups of rats subjected to temporary four-vessel occlusion to produce 15 min of ischaemia, followed by 60 min of reperfusion. In the control animals, mean CBF was 93 +/- 6 ml 100 g-1 min-1, which fell to 5.5 +/- 0.5 ml 100 g-1 min-1 during ischaemia. There was a marked early postischaemic hyperaemia (262 +/- 18 ml 100 g-1 min-1), but 1 h after the onset of ischaemia, there was a significant hypoperfusion (51 +/- 3 ml 100 g-1 min-1). Mean cortical dextran space was 1.58 +/- 0.09 ml 100 g-1 prior to ischaemia. Early in reperfusion there was a significant increase in CBV (1.85 +/- 0.24 ml 100 g-1) with a decrease during the period of hypoperfusion (1.33 +/- 0.03 ml 100 g-1). Therefore, following a period of temporary ischaemia, there are commensurate changes in CBF and CBV, and alterations in the permeability-surface area product at this time may be due to variations in surface area and not necessarily permeability.     

Regional cerebral blood flow correlates of aphasia outcome in cerebral hemorrhage and cerebral infarction

The relationship between recovery from aphasia and regional cerebral blood flow (CBF) was compared in 87 patients, 44 with cerebral hemorrhage and 43 with non-embolic cerebral infarction. CBF values correlated poorly with aphasia outcome in patients with cerebral hemorrhage whereas a tight correlation was demonstrated in patients with non-embolic cerebral infarction. A marked variability of CBF values in the acute and subacute stage might account for the poor correlation between CBF and aphasia outcome in patients with cerebral hemorrhage. On the other hand, a sharp discrimination was achieved between those with a good recovery from aphasia and those with a poor recovery by the dimensions of the hematoma on CT. In non-embolic cerebral infarction, a relative frontal ischemia was associated with motor aphasia while a relative temporal ischemia was associated with sensory aphasia. This dichotomy was not demonstrated in the regional CBF values in patients with cerebral hemorrhage.     

貌似脑瘤的脑型血吸虫病15例临床分析

目的 探讨脑瘤型脑血吸虫病的临床及MRI的特点.方法 对收治的15例脑瘤型脑血吸虫病的临床资料、实验室检查及MRI资料进行回顾性分析.结果 均为慢性脑型血吸虫病肉芽肿型,表现为脑瘤型.脑瘤型脑血吸虫病的MRI表现具有特征性.结论 脑瘤型脑血吸虫病的MRI易误诊为肿瘤,应结合实验室及影像学检查综合分析.     

Effects of ATP on cerebral circulation--morphological observation of cerebral circulation and cerebral vasculature]

Review was made on the effect of adenosine triphosphate, 1.0-3.0 mg/kg intravenously, on the cerebral circulation and the presence of the dilating action on the cerebral blood-vessels in cats. 1. The group of the normal intra-cranial pressure showed, as reported previously, the transient hypotension and its complicated decrease of cerebral blood-circulation at the initial period for 30-100 check, then demonstrating the increase of cerebral blood-flow for 200-1000 check. Its increased volume and duration were dose-dependent. 2. The group of the loaded intracranial pressure of 20-30 mmHg (slightly elevated group) showed the increase of cerebral blood-flow, like the group of the normal intracranial pressure. However, the effect of ATP showed the decrease or disappearance in accordance with the elevation of the loaded pressure. 3. Cerebral vasodilating effect of ATP was promptly observed after the administration, and its degree was 30-50% in photographical observation. 4. Increasing effect on cerebral blood-flow and cerebral vasodilating action of ATP were similar in the pattern to that of vasodilators such as papaverine hydrochloride.     

颅脑损伤后炎症反应与脑水肿

创伤性脑水肿是创伤性脑损伤（traumatic brain iniury，TBI）后的主要继发性病理生理过程之一，也是导致颅内压增高的主要原因。目前国内外多数学者主张将脑水肿分为血管源性、细胞毒性、渗透压性和脑积水性（间质性）四类。过去几十年，根据冷冻性脑损伤模型的研究结果，普遍认为创伤性脑水肿以血脑屏障（BBB）破坏后的血管源性脑水肿为主。但新近研究发现，创伤性脑水肿是血管源性和细胞毒性的混合性水肿，并且以细胞毒性脑水肿为主。[第一段]