神经生长因子预处理对深低温停循环下兔脑皮层神经细胞凋亡的影响

目的 探讨神经生长因子(NGF)预处理对深低温停循环下兔脑皮层神经细胞凋亡的影响.方法 采用深低温下夹闭兔双侧颈总动脉模型.新西兰大白兔幼兔20只随机均分为2组:深低温停循环前48h用生理盐水组(A组)、预处理组-深低温停循环前48h用NGF预处理组(B组),A、B各组分别在降温至20℃时停循环30min、恢复循环复温至常温,72h后处死取兔脑皮层组织标本,采用原位末端标记法(TUNEL法)观察深低温停循环再灌注后兔脑皮层神经细胞凋亡的变化.结果 与A组相比,B组的兔脑皮层神经细胞凋亡数目显著减少,差异具有统计学意义(P=0.009).结论 深低温停循环前用外源性NGF预处理能明显减轻兔脑皮层神经细胞的凋亡,神经生长因子有一定的脑保护作用.     

逆灌脑保护的作用机制研究

目的 旨在探讨维持脑低温是否作为逆灌脑保护的主要作用机制。方法 15℃深低温停循环120min期间，15头猪被分为3组：A组（n=5），停循环；B组（n=5），23—29mmHg压力冷血逆行脑灌注；C组（n=5），34—40mmHg压力冷血逆行脑灌注。然后，在37℃下转流60min。深低温停循环以脑皮层15℃为标准。连续监测脑、食管和灌注血液的温度。激光多普勒血流仪测定脑血流量，脑动、静脉血氧含量计算氧摄取率。结果 在降温和复温期间，脑温度的变化比食管温度要慢。不论停循环还是逆灌保护，脑组织都自然复温2℃-3℃，表明逆灌不能有效地维持停循环期间的脑低温，逆灌能维持躯体低温。逆灌期间，氧摄取率上升，提示逆灌可以提供营养血流到脑组织。结论在猪的急性模型，逆灌产生的脑保护作用机制主要不是维持脑的低温，而是提供营养血流或氧到脑组织。     

深低温停循环脑保护的研究进展

深低温停循环(DHCA)主要用于矫治复杂心血管畸形,其技术关键在于术中作好脑保护,即适宜的脑灌注方法及脑保护液成分。前者包括深低温间断停循环、深低温停循环逆行性脑灌注、深低温停循环后搏动性灌注及选择性顺行脑灌注。目前,国际上多采用逆行性脑灌注加选择性顺行脑灌注方式。     

心跳骤停后脑复苏

心肺复苏（CPR）能使50％以上心跳骤停的患者恢复自主循环。然而,其中大部分患者在复苏之后仍然死亡。高死亡率主要原因是全脑缺血引起神经元损伤。因此,心跳骤停后对大脑功能的恢复和保护治疗就显得十分重要。几年前,控制性降温开始被纳入临床实践,对于院外发生的心跳骤停患者的治疗,这是第1次同时改善生存率和神经系统预后的手段,是随机临床研究的结果。除了控制性降温,其他治疗方法正处在实验或临床研究阶段。这些方法包括溶栓疗法、特殊药物输注方案,或抗细胞凋亡用药等。本文中,我们主要回顾脑复苏的病理生理学知识和可能对复苏治疗有益的几种方法。     

氯胺酮联合亚低温对窒息性心跳骤停大鼠复苏后脑缺血再灌注损伤的影响

目的 探讨氯胺酮联合亚低温对窒息性心跳骤停大鼠复苏后脑缺血再灌注损伤的影响.方法 健康Wistar大鼠50只,4.0～4.5个月,雌雄各半,体重410～510 g,随机分为5组(n=10):假手术组(S组)仅经动、静脉穿刺置管;窒息性心跳骤停组(ACA组)制备窒息性脑缺血模型;氯胺酮组(K组)窒息前5 min腹腔注射氯胺酮100 mg/kg;亚低温组(MH组):窒息开始后维持直肠温30～35℃;氯胺酮+亚低温组(K+MH组):窒息前5 min腹腔注射氯胺酮100 mg/kg,窒息开始后维持直肠温30～35 ℃.成功复苏后,取脑组织,测定脑含水量和海马神经元p-caspase-3的表达水平.结果 与S组比较,ACA组和K组脑含水量升高,p-caspase-3表达上调,MH组和K+MH组p-caspase-3表达上调(P＜0.01),脑含水量差异无统计学意义(P＞0.05);与ACA组比较,MH组和K+MH组脑含水量降低,p-caspase-3表达下调,K组p-caspase-3表达下调(P＜0.01),脑含水量差异无统计学意义(P＞0.05);与K组比较,K+MH组脑含水量降低,p-caspase-3表达下凋,MH组脑含水量降低(P＜0.01),p-caspase-3表达差异无统计学意义(P＞0.05);与MH组比较,K+MH组p-caspase-3表达下调(P＜0.01),脑含水量差异无统计学意义(P＞0.05).结论 氯胺酮联合亚低温可减轻窒息性心跳骤停大鼠复苏后的脑缺血再灌注损伤,该效应较两者单独应用时增强.     

深低温停循环重力脑逆行灌注在主动脉瘤手术中的脑保护作用

目的 探讨深低温停循环重力脑逆行性灌注技术在主动脉夹层动脉瘤手术中对脑和脊髓的保护作用。方法 建立体外循环后，开始降温。肛温17℃时，患者深度头低位（deep trendelenburg position)。控制股静脉回流，股动脉流量降至1．5L／min，升高和维持中心静脉压在20－23cmH2O(1kPa=10.2cmH2O)，即可完成脑逆行性灌注。结果 本组2例患者停循环脑逆行性灌注时间分别为50分钟和116分钟，术后未发生神经系统并发症。结论 深低温停循环重力脑逆行性灌注技术操作简单，能够充分暴露术野，对脑和脊髓有很好的保护作用。     

低温治疗脑缺血的研究进展

低温对脑缺血既有保护作用,又有脑复苏作用,其确切机制虽不清楚,但主要与以下因素有关:低温降低脑代谢率,减少兴奋性氨基酸的释放,增加神经元内泛素合成,抑制氧自由基的产生等。低温的疗效受低温治疗开始的时间、低温的程度及低温持续时间的影响、并且不同低温疗效评价的方法和时间也影响低温脑保护和脑复苏效果的判断。     

冷脑保护液对大脑皮层组织丙二醛、血栓素A2及前列环素的影响

目的　研究深低温停循环间断灌注充氧脑保护液对大脑皮层组织丙二醛 (MDA)、血栓素 A2 (TXA2 )及前列环素 (PGI2 )的影响。　方法　杂种犬 10条 ,随机均分为两组。 A组 :单纯深低温停循环 12 0分钟 ;B组 :深低温停循环后间断灌注充氧脑保护液。两组动物分别于不同时相测定大脑皮层组织 MDA,TXA2 的代谢产物血栓素 B2(TXB2 )及 PGI2 代谢产物 6 - Keto- PGF1a的含量。　结果　恢复循环 45分钟后 ,A组 MDA和 TXB2 含量明显高于心肺转流术前 (P<0 .0 1) ,6 - Keto- PGF1a含量明显低于 B组 (P<0 .0 1)。　结论　深低温停循环间断灌注充氧脑保护液能明显减少恢复循环后大脑皮层组织 MDA和 TXA2 的生成 ,增加 PGI2 的生成 ,发挥其对大脑皮层组织的保护作用。     

深低温低流量灌注与降温期血气管理对乳猪脑保护的对照研究

目的：在深低渐体外循环中比较降温期pH稳态血气管理和深低温阶段低流量灌注对脑保护的作用能力。方法：24头乳猪根据不同的体外循环脑保护处理方法分成4组，A组：深低温停循环、降温期alpha稳态血气管理；B组：深低温停循环、降温期pH稳态血气管理；C组：深低温低流量、降温期alpha稳态血气管理；D组：深低温低流量、降温期pH稳态血气管理。比较不同脑保护方法和体外循环阶段对脑血流（CBF）、脑氧代谢率（CMRO2）、脑乳酸含量、脑水含量和脑电图（EEG）的影响。结果：B组、D组降温末CBF均高于A组、C组；而CMRO2则低于A组、C组；B组、D组降温期EEC平坦波出现早。C组、D组复温期CBF、CMRO2和EEG恢复好于A组、B组。复温末A组、B组颈内静脉乳酸含量显著高于C组、D组，脑水含量组间差异无显著性。结论：深低温体外循环流量灌注对脑保护的作用能力强于降温期pH稳态血气管理，两种方法配合应用具有脑保护的协同作用。     

大血管手术中的脑保护

在主动脉弓部手术中，目前在深低温停循环，逆行性脑灌注，脑分离体外循环等脑保护方法，每种方法都有其一定的适用范围，各有优缺点。ＤＨＣＡ方法方法简单，不用阻断动脉，具有良好的手术野，但脑停循环的安全允许时间受到限制是其不中。ＣＲＣＰ维持了循环的脑低温，向脑组织提供了确定的氧供，消除代谢产物，延长安全允许时间，为防止冷损伤，而采取了“分离低温”。     

Use of ultrasound in neurosurgical operations: a preliminary report

Real-time ultrasound scanning has considerable potential in the neurosurgical operating room for the localization and further characterization of intracranial lesions as well as for planning and guiding the approach to such lesions. With further refinements, the ultrasound scanner may well be considered a surgical instrument and become a valued part of the neurosurgical armamentarium.     

多模态MRI技术评估脑老化及脑老化与脑疾病的关系研究进展

人类脑随年龄增长而退化,即脑老化;其过程与认知能力下降趋势一致,即神经退行性疾病发病风险随年龄增长而逐渐增加。加强对脑老化的认识并筛选相关生物标志物,对于早期诊断神经退行性疾病、预测年龄相关认知能力下降至关重要。本文对多模态MRI技术用于评估脑老化及脑老化与脑疾病关系的研究进展进行综述。     

Difficulty in brainstem death testing in the presence of high spinal cord injury

In the UK, when the standard brain death criteria are met, furtherinvestigations are not necessary. Confirmatory tests can beuseful, however, when it is not possible to carry out all ofthe brainstem tests. We report the case of a patient with multipletrauma and a high spinal cord injury who was apnoeic. Confirmatorytests (EEG, brainstem, auditory evoked potential) were essentialin supporting the diagnosis of brainstem death to allow withdrawalof artificial ventilation, as organ donation was being considered. Br J Anaesth 2004; 92: 760–4     

Enhanced upper respiratory tract airflow and head fanning reduce brain temperature in brain-injured, mechanically ventilated patients: a randomized, crossover, factorial trial

Background. Heat loss from the upper airways and through theskull are physiological mechanisms of brain cooling which havenot been fully explored clinically. Methods. This randomized, crossover, factorial trial in 12 brain-injured,orally intubated patients investigated the effect of enhancednasal airflow (high flow unhumidified air with 20 p.p.m. nitricoxide gas) and bilateral head fanning on frontal lobe braintemperature and selective brain cooling. After a 30 min baseline,each patient received the four possible combinations of theinterventions—airflow, fanning, both together, no intervention—inrandomized order. Each combination was delivered for 30 minand followed by a 30 min washout, the last 5 min of which providedthe baseline for the next intervention. Results. The difference in mean brain temperature over the last5 min of the preceding washout minus the mean over the last5 min of intervention, was 0.15°C with nasal airflow (P=0.001,95% CI 0.06–0.23°C) and 0.26°C with head fanning(P<0.001, 95% CI 0.17–0.34°C). The estimate ofthe combined effect of airflow and fanning on brain temperaturewas 0.41°C. Selective brain cooling did not occur. Conclusion. Physiologically, this study demonstrates that heatloss through the upper airways and through the skull can reduceparenchymal brain temperature in brain-injured humans and theonset of temperature reduction is rapid. Clinically, in ischaemicstroke, a temperature decrease of 0.27°C may reduce therelative risk of poor outcome by 10–20%. Head fanningmay have the potential to achieve a temperature decrease ofthis order.     

Toxicity of photodynamic therapy with photofrin in the normal rat brain

The widespread acceptance of photodynamic therapy (PDT), a potential adjuvant brain tumor therapy under clinical evaluation since 1980, has been partially restrained by its potential toxicity toward normal brain tissue. This study examined PDT-produced injury of normal rat brain as a function of photosensitizer dose. Brain injury was characterized by correlating measurements of the area of cerebral edema using T2-weighted magnetic resonance images, measurement of brain water content at the lesion site, microscopic examination of histological sections through the PDT lesion, and by evaluation of the area of blood brain barrier (BBB) disruption using computerized morphometric analysis of the region of Evans blue (EB) dye-labelled albumin extravasation. Monochromatic red light (630 nm) was delivered intracere-brally using a 5-mm-long cylindrical, diffusion-tip optical fiber at a constant energy dose of 15 joules. A Photofrin dose of 2 mg/kg of body weight produced a transient breakdown in the blood brain barrier around the site of the implanted optical fiber demonstrated by magnetic resonance imaging (MRI), extravasation of EB dye and pallor on hematoxylin and eosin-stained microscopic tissue sections. A much larger area of BBB disruption was seen at a dose of 4 mg/kg of Photofrin, and this drug dose resulted in significant permanent brain injury. In this model, a Photofrin dose of 4 mg/kg body weight is not tolerated by the normal brain. © 1994 Wiley-Liss, Inc.     

The impact of enoxaparin administration in relationship to hemorrhage in mild traumatic brain injury

BackgroundVenous thromboembolism prophylaxis in the general trauma population is well established. However, risk of increased intracranial hemorrhage in traumatic brain injury (TBI) population is of concern. The aim for this study is to identify a reproducible model of mild traumatic brain injury (mTBI), evaluated by clinical and histological markers and test the hypothesis that enoxaparin increases the risk of spontaneous brain hemorrhage.Methods40 male Sprague Dawley rats were randomly assigned to 5 groups: group 1 (sham) with no TBI along with 4 groups comparing mTBI with and without pharmacological intervention using enoxaparin at 24 h and 72 h respectively. Mild traumatic brain injury was induced using a weight drop apparatus, with a clinical endpoint of time to right (TTR), along with histological and spectrophotometer analysis for qualitative hemorrhage.ResultsThere is a statistically significant difference between group 1 (sham) and all other groups with a mean longer time to right of 64 s (p = 0.005) in the mTBI groups. There was a statistically significant difference between group 1 (sham) and all other groups with an increase of 6 g/dL hemoglobin (p < 0.001) in the mTBI groups with no difference in hemorrhage between groups that were treated with enoxaparin.ConclusionThe weight drop apparatus is a reproducible model for mTBI that has correlations with clinical and qualitative data. This model was able to produce clinical signs of concussion, as reflected by longer TTR and increased hemoglobin in the mTBI groups. Upon further analysis, there wasno increase in hemorrhage in the pharmacological intervention groups with enoxaparin.     

Somatomedins in tumour cyst fluid,cerebrospinal fluid,and tumour cytosol in patients with glial tumours

Summary In the present study, the levels of the growth-promoting hormones, somatomedins, were analysed in tumour cyst fluid, CSF, and tumour cytosol, collected from 22 unselected patients with intracranial tumours. All samples contained somatomedin activity. 5/7 CSF samples, taken from patients with tumour mass visible on CT, showed elevated concentrations. 6/9 cyst fluid samples, taken from patients with glioma were elevated compared with normal serum somatomedin levels. Tumour cytosol, taken from 7 patients with malignant glioma contained somatomedins in an elevated level compared with values previously analysed from normal adult brains. These preliminary findings demonstrate for the first time the presence of somatomedins in brain tumours and suggest the use of somatomedins as a possible brain tumour marker.     

Cerebral protection in traumatic brain injury

With advances in the understanding of the pathophysiology of traumatic brain injury, many novel cerebroprotective measures have been developed. Many of them have undergone preclinical trials and have shown promising results, but the results have not translated into clinical benefits. Evidence of these cerebroprotective measures including NMDA‐receptor antagonist, steroids, free radial scavengers, nimodipine, ziconotide, bradykinin receptor antagonist and dexanabinol has been reviewed. Problems encountered in clinical studies of traumatic brain injury are mainly related to the heterogenicity of traumatic brain injury and the design of clinical studies. Given all these difficulties, clear benefit of these measures cannot be shown and an optimum treatment strategy has yet been developed.