早期应用纳洛酮对重型颅脑损伤患者内皮素及神经功能的影响

目的 探讨早期应用纳洛酮对重型颅脑损伤患者内皮素及神经功能的影响及意义。方法 采用按随机配对实验法，将82例重型颅脑损伤患者分为纳洛酮治疗组和对照组，在伤后不同时间予GCS评分、血ET测定、运动功能积分、及GOS预后评定。结果 纳洛酮治疗组的各项指标均较对照组明显改善，两组差异有显著性（P〈0.05）。结论 早期应用纳洛酮治疗重型颅脑损伤，具有改善脑血流、脑代谢，保护脑细胞，改善脑干的缺血缺氧状态，从而利于神经功能恢复，并明显改善预后。     

早期应用盐酸纳洛酮治疗重度颅脑外伤的疗效对照观察

本文就我院自１９９９．１～２００１．５收治的８５例急性重型颅脑损伤病人采用分组对照研究，探讨纳洛酮对重型颅脑损伤的影响。资料与方法１．研究对象：入选对象均符合下条件：（１）有明确的头部外伤史。（２）入院时GCS评分≤８分，平均５．６分。（３）无心、肺、肝、肾等器质性脏器损伤或衰竭。８５例病人按随机分配卡法，随机分入治疗组及对照组，治疗组n＝４５，对照组n＝４０，两组平均年龄之间经t检查，无显著性差异，性别比例之间经x２检验，无显著性差异，两组的病情之间经t检验无显著性差异。２．治疗方法：对照组：采用常…     

过表达生存素对颅脑外伤大鼠神经细胞凋亡和神经功能的影响

目的:观察过表达生存素(Survivin)对颅脑外伤大鼠神经细胞凋亡和神经功能的影响。方法:75只SD大鼠随机分为对照组、模型组和Survivin组。模型组和Survivin组大鼠采用自由落体法构建颅脑外伤大鼠模型,假手术组不做颅脑损伤。假手术组和模型组大鼠经颅内注射对照线相关病毒1×10 11 vg,Su...     

综合外伤急救模式联合危机管理对急诊颅脑损伤患者神经功能及预后的影响

目的 探讨综合外伤急救模式联合危机管理对急诊颅脑损伤患者神经功能及预后的影响.方法 回顾性分析2019-01—2021-01于南阳市第一人民医院西区医院急诊科收治的40例颅脑损伤患者的临床资料.均采取综合外伤急救模式联合危机管理干预.统计急诊干预相关时间、并发症发生率、抢救成功率.干预前及干预后1个月时,以美国国立卫生...     

颅脑外伤

外伤后急性弥漫性脑肿胀的诊断和治疗；前额叶底部对冲性脑挫裂伤31例手术治疗体会；标准大骨瓣减压术在重型颅脑损伤治疗中的应用；重型颅脑创伤后如何做好切除颅骨减压手术；重型颅脑损伤患者术中急性脑膨出的原因及防治；环孢素A对轴索损伤后的神经保护作用；     

纳洛酮对大鼠急性缺血性肾衰的保护作用

为探讨纳洛酮（NAL）对肾脏缺血再灌注损伤中的保护作用，利用大鼠肾脏缺血再灌注致急性缺血性肾功能衰竭（肾衰）模型，观察NAL对肾缺血再灌注后血中丙二醛（MDA）、超氧化物歧化酶（SOD）及肾组织中Na+、K+－ATP酶和Ca2+－ATP酶的影响，并观察组织病理学变化。结果缺血60min再灌注后，血MDA含量明显升高，SOD活力明显降低，肾组织Na+、K+－ATP酶和Ca2+－ATP酶活力均显著降低。用NAL（Ⅰ组为2mg／kg，Ⅱ组为4mg／kg）后，MDA显著下降，SOD和Na+、K+－ATP酶及Ca2+－ATP酶均明显升高，且有量效关系。组织病理学检查显示应用NAL后肾小管上皮细胞的损伤明显减轻，NAL－Ⅱ组明显好于NAL－Ⅰ组。认为NAL对急性缺血性肾衰有一定的保护作用。     

神经外科——颅脑外伤

颅脑损伤后颅骨成形及相关问题分析，AM-36对大鼠液压脑损伤的神经保护作用，重型颅脑损伤合并多发伤的临床救治，超低位大骨瓣开颅颞肌下减压术治疗重型颅脑创伤脑疝病人，豫北农村区域性颅脑创伤急救模式初探，急性重型颅脑损伤87例临床分析[编者按]     

热休克蛋白对颅脑外伤的保护机理

颅脑外伤后除产生内源性脑损害因子外，还有保护因子的产生。热休克蛋白是机体对外来刺激诱导产生的一组应激蛋白，对细胞具有保护作用。本文对热休克蛋白生物学特性，颅脑外伤后热休克蛋白产生的机制以及对脑细胞的保护机理作一综述。     

盐酸纳洛酮治疗中型颅脑损伤

颅脑损伤早期应用大剂量纳洛酮能明显降低颅脑损伤患者的病死率，促进神经功能恢复。改善患者远期生活质量，具有重要意义。我科于2003年2月至2004年4月应用盐酸纳洛酮治疗30例中型颅脑损伤患者，均取得良好效果。     

大小剂量纳洛酮对严重颅脑损伤后细胞凋亡抑制作用的实验研究

目的观察纳洛酮对脑外伤的抗凋亡作用,比较大小剂量纳洛酮对实验性脑损伤后神经细胞凋亡的影响.方法选用家兔77只,随机分成正常组、对照组、大剂量组和小剂量组,分别予非颅脑损伤、颅脑损伤、颅脑损伤后大剂量纳洛酮腹腔注射及颅脑损伤后小剂量纳洛酮腹腔注射处理,15天后均断头处死,于致伤处和对侧处分别取材,利用TUNEL法制作切片,观察及比较各组神经细胞凋亡数量.结果致伤处或对侧处,正常组、大剂量组、小剂量组和对照组神经细胞凋亡数量两两之间比较均有显著差异,值从小到大为:正常组、大剂量组、小剂量组、对照组.结论纳洛酮具有抑制严重颅脑损伤后神经细胞凋亡的作用;大剂量纳洛酮应用可以较显著抑制严重颅脑损伤后的神经细胞凋亡.     

纳洛酮对大鼠颅脑损伤后神经细胞凋亡的影响

目的　探讨纳络酮对大鼠颅脑损伤后神经细胞凋亡的影响。方法　采用Feeney氏自由落体法制备脑损伤动物的模型 ,将 90只大鼠随机分为实验组及对照组 ,于伤后 1 5、60min及2 4h分别给予纳洛酮或 0 .9%氯化钠溶液 ,伤后第 5天断头处死大鼠 ,采用原位末端脱氧核苷酸生物素末端标记 (TUNEL)法测定神经细胞原位凋亡情况 ,并用光镜观察细胞形态学改变。结果　与对照组比较 ,大鼠脑损伤后 1 5及 60min应用纳洛酮可明显减少神经细胞凋亡 ,而伤后 2 4h给药 ,则两组神经细胞的凋亡率差异无显著性 (P >0 .0 5)。结论　早期应用大剂量纳洛酮可明显减少脑损伤后神经细胞的凋亡 ,从而可有效地保护神经细胞功能     

纳洛酮在急性重型颅脑损伤中的应用

目的探讨纳洛酮治疗急性重型颅脑损伤的效果.方法对67例急性重型颅脑损伤病人随机分组对照,观察两组病人生命体征和意识状态变化,并进行统计学分析.结果实验组病例入院3天后平均动脉压异常率为23.5%,呼吸异常率为11.8%,心律异常为29.4%,明显较对照组少.伤后48小时意识转清率实验组与对照组分别是32.4%与30.0%,两者无明显差别.1周后意识转清率实验组64.7%,明显高于对照组48.6%.结论纳洛酮治疗急性重型颅脑损伤,有利于较快恢复生命体征稳定,缩短昏迷时间.     

大鼠颅脑损伤后细胞凋亡及纳络酮的抗凋亡作用

目的 探讨颅脑损伤后神经细胞凋亡的时相特点及其药物调控作用。方法 采用原位末端标记法（TUNEL）结合流式细胞术对外伤组、伤后纳络酮治疗组及对照组大鼠伤侧大脑皮质的细胞凋亡情况进行定量分析。结果 凋亡细胞从伤后24h开始逐渐增多，伤后3－5d发展到项峰，此后逐渐下降；是纳络酮治疗组各时相点凋亡细胞数均明显低于外伤组。结论 外伤后第3－5天是细胞凋亡的高峰期，纳络酮具有显著的抗凋亡作用。     

The impact of acute care medications on rehabilitation outcome after traumatic brain injury

Objectives: To examine the impact of medications with known central nervous system (CNS) mechanisms of action, given during the acute care stages after traumatic brain injury (TBI), on the extent of cognitive and motor recovery during inpatient rehabilitation.

Design: Retrospective extraction of data utilizing an inception cohort of moderate and severe TBI survivors.

Methods: The records of 182 consecutive moderate and severe TBI survivors admitted to a single, large, Midwestern level I trauma centre and subsequently transferred for acute inpatient rehabilitation were abstracted for the presence of 11 categories of medication, three measures of injury severity (worst 24 hour Glasgow Coma Scale, worst pupillary response, intra-cranial hypertension), three measures of outcome (Function Independence Measure (FIM) Motor and Cognitive scores at both rehabilitation admission and discharge and duration of post-traumatic amnesia (PTA)).

Main outcome and results: The narcotics, benzodiazepines and neuroleptics were the most common categories of CNS active medications (92%, 67% and 43%, respectively). The three categories of medications appeared to have no significant outcome on the FIM outcome variables. The neuroleptics affected cognitive recovery with almost 7 more days required to clear PTA in the neuroleptic treated group. The presence of benzodiazepines did tend to obscure the impact of neuroleptics on PTA duration but the negative impact of neuroleptics on PTA duration remained significant.

Conclusions: The results suggest that the use of neuroleptics during the acute care stage of recovery has a negative impact on recovery of cognitive function at discharge from inpatient rehabilitation. Due to the paucity of subjects with hemiplegia in this cohort, conclusions could not be drawn as to the impact of acute care medications on motor recovery.     

盐酸纳络酮对颅脑损伤患者血清C－反应蛋白影响的临床研究

目的通过动态观察盐酸纳络酮对颅脑损伤患者血清C-反应蛋白浓度的影响,进一步探讨盐酸纳络酮在颅脑损伤治疗中的作用。方法将80例颅脑损伤患者随机分为纳络酮组和常规组。纳络酮组在常规治疗的基础上加用盐酸纳络酮,即人院后立即缓慢静脉推注4mg后以0．4mg,／kg／天静脉泵持续静脉滴注,3天后改为0．2mg／kg／天,至第10天停药。两组患者于入院后24小时内和第10天检测血清C-反应蛋白浓度。治疗后3月采用GOS评分比较预后。结果两组患者血清C-反应蛋白浓度明显高于正常对照组（P〈0．05）;纳络酮组血清C-反应蛋白浓度明显低于常规组（P〈0．05）;纳络酮组治疗后3个月GOS评分明显高于常规组（P〈0．05）。结论颅脑损伤患者血清C-反应蛋白浓度明显升高,盐酸纳络酮能显著降低患者血清C-反应蛋白浓度．保护神经功能,改善预后。     

Effect of AVP on brain edema following traumatic brain injury

Objective: To evaluate plasma arginine vasopressin (AVP) level in patients with traumatic brain injury and investigate the role of AVP in the process of brain edema. Methods: A total of 30 patients with traumatic brain injury were involved in our study. They were divided into two groups by Glasgow Coma Scale: severe traumatic brain injury group (STBI, GCS≤8) and moderate traumatic brain injury group ( MTBI, GCS >8). Samples of venous blood were collected in the morning at rest from 15 healthy volunteers (control group) and within 24 h after traumatic brain injury from these patients for AVP determinations by radioimmunoassay. The severity and duration of the brain edema were estimated by head CT scan. Results: plasma AVP levels (ng/L) were (mean±SD): control, 3. 06±1. 49; MTBI, 38. 12±7. 25; and STBI, 66. 61±17. 10. The plasma level of AVP was significantly increased within 24 h after traumatic brain injury and followed by the reduction of GCS, suggesting the deterioration of cerebral injury (P<0. 01). And the AVP level was correlated with the severity (STBI r =0.919, P < 0.01; MTBI r = 0.724, P < 0.01) and the duration of brain edema (STBI r = 0. 790, P < 0. 01; MTBI r = 0. 712, P<0.01). Conclusions: The plasma AVP level is closely associated with the severity of traumatic brain injury. AVP may play an important role in pathogenesis of brain edema after traumatic brain injury.     

不同剂量纳洛酮后处理对大鼠局灶性脑缺血再灌注损伤的影响

目的 探讨不同剂量纳洛酮后处理对大鼠局灶性脑缺血再灌注损伤的影响.方法 成年sD大鼠88只,体重270～330 g,随机分为4组(n=22):假手术组(S组)、脑缺血再灌注组(IR组)和不同剂量纳洛酮后处理组(N_(1,2)组).除S组外,其它3组均采用阻断右侧大脑中动脉90 min、再灌注24 h的方法制备局灶性脑缺血再灌注损伤模型.N_(1,2)组于再灌注即刻分别腹腔注射纳洛酮1、10 mg/kg,S组和m组给予等容量生理盐水.分别于再灌注2、24 h时测定大鼠神经功能障碍评分(NDS);再灌注24 h时测定脑梗死面积和脑组织微管相关蛋白2(MAP2)的表达水平和脑组织血浆容量、徽血管直径和长度.结果 与S组相比,IR组、N_(1,2)组NDS评分均升高,脑梗死面积增大,脑组织MAP2表达水平下调,缺血侧脑组织血浆容量降低,微血管直径和长度减小(P<0.05);与IR组相比,N_2组NDS评分降低,脑梗死面积减小,脑组织MAP2表达水平上调,缺血侧脑组织血浆容量升高,微血管直径和长度增大(P<0.05),N_1组上述指标差异无统计学意义(P>0.05);与N_1组相比,N_2组NDS评分降低,脑梗死面积减小,脑组织MAP2表达水平上调,缺血侧脑组织血浆容量升高,微血管直径和长度增大(P<0.05).结论 纳洛酮后处理可减轻大鼠局灶性脑缺血再灌注损伤,且呈剂量依赖性.     

Plasma free carnitine in severe trauma: Influence of the association with traumatic brain injury

BackgroundMetabolic response to severe trauma requires early nutritional resuscitation. Carnitine is essential for lipolysis, the energy source during this hypercatabolic phase. However l-carnitine is not present in nutritional replacement solutions. Furthermore, free carnitine depletion, defined as carnitine plasma level under 36 μmol/L, was not adequately reported in adult patients with severe trauma. The aim of this study was to assess plasma free carnitine levels and factors of variation in severe trauma.MethodOur observational study concerned 38 trauma patients including 18 with traumatic brain injury (TBI). On the third day after trauma, plasma free carnitine concentration was determined (by enzymatic method) while patients received artificial nutrition.ResultsLow plasmatic free carnitine concentration was evidenced in 95% of the patients with a median value of 18 μmol/L (11–47). Univariate analysis showed that mean arterial pressure, serum urea, CKD-EPI and patients with TBI were significantly associated with plasma free carnitine concentration less than 18 μmol/L. Lower plasma free carnitine concentration was observed in the group of patients with TBI with 17.72 μmol/L (11–36) versus 21.5 μmol/L (11–47) for others patients (p = 0.031). Logistic regression analysis showed that severe trauma with TBI and CKD-EPI above 94 mL/min/1.73 m2 appeared to be independent predictor of lower free carnitine plasmatic concentration (Goodness of fit = 0.87 and AUC = 0.89).ConclusionOur observations support hypotheses that plasma free carnitine concentration is lowered in severe injured patients especially for TBI patients and patients with estimated GFR above 94 mL/min/1.73 m².