利多卡因对心脏术后脑保护效果的Meta分析

背景：虽然心脏手术日趋成熟,但术后认知障碍发生率仍然较高。利多卡因对脑的保护效应的研究结果不一。 目的：分析利多卡对心脏术后脑保护效果。 方法：在PubMed,Cochrane databases,CNKI和Ovid等数据库中系统检索有关利多卡因、心脏手术及脑保护的前瞻性的随机对照研究。提取术后认知障碍发生率及脑代谢相关的指标用于疗效评价,结果以优势比(OR)、加权均数差(WMD)和 95%可信区间(CI)表示。提取的资料采用Review Manager Version 5软件进行分析。 结果与结论：共有5篇含有术前和术后的神经心理学测试的文献及2篇关于术中脑代谢测量的文献入选。合并后的结果显示认术后的认知障碍和术前的差异无显著性意义,但在亚组分析中显示低年龄组和低剂量组的术后认知障碍较术前减少 (P < 0.05)。术中应用利多卡因能够在手术中降低动脉-颈内静脉血氧含量差,脑氧摄取率)及脑乳酸产生量(P < 0.05)。死亡及退出患者总数差异无显著性意义。结果说明现有证据不足以证明利多卡因有脑保护的作用,但应用在合适的临床情况下,利多卡因是有脑保护的作用的。     

大鼠额叶皮质损害和胚脑移植的脑电地形图及形态学研究

用ＮＤＣ－２００型脑电地形图仪对单侧额叶皮质损害及损害后移植胚服皮质的大鼠进行脑电功率谱及脑电地形图的检查。结果发现大鼠伤额叶皮质Ｄｅｌｔａ波和Ｔｈｅｔａ波与Ａｌｐｈａ波和Ｂｅｔａ波之比明显主于健侧。损害后３ｄ，２周，４周，８周，其结果无差别。额叶皮质损害后２周接受了胚脑皮     

利多卡因对大鼠SAH后神经细胞凋亡和迟发性脑血管痉挛的保护作用

目的:探讨利多卡因对大鼠蛛网膜下腔出血(SAH)后神经细胞凋亡和迟发性脑血管痉挛的保护作用。方法:将60只成年大鼠分为假手术组(sham)、SAH组(SAH)和lidocaine处理组(lidocaine)。采用枕大池二次注血法制备动物模型。lidocaine组注射盐酸利多卡因。分别于不同时间灌注后取脑。取用部分基底动脉行苏木精-伊红染色法(HE)观察形态改变和测量基底动脉的管径和管壁的厚度,使用脱氧核糖核酸(DNA)断裂的原位末端标记(TUNEL)法测定海马CA1区神经细胞的凋亡情况。结果:HE染色显示,利多卡因组从第3 d开始内径周长增加,管壁厚度缩小。TUNEL检测显示:SAH组凋亡细胞随时间逐渐增加,而利多卡因组的凋亡细胞逐渐减少。结论:利多卡因能明显减轻大鼠SAH后迟发性的脑血管痉挛及减少海马CA1区神经细胞的凋亡,具有一定的保护作用。     

利多卡因治疗重度颅脑外伤的临床研究

目的 探讨应用利多卡因经静脉注射对重度颅脑外伤患者的治疗作用。方法 重度颅脑外伤患者60例（GCS≤8分），随机分为两组，对照组30例，伤后予常规治疗；治疗组30例，伤后3d内予常规治疗加利多卡因静脉注射治疗14d。治疗前后均作GCS评分、腰穿测定颅内压、头部CT、ECT、TCD检查。结果 治疗组利多卡因治疗2～5d即出现出现意识、肢体功能好转、脑血供改善、脑水肿吸收；10d后肢体功能明显恢复，脑血供和颅内血流速度接近正常，脑水肿消退，颅内压接近正常。对照组患者同期治疗后观察头部ECT、TCD、CT未见明显变化，意识、肢体功能、脑血供改善不明显、脑水肿消退缓慢。结论 早期应用利多卡因静脉注射能缓解颅脑损伤患者脑血管痉挛，改善脑微循环，减轻脑缺血引起的脑水肿，使颅内压下降，促进脑功能恢复。     

神经节苷脂GM1及其脑保护机制

神经节甘脂是一组含有唾液酸的鞘糖脂,神经节甘脂GM1(即单唾液酸四已糖神经节甘脂)是哺乳类神经节甘脂的主要种类.神经节甘脂GM1具有一定的脑保护作用,关于探讨其脑保护作用及可能机制的研究很多,本文仅就目前较为公认的脑保护机制作一简述.     

神经节苷脂GM1及其脑保护机制

神经节甘脂是一组含有唾液酸的鞘糖脂,神经节甘脂ＧＭ１（即单唾液酸四已糖神经节甘脂）是哺乳类神经节甘脂的主要种类。神经节甘脂ＧＭ１具有一定的脑保护作用,关于探讨其脑保护作用及可能机制的研究很多,本文仅就目前较为公认的脑保护机制作一简述。     

利多卡因治疗重度颅脑外伤的临床研究

目的探讨应用利多卡因经静脉注射对重度颅脑外伤患者的治疗作用.方法重度颅脑外伤患者60例(GCS≤8分),随机分为两组,对照组30例,伤后予常规治疗;治疗组30例,伤后3d内予常规治疗加利多卡因静脉注射治疗14d.治疗前后均作GCS评分、腰穿测定颅内压、头部CT、ECT、TCD检查.结果治疗组利多卡因治疗2～5d即出现出现意识、肢体功能好转、脑血供改善、脑水肿吸收;10d后肢体功能明显恢复,脑血供和颅内血流速度接近正常,脑水肿消退,颅内压接近正常.对照组患者同期治疗后观察头部ECT、TCD、CT未见明显变化,意识、肢体功能、脑血供改善不明显、脑水肿消退缓慢.结论早期应用利多卡因静脉注射能缓解颅脑损伤患者脑血管痉挛,改善脑微循环,减轻脑缺血引起的脑水肿,使颅内压下降,促进脑功能恢复.     

脑创伤后脑微血管扫描电镜观察及临床意义

目的：探讨急性颅脑损伤后扫描电镜下脑微血管形态学改变，为脑损伤后继发性损害提供微循环基础。方法：制作大鼠液压冲击脑损伤模型，复合甲基丙烯酸甲酯脑微血管铸型，50％盐酸腐蚀脑组织，制作脑微血管标本，扫描电镜观察正常大鼠正常大鼠脑微血管和急性脑损伤后3、12、48、72h脑微血管形态学的改变。结果：对照组脑内有较稠密的微血管，分布均匀，外形规则、平滑，粗细均匀，行走弯曲自然。脑损伤后3h观察到小动脉行走僵硬，毛细血管充盈差，吻合减少，行走过度弯曲或形成盲端。24h和48h的血管有较多的渗出，铸型剂聚集或囊性扩张。结论：急性颅脑损伤后脑微血管功能失调是导致加重继发性脑缺血缺氧的重要原因。     

轻型颅脑损伤的脑电地形图

我们分析了119例主诉较重但临床检查与头颅CT扫描无阳性发现的轻型颅脑损伤病人的BEAM,结果显示BEAM的异常率达61.4％。BEAM检测出的脑电功能异常部位与受伤机制相符,对轻型颅脑损伤有辅助诊断价值。     

镁剂在颅脑损伤中的保护作用

镁离子 (Mg2 + )是机体内重要的细胞内阳离子 ,研究表明 Mg2 + 不仅在脑组织具有重要的调节功能 ,而且对颅脑损伤具有一定的保护作用 ,因而创伤性颅脑损伤后血液游离Mg2 + 的检测还具有诊断和预后的价值。1　 Mg2 + 颅脑损伤后的变化Smith等 〔1〕采用 31 P磁共振分光技术 (MRS)检测颅脑液压伤后脑组织及神经细胞内 Mg2 +含量明显下降 ,受伤脑区细胞内 Mg2 +含量下降最显著 ,其下降程度与脑损伤程度相关。Altura〔2〕等采用单一 Mg2 +选择电极法测定 98例脑卒中患者血清中游离 Mg2 + 和总 Mg2 + 含量 ,结果显示游离 Mg2 +明显下降 ,…     

Potentially toxic serum lidocaine concentrations following spray anesthesia for bronchoscopy

Summary Serum lidocaine concentrations were measured in a series of ten patients during and after topical lidocaine spray anesthesia used for diagnostic fiberoptic bronchoscopy. Mean total dose of lidocaine ranged from 480–720 mg. Peak serum lidocaine concentrations averaged 3.6 g/ml (range: 1.9 to 7.4 µg/ml), and were attained shortly after the start of the procedure. Repeated topical administration of lidocaine spray therefore may lead to large cumulative doses and serum concentrations which are in the therapeutic or potentially toxic range.Supported in part by Grant Oc 10/6-3 from Deutsche Forschungsgemeinschaft und by Grant MH-34223 from the United States Public Health Service     

The Extracellular Space in the Edematous Human Cerebral Cortex: An Electron Microscopic Study Using Cortical Biopsies

In a vascular anomaly showing moderate edema, the extracellular space appeared apparently normal, exhibiting a membrane to membrane space of about 20?nm in width. In congenital hydrocephalus, this space appeared notably enlarged and occupied by an electron transparent, nonproteinaceous interstitial edema fluid, due to abnormal accumulation of cerebrospinal fluid. In brain trauma, the distended extracellular space contained either electron-lucid nonproteinaceous or electron-dense proteinaceous edema fluid. Hemorrhagic foci, fibrinoid material, and non-nervous invading cells, such as macrophages and monocytes, were also found. In brain tumors, the widened extracellular space showed electron-dense proteinaceous edema fluid and bundles of fibrinoid material. The enlarged extracellular space found in congenital hydrocephalus, vascular anomalies, brain trauma, and tumors is closely related to the clinical symptoms exhibited by the patients under study.     

Cerebral reactive hyperaemia and arterial pressure in anaesthetized goats

The effects of arterial pressure on cerebral reactive hyperaemia were studied in anaesthetized goats measuring electromagnetically middle cerebral artery flow and performing arterial occlusions of 5–30 s. Under normotension (mean arterial pressure, MAP = 11± 0.3 kPa), reactive hyperaemia (peak hyperaemic flow to control flow and repayment to debt ratios) increased, and cerebrovascular resistance during peak hyperaemic flow decreased, as ischaemia duration lengthened; the virtual maximal changes were obtained after 20 s ischaemia. During hypertension by aorta constriction (MAP = 18 ± 0.7 kPa) or by i. v. infusion of noradrenaline (MAP = 19 ± 0.8 kPa) middle cerebral artery flow did not change significantly and cerebrovascular resistance increased 25 and 46%, respectively (P < 0.05). During both types of hypertension reactive hyperaemia was over 50% higher, and the decrement in cerebrovascular resistance during peak hyperaemic flow was also higher, than under normotension. During hypotension by constriction of the inferior vena cava (MAP = 5 ±.5 kPa) or by i. v. infusion of isoproterenol (MAP = 6±.5 kPa), middle cerebral artery flow decreased 35% or did not change, and cerebrovascular resistance decreased 41 and 45 %, respectively (P < 0.05). In these conditions, reactive hyperaemia and the decrement in cerebrovascular resistance during peak hyperaemic flow were reduced SOY, and it was similar in both types of hypotension. The absolute levels of cerebrovascular resistance obtained during peak hyperaemia were similar during normotension, hypertension and hypotension. Thus, arterial pressure is a main determinant of postocclusive cerebral reactive hyperaemia, and myogenic mechanisms may be of significance in determining the early stage of cerebral reactive hyperaemia after brief ischaemias. Adrenergic mechanisms might be of minor significance in this type of cerebral reactive hyperaemia.     

Peculiarities of nerve conduction block produced by lidocaine and ajmaline

The development of tonic and use-dependent block of nerve conduction under the effect of antiarrhythmic drug ajmaline and local anesthetic lidocaine was examined on sciatic nerve of Rana ridibunda. Ajmaline and lidocaine attenuated the amplitude of action potential by half during 120 and 13 minutes, respectively. Ajmaline produced virtually immediate use-dependent block of conductance, while it was minor in lidocaine-treated nerve preparation. __________ Translated from Byulleten’ Eksperimental’noi Biologii i Meditsiny, Vol. 143, No. 3, pp. 262–266, March, 2007     

山莨菪碱保护缺血小肠的机理探讨

山莨菪碱(654-2)具有保护缺血、缺氧组织细胞的作用,其机制尚不清楚。本工作观察654-2是否具有钙拮抗作用。研究发现,1.肠系膜动脉灌注654-2可显著减轻缺血小肠的粘膜损伤和组织内钙积聚。2.654-2可降低高钾去极化豚鼠回肠对钙的收缩反应,使钙拮抗作用曲线显著右移。3.连续静脉注射654-2 5mg/kg明显抑制心功能,病理检查显心衰样心肺损伤。结果提示,654-2具有钙拮抗样作用,可能是其具有细胞保护作用的重要机理之一。     

多巴胺对出血性脑卒中大鼠胶质纤维酸性蛋白和脑源性神经营养因子表达的影响及保护机制

目的：探讨多巴胺（DA）对出血性脑卒中大鼠的胶质纤维酸性蛋白（GFAP）和脑源性神经营养因子（BDNF） 表达的影响及保护机制。方法：建立出血性脑卒中大鼠模型,将大鼠随机分为假手术组、脑出血模型组（ICH 组）和DA 组（ 脑出血模型给予DA 组）。分别比较3 组大鼠的神经功能障碍评分、神经元形态、脑水肿、细胞凋 亡和脑组织形态变化;免疫组织化学染色法检测脑组织中GFAP 和BDNF 蛋白的表达。结果：与假手术组相比较, ICH 组神经功能障碍评分显著降低;与ICH 组相比,DA 组神经功能障碍评分显著升高。与假手术组比较,ICH 组尼氏小体数量显著减少;与ICH 组相比,DA 组尼氏小体数量明显增加;ICH 组脑组织含水量和细胞凋亡数量 显著高于假手术组;与ICH 组相比,DA 组脑组织含水量和细胞凋亡数量均显著降低。ICH 组脑组织出现了不同 程度的水肿,其中一部分神经细胞出现了明显肿胀,间质之间明显增宽,神经元结构受到了严重破坏,严重的 神经元出现坏死,且有大量的炎性细胞浸润;DA 组大鼠的脑组织形态得到明显的改善。与假手术组相比,ICH 组脑组织中GFAP 蛋白阳性表达显著增加,BDNF 蛋白阳性表达显著降低;与ICH 组大鼠相比,DA 组脑组织中 GFAP 阳性表达明显减少,BDNF 蛋白阳性表达明显增多。结论：DA 能抑制脑组织中GFAP 表达,促进BDNF 的 表达,改善脑出血的神经功能障碍,进而对出血性脑卒中受损脑组织起到保护作用。     

利多卡因后处理减轻大鼠肺缺血再灌注损伤

 目的 探讨利多卡因后处理对肺缺血再灌注损伤的保护作用。方法 72只大鼠随机分为四组,每组18只：假手术组、I-R组（ischemia reperfusion, I-R）、缺血后处理组（ischemic postconditioning, IPC）和利多卡因后处理组。采用夹闭左肺门45min,然后复灌2h的方法建立在体肺I-R模型。利多卡因后处理组再灌注即刻泵入利多卡因4mg/kg, 而后4mg/kg·h持续再灌注2h。测定PaO2、检测肺组织W/D、MDA和血清TNF-α浓度,并对肺组织进行组织形态学检查。结果 再灌注后利多卡因组的PaO2显著高于I-R组（P＜0.05）;再灌注2h后利多卡因组的MDA（7.03±1.17 μmol/L）明显低于I-R组（8.77±1.42μmol/L）（P＜0.05）;再灌注2h后利多卡因组TNF-α浓度（1.69±0.34 μg/L）低于I-R组（2.52±0.54μg/L）（P＜0.05）。肺组织形态学检查发现利多卡因组的肺水肿和中性粒细胞积聚较I-R组明显减轻。结论 利多卡因后处理可以减轻过氧化损伤和TNF-α的表达,减轻肺水肿,具有肺保护效应。     

芍药苷对脑缺血损伤的保护作用及其对脑血管通透性的影响

目的观察芍药苷（peoniflorin,PF）注射液对脑缺血损伤的保护作用及其对脑血管通透性的影响。方法采用线栓法闭塞大脑中动脉建立大鼠局灶性脑缺血模型（MCAO）,各组分别进行行为学评分,脑组织含水量和脑梗塞面积测定及免疫组化检测脑组织中水通道蛋白-4（AQP4）的表达。此外,检测PF对脑缺血再灌注损伤小鼠脑血管通透性的影响。结果PF注射给药可显著改善脑缺血的神经损伤症状,降低脑组织的含水量,缩小脑梗死面积,降低脑血管通透性,减少AQP4阳性细胞的表达。结论芍药苷注射液对脑缺血有明显的保护作用,该作用可通过调节AQP4的表达而降低脑血管通透性来完成。     

Cerebral circulation in acute arterial hypertension—protective effects of sympathetic nervous activity

The cervical sympathetic chain was stimulated electrically at 6 or 3 Hz on one side in anesthetized cats. Acute arterial hypertension was induced by ligation of the aorta. Evans blue was given as tracer for protein leakage. The regional blood flow in the brain was determined by using labelled microspheres. At high blood pressures there was a multifocal breakdown of the blood-brain barrier. The regions with breakdown had 10–20 times the normal flow rates. With a maintained hypertension regions which were overperfused at 5 min were still overperfused at 10 min, but there was little addition of new overperfused areas. Normalization of the pressure resulted in almost twice the normal flow rates in previously overperfused regions. The breakdown of the blood-brain barrier was restricted to the non-stimulated side, or more marked on that side. The protective effect of the sympathetic stimulation lasted more than 10 min. The results indicate that acute arterial hypertension tends to cause forced and long-lasting vasodilation in some areas in the brain but regions which are resistant to the acute rise have an increase in the vascular tone. Sympathetic activity helps in developing this tone. Normalization of the blood pressure results in partial recovery of the vascular tone in previously overperfused regions and normalization in other areas.     

Use-dependent inhibition of polymodal C-fiber cutaneous sensory units in cats by lidocaine and N-propylajmaline

Group for Biomechanics and Regulation of the Circulation, Institute of Experimental Cardiology, All-Union Cardiologic Scientific Center, Academy of Medical Sciences of the USSR, Moscow. (Presented by Academician of the Academy of Medical Sciences of the USSR V. N. Smirnov.) Translated from Byulleten' Éksperimental'noi Biologii i Meditsiny, Vol. 113, No. 3, pp. 248–250, March, 1992.