不同时间迷走神经电刺激对大鼠心肺复苏预后的影响

目的探讨不同时间迷走神经电刺激(vagus nerve stimulation,VNS)对心脏骤停(cardiac arrest,CA)/心肺复苏(cardiopulmonary resuscitation,CPR)后大鼠预后的影响。方法采用改良经皮心外膜电刺激诱导心室颤动方法建立大鼠CA模型。53只雄性SD大鼠随机(随机数字法)分成假手术组(SHAM,n=5)、CPR组(n=12)和VNS组(n=36)。SHAM组不经历CA/CPR;VNS治疗分别设置在CA前30 min(PRE组,n=12)、自主循环恢复(recovery of spontaneous circulation,ROSC)后5 min(POST5组,n=12)以及ROSC后30 min(POST30组,n=12),以统一的刺激参数给予迷走神经电刺激30 min。观察大鼠ROSC后24、48、72 h的神经功能缺损评分和72 h生存率。采用TUNEL染色检测ROSC后72 h的大鼠脑组织皮质区细胞凋亡情况,采用免疫荧光检测α7烟碱型乙酰胆碱受体(α7 subunit-containing nicotinic acetylcholine receptor,α7nAChR)的表达。计量资料组间比较采用单因素方差分析,生存率采用Kaplan-Meier分析和Log-rank检验。以P<0.05为差异有统计学意义。结果与CPR组(生存率为33.33%)相比,CA前VNS处理(PRE,生存率为75%)和CA后VNS处理(POST5组生存率75%;POST30组生存率83.33%)均可显著提高大鼠CPR后72 h生存率(P<0.05),降低ROSC后的神经功能缺损评分,降低脑皮质细胞凋亡阳性率,而VNS各处理组间差异无统计学意义(P>0.05)。VNS处理后脑皮质α7nAChR的表达较CPR组增加。结论CA前和ROSC后5 min和30 min给予VNS处理均对CA/CPR大鼠具有脑保护的作用,其机制可能与激活α7nAChR介导的抗炎与抗凋亡效应有关。     

胰岛素对心肺复苏大鼠神经元凋亡及Bcl-2,Bax mRNA表达的影响

目的 探讨脑室内注射胰岛素对心肺复苏(cardiopulmonary resuscitation,CPR)后大鼠海马CA1区神经元凋亡和对抑凋亡因子Bcl-2,促凋亡因子Bax mRNA表达的影响.方法 实验地点在首都医科大学宣武医院试验动物中心.30只雄性SD大鼠随机(随机数字法)分为假手术组(对照组,n=6)、心肺复苏组(复苏组,n=12)及CPR后胰岛素干预组(胰岛素组,n=12).经食道超速起搏诱发6min室颤制备大鼠CPR模型;以CPR后大鼠恢复室上性心率、收缩压超过60 mmHg(1 mmHg=0.133 kPa)并持续10 min以上,作为自主循环恢复(ROCS)标准;ROCS 10 min后,胰岛素组大鼠经立体定位仪定位,脑室内注射12.5 μL(1 U)胰岛素,其余2组大鼠注射等量生理盐水.维持生命体征,CPR后24,72 h,应用实时荧光PCR (Realtime-PCR)测定海马CA1区神经元Bcl-2,Bax mRNA的表达量;CPR后7d,应用TUNEL染色检测海马CA1区神经元凋亡;CPR前后监测大鼠静脉血糖变化.计量资料采用均数±标准差(-x±s),组间比较采用单因素方差分析(ANOVA);相关性统计应用Pearson相关分析,以P＜0.05为差异具有统计学意义.结果 ①CPR后24,72 h,胰岛素组大鼠Bcl-2 mRNA表达量均高于复苏组(1.45±0.05) vs.(0.79±0.01);(0.95±0.06) vs.(0.35±0.03),差异具有统计学意义(P＜0.01).组内比较发现,胰岛素组、复苏组72 h表达均低于24 h(P＜0.01).而胰岛素组与复苏组Bax mRNA表达差异无统计学意义(P＞0.05),胰岛素组、复苏组72 h与24h比较差异无统计学意义(P＞0.05).②CPR后7d,胰岛素组大鼠海马CA1区神经元凋亡计数,复苏组(124.75±17.35)个/mm2明显高于对照组(5.12±3.26)个/mm2和胰岛素组(92.79±7.49)个/mm2,差异具有统计学意义(P＜0.01).③各组大鼠各时间点外周静脉血糖比较无统计学意义(P＞0.05).结论 脑室内注射1U胰岛素,能够促进CPR后大鼠神经元促凋亡因子Bcl-2 mRNA的表达,抑制神经元凋亡,具有神经保护作用.脑室注射1U胰岛素不降低外周血糖.     

经右心室电刺激致颤建立家兔心脏骤停模型

目的：建立一种简单、有效、稳定的家兔电刺激致颤心脏骤停（ CA）后脑复苏模型。方法选用20只新西兰雄性家兔,采用体表胸壁及心内膜下交流电诱发室颤的方法制作CA模型,CA 4 min后开始心肺复苏（CPR）。记录手术操作时间（TOP）、自主循环恢复时间（TROSC）、恢复率,除颤、肾上腺素次数,24 h、72 h存活率以及进行72 h大脑皮质凋亡细胞检测。另取10只兔为对照组,只进行致颤前手术操作。结果①20只家兔全部诱发CA成功,室颤发生率为100％。自主循环恢复率为80％;24 h、72 h存活率为50％、30％;除颤和肾上腺素次数为1．20±0.89、1．60±0．75;TOP和TROSC分别为（79±25）min、（268±33）s。②血浆神经元特异性烯醇化酶（NSE）水平显著升高,ROSC 72 h略有回降,但仍高于造模前（P＜0．05）。③与对照组比较,ROSC后72 h大脑皮质区出现了较多神经细胞的凋亡（P＜0．05）。④神经功能评分（NDS）在复苏后3 h时最低,以后渐趋好转。结论该模型操作简单、结果稳定、复苏成功率高,是一个较为理想的心肺脑复苏研究模型。     

应用反复低血压及双侧颈总动脉阻断法建立血管性痴呆大鼠模型

目的:通过反复低血压及双侧颈总动脉阻断后建立血管性痴呆大鼠模型,观察大鼠学习记忆能力和脑组织病理学变化。方法:实验于1999-09/2000-01在重庆医科大学第一附属医院神经病学研究所完成。选择健康雄性Wistar大鼠30只,随机分3组,假手术组10只、反复脑缺血后2周组10只、反复脑缺血后12周组10只。采用反复股动脉抽血/回输(25mL/kg)和双侧颈总动脉阻断(10min)法建立血管性痴呆大鼠模型。进行跳台试验时,让大鼠在箱内适应5min后再放到平台(安全区)上并通电,记录大鼠第1次步下平台的时间,即潜伏期,及5min内大鼠步下平台被电击的次数,即错误次数。24h和48h后重复上述试验,但一开始即将大鼠放到平台上并通电。然后进行穿梭箱试验,其参数设置为:蜂鸣(条件刺激)时间5s,电刺激(非条件刺激)时间20s,电流强度3mA,间隔30s,循环20次。即给予声刺激(蜂鸣)5s,期间如大鼠(主动)逃避到箱的另一端,蜂鸣停止并转为间隔期,否则给予电击;电击期间如大鼠逃避到箱的另一端,电击停止并转为间隔期,否则持续被电击20s;间隔30s后又给予声刺激,重复20次为1个循环。计算机自动控制并记录大鼠在1个循环中被电击次数、被电击时间和主动逃避时间。每天1个循环(箱内适应5min后开始),连续5d。常规苏木精-伊红染色,甲酚紫/酸性品红染色观察脑组织病理学变化。结果:纳入动物30只,实验过程中死亡6只,进入结果分析24只。①跳台试验结果:与假手术组比较反复脑缺血后2周组和反复脑缺血后12周组的错误次数明显增多[以第3天为例,假手术组、反复脑缺血后2周组、反复脑缺血后12周组分别为(1.3±1.0),(9.2±2.0),(12.9±2.3)次,P<0.01],潜伏期显著缩短[以第3天为例,假手术组、反复脑缺血后2周组、反复脑缺血后12周组分别为(193.6±68.9),(20.3±8.2),(12.0±4.4)s,P<0.01]。②程控穿梭箱试验结果:第5天与假手术组比较反复脑缺血后2周组和反复脑缺血后12周组在1个循环中被电击次数明显增多[假手术组、反复脑缺血后2周组、反复脑缺血后12周组分别为(5.5±1.2),(14.2±2.6),(17.7±2.6)次,P<0.01],被电击时间明显增多[假手术组、反复脑缺血后2周组、反复脑缺血后12周组分别为(19.3±8.1),(129.2±23.4),(178.2±35.5)s,P<0.01],主动逃避时间明显减少[假手术组、反复脑缺血后2周组、反复脑缺血后12周组分别为(38.2±6.8),(11.2±5.0),(3.4±3.1)s,P<0.01]。③脑组织神经元改变结果:术后2周大鼠出现明显的学习和记忆障碍,大脑皮质、海马CA1和CA4区神经元丢失分别为29.8%,92.1%,24.4%,但无明显的肢体瘫痪;12周后大鼠学习和记忆障碍进一步加重,大脑皮质、海马CA1和CA4区神经元丢失分别为35.8%,94.0%,30.2%,但脑损害无明显加重。结论:反复低血压及双侧颈总动脉阻断法能高度模拟血管性痴呆的临床特点,是一种可靠、简易而实用的血管性痴呆大鼠模型。     

兔室颤心搏骤停模型的建立

目的 建立一种简单、方便、有效的兔心肺腩复苏(CPcR)模型.方法 采用体表交流电诱发室颤的方法制作兔心跳骤停(CA)模型,依据CA时间的长短,27只新西兰大白兔随机分为CA 8min、CA 5min和CA 3min组,每组9只,随后进行胸外心肺复苏术(CPR).自主循环恢复(ROSC)后4 h检测血肌钙蛋白I水平,72 h后处死动物,取海马组织尼氏染色和TUNEL法凋亡细胞检测,计算每40×倍视野下海马CAI区尼氏染色阳性细胞数和凋亡细胞数.另取2只兔作为对照组,只进行外科操作小进行敛颤和CPR.各组数据依据正态检验结果用单因素方差分析(one-way ANOVA)或秩和检验(Mann-Whitney rank),多重比较用ISD-t检验,ROSC率的比较用行X列连表χ2检验,两样本均数的比较用t检验,P＜0.05表示差异具有统计学意义.结果 CA 8 min,CA 5 min和CA 3 min组各有4,5,7只动物ROSC,各组间ROSC率差异无统计学意义.ROSC后各组动物的存活时间分别为(1.67±2.55)h,(37.78±30.27)h,(12.0±14.97)h,CA 3 min组和其他两组之间差异具有统计学意义(P＜0.05).ROSC后4 h三组之间血浆肌钙蛋白水平分别为(0.71±0.07)ne/mL,(0.55±0.08)ng/mL,(0.45±0.06)ng/mL,CA 3 min组和其他两组之间差异具有统计学意义(P＜0.05).与对照组相比,ROSC后72 h海马CA1区出现了神经元细胞的缺失和凋亡,CA 3 min组和对照组尼氏染色阳性细胞数分别为(34.33±6.19),(55.75±5.91)(P＜0.01),对照组中海马Cal区未见有凋亡细胞.结论 兔CA 3 min后进行CPR有较长的存活时间,ROSC后72 h海马CA1区可见神经元细胞缺失和凋亡,因此该模型可能是一个比较理想的CPCR研究模型.     

2Hz电针减轻神经源性痛大鼠的痛觉超敏和冷诱发的持续性疼痛

目的 :已知电针能减轻大鼠辐射热引起的疼痛和急、慢性炎症痛 ,本文探讨电针能否减轻大鼠神经源性痛。方法 :将大鼠右侧L5/L6 脊神经结扎 ,用引起 5 0 %缩足的机械刺激阈值评价机械性痛觉超敏 ,用大鼠 5min内在 5± 1℃冷板上的缩足次数反映冷诱发的持续性疼痛。用韩氏穴位神经刺激仪给予电刺激 ,波宽 0 .6ms ,频率 2Hz ,电流强度为 0 .5 ,1和 2mA ,各 10min ,共刺激 30min。结果 :2Hz电针能减轻痛觉超敏 (持续 1h)和冷诱发的持续性疼痛 (持续 12小时 )。电针前15min皮下注射纳洛酮 (1mg/kg)能阻断电针对冷诱发的持续性疼痛的作用 ,但不能阻断对痛觉超敏的作用。结论 :低频 (2Hz)电针可能通过阿片机制减轻持续性的神经源性疼痛 ,低频电针也能减轻机械性痛觉超敏 ,该作用可能不是通过阿片机制完成的。     

心肺复苏对室颤频率的影响

目的:观察除颤前心肺复苏(CPR)对室颤频率的影响.方法:将32只健康家猪分为4组,每组动物8只,分别制作闭胸电诱发室颤模型:A组室颤3 min后给予直接除颤:B组室颤3 min后予CPR 2 min后再进行除颤;C组室颤7 min后进行直接除颤;D组室颤7 minn后予CPR 2 min后再进行除颤.结果:室颤发生后频率随时间延长逐渐下降,1 min时室颤频率为12.3±1.8 Hz,3 min时为8.1±1.4 Hz,7 min时为6.8±1.2 Hz(P＜0.05),B组和D组CPR后室颤频率显著增加(B组:13.1±2.1 Hz,D组:10.4±1.5,P＜0.05).A组和B组各8例均经除颤后立即恢复自主循环.除颤后立即恢复自主循环者C组有2例、D组5例:除颤后出现无脉性心电活动,经CPR后恢复自主循环者C组有6例、D组3例(P＞0.05).结论:除颤前CPR可增加室颤的频率,可改善长时间室颤的自主循环恢复率.     

电刺激大鼠上矢状窦旁硬脑膜后血浆降钙素基因相关肽和P物质的变化

目的观察电刺激上矢状窦旁硬脑膜对大鼠血浆降钙素基因相关肽(CGRP)和P物质浓度的影响。方法 13只大鼠随机分为对照组(n=6)和电刺激组(n=7)。对照组行假刺激,电刺激组以20 Hz、4 mA和250μs的方波电流刺激上矢状窦旁硬脑膜,使用放射免疫法比较血浆CGRP和P物质的浓度。结果对照组与电刺激组的血浆CGRP浓度相比有显著性差异(50.60±7.16 pg/ml vs 42.20±4.82 pg/ml,P=0.029),而血浆P物质浓度相比无显著性差异(308.59±43.07 pg/ml vs 264.60±60.28pg/ml,P=0.165)。结论电刺激上矢状窦旁硬脑膜能够降低大鼠血浆CGRP浓度,而P物质浓度无明显变化。     

弥散加权成像评价大鼠复苏后脑损伤研究

目的:对比分析不同时间点弥散加权成像(DWI)检查对评估大鼠心脏骤停(CA)模型心肺复苏(CPR)后脑水肿的价值。方法:将20只体重为(506±13)g的雄性SD大鼠随机分为sham组(n=6)、ROSC 6 h(n=7)组及ROSC24h组(n=7),利用气管插管制作大鼠心脏骤停窒息模型。模型组大鼠恢复自主循环(ROSC)6 h及24 h后行DWI序列扫描,假手术组于术后6 h扫描。对比分析各组大鼠全脑表观弥散系数(ADC值)及水通道蛋白4(AQP4)免疫组化结果的差异。结果:14只大鼠接受了CPR,12只大鼠成功ROSC其中2只未能ROSC,其余6只大鼠接受了假手术。ROSC6h组大鼠全脑ADC值明显低于sham组及ROSC 24 h组(P0.05);sham组与ROSC24h组全脑ADC值无统计学差异(P0.05)。ROSC6h组及ROSC24组大鼠神经细胞AQP4抗体表达均为阳性,ROSC6h染色强度明显高于ROSC 24 h组。结论:ADC值可用于CA/CPR后复苏早期(ROSC 6 h)脑水肿评估,但是在复苏后期(ROSC 24 h)评估脑水肿受限。     

胞二磷胆碱提高心肺复苏效果和减轻心肌损伤的作用研究

目的 探讨胞二磷胆碱在心肺复苏(CPR)中对于提高自主循环恢复(ROSC)率和减轻心脏损伤的作用.方法 按随机数字表法将SD大鼠分为对照组(未窒息,5只)、模型组(10只)、肾上腺素组(10只)、胞二磷胆碱组(10只),用窒息法复制心搏骤停(CA)动物模型并进行CPR,各组分别于复苏前5 min和复苏开始时给2次药,对照组和模型组给予等量生理盐水.各组于CPR期间及复苏成功后2h内测定血流动力学指标,然后处死大鼠取心脏组织,检测ATP酶、超氧化物歧化酶(SOD)、丙二醛(MDA)水平,评估大鼠心肌缺血/再灌注损伤情况.结果 胞二磷胆碱组和肾上腺素组ROSC率高于模型组(90％、80％比20％,均P＜0.01),平均复苏时间(s)显著短于模型组(53±10、55±9比95±7,均P＜0.01);复苏后2h末心率(HR,次/min)、平均动脉压(MAP,mm Hg,1 mm Hg=0.133 kPa)均显著高于模型组(HR:222.78±41.55、167.75±11.76比131.50±0.70,MAP:36.53±8.69、39.30±6.45比30.19±5.15,均P＜0.01).胞二磷胆碱组复苏后心功能[左室内压上升/下降最大速率(±dp/dt max)]逐渐平稳并显著高于模型组和肾上腺素组;肾上腺素组虽高于模型组,但下降趋势明显.胞二磷胆碱组Na+-K+-ATP酶(μmol· mg-1· h-1)和SOD活性(U/mg)显著高于模型组和肾上腺素组(Na+-K+-ATP酶:7.35±0.20比5.11 ±0.69、4.70±0.41,SOD活性:320.65±47.25比225.79±24.64、253.67±12.00,均P＜0.01),而MDA含量(mmol/mg)显著低于模型组和肾上腺素组(8.19±1.64比16.59±1.27、14.65±0.93,均P＜0.01),且上述指标与对照组比较无明显差异;模型组和肾上腺素组上述各指标也无明显差异.结论 胞二磷胆碱可提高CPR成功率,并且与肾上腺素相比可减轻心肌缺血/再灌注损伤,改善复苏后心功能.     

Model of cardiac arrest in rats by transcutaneous electrical epicardium stimulation

Objective

To establish a new model of cardiac arrest (CA) in rats by transcutaneous electrical epicardium stimulation.

Methods

Two acupuncture needles connected to the anode and cathode of a stimulator were transcutaneously inserted into the epicardium as electrodes. The stimulating current was steered to the epicardium and the stimulation was maintained for 3 min to induce CA. Cardiopulmonary resuscitation (CPR) was performed at 6 min after a period of nonintervention.

Results

CA was successfully induced in a total of 20 rats. The success rate of induction was 12/20 at the current intensity of 1 mA; and reached 20/20 when the current intensity was increased to 2 mA. After the electrical stimulation, the femoral blood pressure quickly dropped below 25 mm Hg and the arterial pulse waveform disappeared. The average time from the electrical stimulation to CA induction was 5.10 (±2.81) s. When the electrical stimulation stopped, 18/20 rats had ventricular fibrillation and 2/20 rats had pulseless electrical activity. CPR was performed for averagely 207.4 (±148.8) s. The restoration of spontaneous circulation (ROSC) was 20/20. The death rate within 4 h after ROSC was 5/20, and the 72-h survival rate was 10/20. There were only two cases of complications, a minor muscle contraction and a minor lung lobe injury.

Conclusion

The model of CA in rats induced by transcutaneous electrical epicardium stimulation is a stable model that requires low-intensity current and has fewer complications. This model may provide another option for experimental research of CA induced by malignant arrhythmia (especially VF).     

犬室颤心脏骤停模型的研究与改进

目的建立一种简单、有效、稳定的犬心脏骤停（CA）模型,为心肺脑复苏的实验研究奠定基础。方法选用健康成年犬30只,体质量（15±2）kg,雌雄不限,麻醉后经右颈外静脉置电极导管至右心室,以5mA电流诱发室颤的方法制作CA模型,根据CA时间不同随机分为CA3 min组、CA5 min组和CA8 min组,每组10只,随后进行电除颤及标准胸外心肺复苏术,比较各组的复苏成功率及存活情况。结果诱颤后所有犬心电图均显示室颤波,动脉血压下降并失去波动;各组自主循环恢复（ROSC）情况为CA 3min组：90％（9／10）、CA5min：80％（8／10）、CA8min：20％（2／10）;ROSC率CA3 min组和CA5 min组比较差异无统计学意义（P〉0.05）,CA8 min组与其他2组之间比较差异具有统计学意义（P〈0.05）;CA3rain组与CA5min、CA8 min组存活时间比较差异有统计学意义（P〈0.05）。结论犬经右心室导管诱发室颤制作的心脏骤停模型稳定且可靠,CA3 min后开始复苏具有较好的ROSC率和存活时间,能满足心肺脑复苏基础研究的需要。     

低频电疗对白鼠周围神经损伤后脊髓后角神经细胞活动电位的影响

背景迄今为止有关低频电疗缓解疼痛作用机制的研究寥寥无几,且有关低频电疗对脊髓后角神经细胞活动电位的影响尚不清楚.目的应用周围神经损伤的动物模型,观察低频电疗对被机械性刺激和温度刺激所引发的脊髓后角神经细胞活动电位(膜电位)的影响,并观察纳洛酮干预后的效应.设计随机对照动物实验.单位延边大学医学院附属医院神经内科.材料实验于2004-02/10在延边大学医学院中心实验室进行.取80只SD雄性白鼠,随机取60只手术分离出坐骨神经,将坐骨神经的2个分支胫神经和腓肠神经结扎后切断,留下腓神经作为实验组,其余20只经手术分离出坐骨神经后放原位,重新缝合皮肤作为对照组.方法①疼痛测定手术1周后用机械性刺激和温度刺激每5 s刺激大鼠一次,共刺激10次后测定躲避反应的频率(0%～40%为轻度疼痛,40%～70%为中度,70%以上为重度).②对照组和实验组中重度疼痛的大鼠测定自发的和被机械性刺激和温度刺激所引发的脊髓后角神经细胞膜电位.③实验组大鼠用环状电极在腿部进行经皮低频电刺激(电流3 mA,时间10 min,频率10 Hz),测定刺激前后脊髓后角神经细胞膜电位.④实验组低频电刺激的同时,经尾部静脉注射纳洛酮,测定注射纳洛酮前和注射10 min后脊髓后角神经细胞膜电位.结果经补充后80只大鼠进入结果分析.①实验组被机械性刺激和温度刺激所引发的躲避反应频率明显高于对照组(P＜0.01).②实验组被机械性刺激和温度刺激所引发的脊髓后角神经细胞膜电位明显高于对照组(P＜0.01).③实验组经低频电刺激10 min后,被机械性刺激和温度刺激所引发的脊髓后角神经细胞的膜电位明显低于刺激前[每10 s(102.6±0.86),(136.9±1.46)次;每10 s(175.2±1.28),(240.8±1.51)次,P＜0.01].④实验组注射纳洛酮10 min后,被机械性刺激和温度刺激所引发的脊髓后角神经细胞的膜电位明显高于注射前[每10 s(174.5±0.41),(235.4±1.41)次,P＜0.01].结论低频电刺激能有效抑制被无害刺激所引发的脊髓后角神经细胞的活动电位,且静脉注射纳洛酮(8 mg/kg)可使之逆转到治疗前的水平,说明低频电疗可能是刺激中枢神经系统使其分泌内源鸦片物质,作用于脊髓后角细胞使其活性降低,从而达到缓解疼痛的目的.     

自控经皮耳神门穴电刺激在焦虑产妇剖宫产术前准备中的应用

目的探讨自控经皮电刺激耳神门穴用于焦虑产妇剖宫产术前准备的可行性。方法选择Zung氏焦虑自评分（SAS）〉30分的择期剖宫产产妇60例,随机分为两组,观察组（n=30）产妇入手术室后行自控穴位电刺激,取耳神门穴,频率为1．5Hz,强度由产妇自己掌握,持续刺激30min。对照组（n=30）不进行电刺激。比较两组产妇入室时（T0）及刺激30min后（T1）的心率（HR）、平均动脉压（MAP）、胎儿心率变化;比较产妇焦虑VAS评分、血浆血管紧张素Ⅱ水平。结果观察组产妇刺激30min后HR为（72±9）次／min,MAP（84±11）mmHg,焦虑VAS评分（49．8±20．8）分,血浆血管紧张素Ⅱ水平（73．9±21．8）ng／L,均低于对照组,差异有统计学意义（t分别为2．143,2．648,3．576,2．163;P均〈0．05）;胎心率比较差异无统计学意义（P〉0．05）。结论自控经皮电刺激耳神门穴具有明显的镇静、降压、抑制应激反应作用,可用于焦虑产妇剖宫产的术前准备。     

A simpler cardiac arrest model in rats

Two disadvantages of electrical induction of cardiac arrest used currently are that it is a technically complicated procedure and the consequent thermal injury, which prompts us to search for a simpler method with less adverse effect to induce ventricular fibrillation (VF) in rats. Different potential (18, 24, 30, and 36 V) of alternating current (AC) were administered to elicit VF in 15 rats via pacing electrode placed in esophagus. Four minutes after onset of VF, conventional cardiopulmonary resuscitation (CPR) was initiated. Restoration of spontaneous circulation was defined as the return of supraventricular rhythm with a mean aortic pressure of 20 mm Hg or greater for a minimum of 5 minute. Ventricular fibrillation was achieved by short interval of AC stimulation in all of the rats. After the termination of prolonged AC stimulation, electrocardiogram indicated VF occurred in 6 of 15 rats, asystole in 3 of 15 rats and pulseless electrical activity in 6 of 15 rats. Before CPR, however, electrocardiogram indicated that only 2 of 15 and 4 of 15 animals remained in VF and pulseless electrical activity, respectively, whereas 9 of 15 animals presented as asystole. After CPR, 11 of 15 animals were resuscitated. Necropsy showed that there was no gross evidence of thermal injury on the surface layer of the heart. Therefore, development of a rat cardiac arrest model by transesophageal AC stimulation is simpler and less adverse effect, which may have practical significance for facilitating experimental investigation on cardiac arrest and CPR.     

心肺复苏的质量对复苏后炎症反应的影响

目的 评价临床上常见的不标准心肺复苏(N-CPR)和2005年国际CPR指南推荐的标准心肺复苏(S-CPR)对心脏停搏(CA)猪复苏后炎症反应的影响.方法 18头猪被随机均分成两组,经麻醉、插管、机械通气后,应用程控刺激方法制备心室纤颤(VF)模型.S-CPR组应用2005年指南推荐的CPR方式;N-CPR组模拟临床上经常出现的低质量CPR方式.VF 4 min后开始进行CPR,CPR 9 min后进行电除颤及高级生命支持,自主循环恢复(ROSC)后进行各项指标观察.24 h仍存活的猪经处死后取脑、心、肝、肾组织,应用免疫组化法检测核转录因子-kB(NF-kB)的表达.实验期间连续监测CPR后3、6和9 min的血流动力学变化,并抽取基础状态、CPR 9 rain、ROSC 4 h的静脉血,测定血清肿瘤坏死因子-a(TNF-α)、白细胞介素-1β(IL-1β)的浓度.结果 与N-CPR组比较,S-CPR组ROSC率(22.2%比88.9%)及24 h存活率(22.2%比88.9%)明显提高(P均＜0.05);CPR后3、6和9 min心排血量(CO)和平均动脉压(MAP)也均显著升高(P均＜0.01);并且CPR后9 min和ROSC 4 h血清促炎症因子TNF-α、IL-1β]水平和各组织NF-kB表达程度均降低.结论 高质量的CPR后不仅能提高CA猪的生存率,也明显改善CPR后的炎症反应.     

Evaluating the Effectiveness of Dispatch-assisted Cardiopulmonary Resuscitation Instructions

Objectives: To determine the frequency of agonal breathing during cardiac arrest (CA), its impact on the ability of 9‐1‐1 dispatchers to identify CA, and the impact of dispatch‐assisted cardiopulmonary resuscitation (CPR) instructions on bystander CPR rates. Methods: A before‐after observational study enrolling out‐of‐hospital adult CA patients where resuscitation was attempted in a single city with basic life support with defibrillation/advanced life support tiered emergency medical services. Victim, caller, and system characteristics were measured during two successive nine‐month periods before (control group) and after (intervention group) the introduction of dispatch‐assisted CPR instructions. Results: There were 529 CAs between July 1, 2003, and December 31, 2004. Victim characteristics were similar in the control (n= 295) and intervention (n= 234) period; mean age was 68.3 years; 66.7% were male; 50.1% of CAs were witnessed; call‐to‐vehicle stop was 6 minutes, 37 seconds; ventricular fibrillation/ventricular tachycardia occurred in 29.9%; and the survival rate was 4.0%. Dispatchers identified 56.3% (95% confidence interval [CI] = 48.9% to 63.0%) of CA cases; agonal breathing was present in 37.0% (95% CI = 30.1% to 43.9%) of all CA cases and accounted for 50.0% (95% CI = 39.1% to 60.9%) of missed diagnoses. Callers provided ventilations in 17.2% and chest compressions in 8.3% of cases as a result of the intervention. Long time intervals were observed between call to diagnosis (2 minutes, 38 seconds) and during ventilation instructions (2 minutes, 5 seconds). Bystander CPR rates increased from 16.7% in the control phase to 26.4% in the intervention phase (absolute rate, 9.7%; 95% CI = 8.5% to 11.3%; p = 0.006). Conclusions: This trial demonstrates an increase in bystander CPR rate after the introduction of dispatch‐assisted CPR. Agonal breathing occurred frequently and had a negative impact on the recognition of CA. There were long time intervals between call initiation and diagnosis of CA and during mouth‐to‐mouth ventilation instructions.     

Changes in expression of Nogo receptor 1 in hippocampus and cortex after cardiopulmonary resuscitation in rats

The aim of this study was to investigate changes in Nogo receptor 1 (NgR₁) expression in the cerebrum after cardiopulmonary resuscitation (CPR) in rats. Cardiac arrest was induced by alternating current in 50 SD rats through transcutaneous electrical epicardium stimulation, and CPR was performed with the Utstein mode 6 minutes after cardiac arrest. Rats were killed 1, 3, and 7 days after CPR. We performed immunofluorescence with antibodies against NgR₁ to map the distribution of NgR₁ in the rat cerebrum, whereas quantitative polymerase chain reaction was performed for quantitative analysis of NgR₁ messenger RNA (mRNA). There was a striking transient up-regulation of the NgR₁ protein and mRNA in both the hippocampus and cortex in response to CPR. Nogo receptor 1 proteins were strongly expressed in hippocampal neurons 1 and 3 days after CPR (P < .001 for 1 day and P < .05 for 3 days, vs the control group, respectively), which returned to the basal level 7 days after CPR. In the cortex, staining moderately increased 1 day after CPR and got the peak level after 3 days (P < .001), returning to normal expression levels on day 7. The levels of NgR₁ mRNA in the hippocampus and cerebral cortical cortex showed the same trend with staining. The changes were significantly different between day 3 and baseline in both the hippocampus and cortex (P < .05, respectively). Furthermore, there were significant differences between the hippocampus and cerebral cortical cortex at 1 day and 3 days after the CPR (P < .05, respectively). There was a transient increase in NgR₁ in the vulnerable areas of the rat brain after CPR. Blockade of NgR₁ may be important in maintaining the high regenerative capacity of neurons during the time window when NgR₁ expression increases.     

神经阻滞的注射针定位中电刺激强度与针尖-神经干距离及针尖斜面方向关系的实验研究

目的：探讨神经阻滞注射针定位技术的针尖-胫神经干距离与刺激电流强度关系,为神经阻滞技术的临床应用提供理论依据。方法：新西兰大白兔7只,体重2.5±0.5kg,雌雄不限。兔大腿后外侧纵向切口暴露胫神经干14条,以三维定位仪定位针尖与神经干间距离,分别于针尖-神经干距离为0mm、1mm、2mm、3mm、4mm、5mm处调节刺激器电流（直流电方波输出,波宽0.2ms,频率2Hz）强度,记录诱导靶肌肉收缩的最低刺激电流。结果：最低电流刺激强度分别为：0.28±0.07mA（0mm）、0.34±0.08mA（1mm）、0.44±0.10mA（2mm）、0.58±0.15mA（3mm）、0.74±0.17mA（4mm）、0.91±0.21mA（5mm）。以针尖-神经干距离为自变量X,最低电刺激强度均数为应变量Y,直线回归分析示两者间存在线性回归关系,方程为Y=0.13X+0.22, 决定系数r2=0.974。结论：注射针定位中针尖-神经干距离与刺激电流强度呈线性回归关系,对临床神经阻滞中的注射针定位有指导意义。