小鼠心脏骤停动物模型的建立

目的 建立一种小鼠心脏骤停模型，为心肺复苏的实验研究奠定基础。方法 选用健康小鼠15只，体重30～50g，雌雄不限，麻醉后插入导管至左颈总动脉测压，实验中全程监测心电图。应用经食管心脏起搏的方法对小鼠诱发室颤或无脉性电活动并维持4min，然后开始常规心肺复苏。结果 经食管心脏快速起搏可以导致血压迅速下降，停止心脏起搏刺激后，15只小鼠中有14只心电图表现为无脉性电活动，1只表现为一条直线，未诱出持续性室颤。全部小鼠均复苏成功。结论 经食管心脏起搏诱发小鼠心脏骤停的动物模型具有操作简单、重复性好和模型稳定的特点，能够满足心肺复苏基础研究的需要。     

参附注射液对家兔缺氧型心搏骤停-心肺复苏模型血清心肌肌钙蛋白T的影响

目的　探讨参附注射液 (SF)对家兔缺氧型心搏骤停 -心肺复苏 (CA -CPR)模型血清心肌肌钙蛋白T (cTnT)的影响。方法　普通家兔 30只 ,用夹闭气管法复制缺氧型CA -CPR模型 ,用随机数字表法随机分为SF组、纳洛酮组和生理盐水组 ,每组 10只。 3组在自主循环恢复后 8、 15、 2 2min分别静注SF、纳洛酮、生理盐水 ,并分时点检测血清cTnT值。结果　参附组cTnT值在复苏后 6 0、 12 0min明显低于生理盐水组 (P <0 0 5 )。结论　SF对CPR期间cTnT的升高有明显的抑制作用。     

插入式腹主动脉按压对心搏骤停兔心肺脑复苏的实验研究

目的：探讨插入式腹主动脉按压心肺复苏（IAAC-CPR）对心搏骤停兔心肺脑复苏的效果。方法健康新西兰大白兔10只,雌雄不拘,按随机数字表法分为传统胸外按压心肺复苏（CC-CPR）组和IAAC-CPR组,每组5只。经颈静脉快速推注冰氯化钾并夹闭气管导管制备心搏骤停模型;心搏骤停3 min后开始实施心肺复苏（CPR）,CC-CPR组为呼吸机辅助通气+胸外按压;IAAC-CPR组为呼吸机辅助通气+胸外按压+腹主动脉按压。观察CPR过程中血流动力学和脑皮质血流的变化;记录自主循环恢复（ROSC）时间,观察动物24 h生存情况、24 h神经功能评分及腹部器官情况等。结果 IAAC-CPR组复苏后30、60、90、120 s时脑血流量（CBF,PU值）及平均动脉压（MAP,mmHg,1 mmHg＝0.133 kPa）均明显高于CC-CPR组（CBF 30 s：16.1±6.0比7.8±2.2,60 s：91.6±11.8比57.3±23.2,90 s：259.9±74.9比163.6±50.3,120 s：301.5±60.5比208.4±23.8;MAP 30 s：46.4±9.4比31.4±8.7,60 s：55.8±13.8比34.0±11.5,90 s：61.2±11.5比38.2±10.1,120 s：63.6±11.8比40.2±10.2;均P＜0.05）。与CC-CPR组比较,IAAC-CPR组ROSC所需时间明显缩短（s：182.0±59.0比312.6±86.6,t＝2.787,P＝0.024）,24 h神经功能评分明显下降（分：2.4±1.7比4.6±0.6,t＝2.974,P＝0.023）;而复苏成功率（80.0%比60.0%,χ2＝0.000,P＝1.000）、24 h存活率升高（80.0%比40.0%,χ2＝0.417,P＝0.519）,但差异无统计学意义。ROSC后24 h尸解动物均未发现肝脏损伤。结论在心搏骤停兔复苏早期,IAAC-CPR较CC-CPR取得了更好的脑血流灌注,明显减轻了心搏骤停兔的神经系统功能损伤,且无腹部器官损伤。     

α-甲基去甲肾上腺素对家兔心肺复苏后早期心功能及心肌组织形态学影响的实验研究

目的 通过对血流动力学指标、心肌损伤标志物cTnT及心肌组织形态学观察,明确α-甲基去甲肾上腺素(α-MNE)是否町减轻复苏后心肌损伤、改善心脏功能.方法 兰州市兽医研究所提供18只清洁级家兔,体质量2.5～3.5 kg,雌雄不拘,通过体外致颤法建立家兔心肺复苏模型.按数字随机法随机分为三组:A组手术对照组,仪行麻醉、手术、气管插管,但不致颤;B组:肾上腺素组,在复苏时使用标准剂量肾上腺素(30 μg/ks);C组:α-MNE组,在复苏时使用α-MNE(100 μg/kg).动态观察致颤前15 min、复苏后30 min,60 min,120 min,180 min,240 min左室舒张末压(LVEDP)、左室内压上升和下降最大速率(peak±dp/dt)及心肌损伤标志物cTnT变化,在复苏后240 min处死家兔取心肌组织进行光镜检查.统计学处理数据采用Spss 10.0软件处理,组间比较采用ANOVA方差分析.结果 与A组比较,其余两组复苏成功后LVEDP明显升高(P<0.01),peak±dp/dt显著F降(P<0.01);C组与同时相B组比较,LVEDP升高幅度明显降低(P<0.05),peak ±dp/dt降低程度显著减轻(P<0.05);与A组比较,其余两组复苏成功后cTnF明显升高(P<0.01),但C组升高幅度明显小于B组(P<0.05).B、C组光镜下均见心肌损伤,但C组心肌损伤较B组轻.结论 α-甲基去甲肾上腺素可减轻复苏后心肌损伤、改善心脏功能,对复苏后心脏具有一定有保护作用.     

Ventricular fibrillation induced by transoesophageal cardiac pacing: a new model of cardiac arrest in rats

OBJECTIVE: To investigate whether transoesophageal cardiac pacing can induce ventricular fibrillation (VF) and how long the cardiac pacing has to be sustained to prevent the reversion of the VF induced. METHODS: A pacing electrode was inserted orally into the oesophagus and high-frequency ventricular pacing was performed so as to elicit VF in 25 Sprague-Dawley rats. Incidences of VF and time of cardiac pacing were observed and recorded. Four minutes after onset of VF cardiopulmonary resuscitation (CPR) was initiated. RESULTS: A short interval of high-frequency ventricular pacing caused an immediate drop of blood pressure, loss of pulse and increase of right atrial pressure in the same time frame. When the cardiac pacing was terminated, VF was elicited at least once or more than once in all of the 25 rats. However, the VF elicited by the burst stimulation could be defibrillated spontaneously. With the prolongation (120-180 s) of cardiac pacing, the incidence of defibrillation of VF decreased from 100 to 0%. VF persisted in 19 of 25 animals, developed into asystole in 5 of 25 animals and converted into pulseless electrical activity in 1 of 25 animals prior to CPR. Following CPR 22 of 25 animals were resuscitated. CONCLUSIONS: Transoesophageal cardiac pacing can induce VF in rats. However, the cardiac pacing is required for at least 120-180 s to ensure that VF does not spontaneously convert. We can use the technique to establish a new and simpler rat cardiac arrest (CA) model, which may facilitate experimental investigation on CPR.     

Erythropoietin improved initial resuscitation and increased survival after cardiac arrest in rats

Introduction

Recent data have demonstrated potent cardioprotective and neuroprotective effects of the application of growth hormones like erythropoietin (EPO) after focal cardiac or cerebral ischemia. In order to assess possible benefits regarding survival and resuscitation conditions, EPO was tested against placebo in a model of cardiac arrest in the rat.

Methods

Thirty-four male Wistar rats were randomized into two groups (EPO versus control; n = 17 per group). Under anesthesia, cardiac arrest was induced by asphyxia after neuromuscular blockade. After 6 min of global ischemia, animals were resuscitated by external chest compression combined with epinephrine administration. An intravenous bolus of recombinant human EPO (rhEPO, 3000 UI kg⁻¹ body weight, i.v.) or saline (in control group) was performed 15 min before cardiac arrest, by a blinded investigator. Restoration of spontaneous circulation (ROSC), survival at 1, 24, 48 and 72 h and hemodynamic changes after cardiac arrest were studied.

Results

Survival to 72 h was significantly improved in the EPO group (n = 15/17) compared to the control group (n = 7/17). All the EPO-treated rats were successfully resuscitated whereas only 13 of 17 control animals resuscitated. EPO-treated animals required a significantly smaller dose of epinephrine before resuscitation, compared to control rats. Time course of systolic arterial blood pressure after resuscitation revealed no significant differences between both groups.

Conclusion

EPO, when administrated before cardiac arrest, improved initial resuscitation and increased the duration of post-resuscitation survival.     

心肺复苏质量对心博骤停猪血流动力学及氧代谢的影响

目的 应用O-CPR技术控制心肺复苏(CPR)质量,以观察在心脏骤停动物模型实施不同质量的CPR对复苏期间血流动力学和氧代谢的影响.方法 18头体质量为(30±1)kg的北京长白猪麻醉后,右侧股静脉送入Swan-Ganz导管并连接爱德华VigianceⅡ连续心排血量监测仪,左侧颈内静脉置管并放置电极到右心室,并分别行主动脉、右心房置管,连续记录血流动力学各指标,然后使用医用程控刺激仪电击致动物心博骤停,在室颤4 min后,将实验猪随机分为2组,标准CPR组和不标准CPR组,利用飞利浦HeartStart MRx监护仪/除颤器的O-CPR进行质量控制,监测胸外按压的深度、频率和回弹等.其中标准CPR组在复苏时进行标准胸外按压,频率为100次/min,按压通气比为30:2,按压深度为38～51 mm,胸廓充分回弹;不标准CPR组按压频率和按压通气比不变,但是按压深度为标准按压的60%～70%,每次胸廓回弹均不完全.在按压和通气9 min后开始电除颤.在各个时间点监测心排血量(CO)、平均主动脉压(MAP)等,计算冠脉灌注压(CPP),监测动静脉血气并计算氧输送量(DO2)和氧耗量(VO2)等,记录复苏成功的实验猪头数.数据处理采用SPSS 11.5统计软件进行y2检验和两个样本的t检验.结果 标准CPR组的自主循环恢复(ROSC)的成功率达90.9%,明显高于不标准者的28.6%(P=0.013),标准CPR组主要血流动力学指标CPP、CO、MAP高(P<0.05),全身血液氧合程度好,D02和VO2高于对照组(P<0.05).结论 在室颤心脏骤停猪模型中,应用规范化标准心肺复苏较不标准者能够明显提高CPP和CO2改善复苏期间的血流动力学,并可以提高DO2和VO2,对氧代谢的改善产生积极作用,因此ROSC成功率明显提高.     

体外膜肺氧合在抢救危重心脏病患者心搏骤停中的作用

目的观察体外膜肺氧合对危重心脏患者心搏骤停后常规心肺复苏困难者的治疗效果。方法本院自2005年9月至2006年5月行体外膜肺氧合(ECMO)治疗危重心脏病患者37例,回顾性分析其中11例发生心搏骤停实施常规心肺复苏无效或复苏后持续低心排而行ECMO循环辅助患者的病历资料。结果5例为心脏术后患者,其中3例心肺复苏(CPR)的同时紧急建立体外循环再次手术,之后因低心排而行ECMO。7例患者床旁建立ECMO,ECMO支持治疗(134．0±113．0)h。8例顺利停机,6例存活出院,其中2例经心脏移植后出院。3例不能顺利脱机者由于ECMO辅助期间循环功能恶化,并最终死于多器官功能衰竭。ECMO期间出现的并发症包括出血、神经精神系统异常、肢体缺血坏死和多脏器功能不全。结论ECMO可以为心搏骤停的患者提供最快的心肺功能支持,为赢得抢救时机和提高抢救质量提供了又一途径,在危重患者心肺复苏中具有良好的疗效。     

经股静——动脉心肺转流术心肺脑复苏机制的探讨

目的观察犬电击致室颤/心跳骤停(VF/CA)8min后经开胸心肺复苏(CPR)和/或经股静-动脉心肺转流(CPB)心肺复苏对心脏复苏和脑脊液(CSF)内乳酸(LA)含量的影响.方法采用犬经胸壁电击VF/CA8min,经CPR恢复自主循环(RSC)后观察4h内CSF内LA含量的变化.9只犬分为两组,Ⅰ组(n＝5)采用开胸心脏按压等方法复苏,Ⅱ组(n＝4)于开胸心脏按压同时经一侧股静、动脉心肺转流,并维持2h.结果Ⅱ组RSC时间较Ⅰ组显著缩短(6.3±2.1minvs13.6±5.9min,P＜0.05);Ⅱ组CPB后室颤波幅较Ⅰ组明显提高;Ⅰ组RSC后30、60、120和240minCSF内LA含量均较CA前明显升高(10.7±3.3、8.8±3.8、7.8±3.5、5.6±1.0vs3.2±1.0,P均＜0.05),而Ⅱ组RSC后除30min外各时点CSF内LA含量均较CA前无明显升高(4.1±2.6、3.9±2.4、2.6±1.7vs3.0±0.4,P均＞0.05),且明显低于Ⅰ组各值(P均＜0.05).结论CA后经开胸CPR辅以CPB能提高心脏复苏的有效性,抑制单一开胸CPR后发生的CSF内LA含量升高,提示其能减轻脑内糖无氧代谢,改善脑氧供需关系,对脑复苏有利.     

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).     

The impact of airway management on quality of cardiopulmonary resuscitation: An observational study in patients during cardiac arrest

Background

Minimising interruptions in chest compressions is associated with improved survival from cardiac arrest. Current in-hospital guidelines recommend continuous chest compressions after the airway is secured on the premise that this will reduce no flow time. The aim of this study was to determine the effect of advanced airway use on the no flow ratio and other measures of CPR quality.

Methods

Consecutive adult patients who sustained an in-hospital cardiac arrest were enrolled in this prospective observational study. The quality of CPR was measured using the Q-CPR device (Phillips, UK) before and after an advanced airway device (endotracheal tube [ET] or laryngeal mask airway [LMA]) was inserted. Patients receiving only bag-mask ventilation were used as the control cohort. The primary outcome was no flow ratio (NFR). Secondary outcomes were chest compression rate, depth, compressions too shallow, compressions with leaning, ventilation rate, inflation time, change in impedance and time required to successfully insert airway device.

Results

One hundred patients were enrolled in the study (2008–2011). Endotracheal tube and LMA placement took similar durations (median 15.8 s (IQR 6.8–19.4) vs LMA median 8.0 s (IQR 5.5–15.9), p = 0.1). The use of an advanced airway was associated with improved no flow ratios (endotracheal tube placement (n = 50) improved NFR from baseline median 0.24 IQR 0.17–0.40) to 0.15 to (IQR 0.09–0.28), p = 0.012; LMA (n = 25) from median 0.28 (IQR 0.23–0.40) to 0.13 (IQR 0.11– 0.19), p = 0.0001). There was no change in NFR in patients managed solely with bag valve mask (BVM) (n = 25) (median 0.29 (IQR 0.18–0.59) vs median 0.26 (IQR 0.12–0.37), p = 0.888). There was no significant difference in time taken to successfully insert the airway device between the two groups.

Conclusion

The use of an advanced airway (ETT or LMA) during in-hospital cardiac arrest was associated with improved no flow ratio. Further studies are required to determine the effect of airway devices on overall patient outcomes.     

亚低温治疗犬心脏骤停复苏后心功能研究

目的 明确亚低温对室颤复苏后犬心功能及心律失常的影响.方法 12头比格犬随机(随机数字法)分成两组(n=6):常温复苏组(37.0±0.2)℃和亚低温组(34.0±0.2)℃,通过快速电刺激诱导室颤,7 min后行心肺复苏,动态观察比较两组犬的心率、左心室收缩力指数、室性心律失常、除颤能量、肾上腺素用量及复苏后1周心超变化.结果 ①与室颤前比较,两组犬左心室收缩力指数在复苏后均有不同程度降低(P＜0.05),但亚低温组下降幅度小于常温组,且心率低于常温组(141±19)次/minvs.(163±31)次/min,P＜0.05.②与常温组比较,亚低温组犬室性心律失常发生的次数明显减少(P＜0.05),但是除颤次数、肾上腺素用量差异无统计学意义(P＞0.05).③复苏后1周,两组犬的心超结果显示,心脏结构及射血分数均恢复正常.结论 亚低温治疗可改善心脏骤停复苏后心肌收缩力,降低室性心律失常发生率.本研究结果提示,亚低温对复苏后心功能有一定的保护作用.     

急性心肌梗死心肺复苏后紧急介入治疗的作用

目的探讨紧急介入治疗能否改善急性心肌梗死心肺复苏后患者的预后。方法回顾性分析院前及急诊室发生心脏骤停的急性心肌梗死患者32例,分为在心肺复苏后同时进行紧急介入治疗组(n= 12)和保守治疗组(n=20)．比较两组的住院期间病死率、严重心律失常、心力衰竭、心原性休克和严重出血的发生率。结果介入组住院期间死亡2例(17%),保守组死亡14例(70%),p＜0．01;心肺复苏后发生心力衰竭者两组分别为3例(25%)和16例(80%),P＜0．01;两组的严重心律失常、心原性休克和严重出血发生率差异无统计学意义(P＞0．05);Logistic回归分析表明,急诊介入治疗能显著降低病死率,而心肺复苏时间＞20min,将增加病死率。结论早期紧急介入治疗能显著改善急性心肌梗死心肺复苏患者的预后。     

Effect of hypertransfusion on the gastrointestinal tract after cardiac arrest in a porcine model

BACKGROUND:

This study aimed to determine the potential protective effect of inducing hypertransfusion to the gastrointestinal tract following a porcine model of cardiac arrest and cardiopulmonary resuscitation (CPR) by evaluating the influence of gastrointestinal ultrastructure, ATPase and serum diamine oxidase.

METHODS:

Ventricular fibrillation was induced by programmed electrical stimulation in 16 male domestic pigs (n=8/group). Four minutes after ventricular fibrillation, CPR was performed. The pigs that successfully restored spontaneous circulation received intravenous infusion of either norepinephrine to maintain the mean arterial pressure at 130% of the baseline before ventricular fibrillation or normal saline. Serum diamine oxidase and gastrointestinal ATPase activity were determined, and histopathological examination of the gastrointestinal tract was performed by light and electron microscopy.

RESULTS:

CPR caused significant injury to the gastrointestinal tract, elevating serum diamine oxidase and causing destruction of intestinal microvillus in control animals. Na⁺-K⁺ ATPase and Ca²⁺ ATPase activity in gastric tissue were significantly elevated in animals receiving hypertransfusion treatment compared with the control animals. Hypertransfusion also significantly reduced serum diamine oxidase to below control levels after CPR. Moreover, severe injury sustained by the gastrointestinal tissue was markedly ameliorated under hypertransfusion conditions compared with the control animals.

CONCLUSIONS:

Gastrointestinal injury and abnormal energy metabolism were strikingly evident following CPR. Hypertransfusion inducing hypertension can improve energy metabolism and ameliorate gastrointestinal mucosal injury, indicating that hypothermia significantly ameliorates gastrointestinal injury sustained following cardiac arrest.KEY WORDS: Cardiopulmonary resuscitation, Cardiac arrest, Gastrointestinal tract, Diamine oxidase, Ultra structure     

Association of serum lactate and survival outcomes in patients undergoing therapeutic hypothermia after cardiac arrest

Introduction

Recent studies have suggested that serum lactate may serve as a marker to predict mortality after resuscitation from cardiac arrest (CA). The relationship between serum lactate and CA outcomes requires further characterization, especially among patients treated with therapeutic hypothermia (TH) and aggressive post-arrest care.

Methods

A retrospective analysis of patients resuscitated from non-traumatic CA at three urban U.S. hospitals was performed using an established internet-based post-arrest registry. Adult (≥18 years) patients resuscitated from CA and receiving TH treatment were included. Logistic regression analysis was used to adjust for potential confounders to survival outcomes. Survival to discharge served as the primary endpoint.

Results

A total of 199 post-CA patients treated with TH between 5/2005 and 11/2011 were included in this analysis. The mean age was 56.9 ± 16.5 years, 85/199 (42.7%) patients were female, and survival to discharge was attained in 84/199 (42.2%). While lower initial post-CA serum lactate levels were not associated with increased survival to discharge, subsequent lactate measurements were significantly associated with outcomes (24-h serum lactate levels in survivors vs. non-survivors, 2.7 ± 0.5 vs. 4.2 ± 0.4 mmol/L, p < 0.01). Multivariable logistic regression confirmed this relationship with survival to discharge (p < 0.01).

Conclusion

Lower serum lactate levels at 12 h and 24 h, but not initially following cardiac arrest, are associated with survival to hospital discharge after resuscitation from CA and TH treatment. Prospective investigation of serum lactate as a potential prognostic tool in CA is needed.     

高渗盐对心搏骤停鼠脑复苏的作用

目的研究高渗盐对心搏骤停复苏后脑组织的保护作用及其机制,探讨脑复苏治疗的有效方法。方法大鼠窒息导致心搏骤停模型复制成功后,实验两组于复苏即刻分别静脉注射生理盐水、10%高渗盐,比较两组大鼠复苏前及复苏后各时间点平均动脉压值、自主循环恢复(ROSC)时间、动脉血与脑匀浆丙二醛(MDA)、脑干湿质量比、神经功能缺损评分(NDS)及脑海马组织病理改变。结果两组大鼠复苏前平均动脉压值差异无统计学意义(P>0.05),而复苏后各时间点平均动脉压值高渗盐组均高于对照组(P<0.05);高渗盐组较对照组能显著改善自主循环恢复时间(P<0.01),提高24、48hNDS(P<0.05),减轻大脑湿质量(P<0.01)及减轻脑组织病理损伤;但对1h动脉血MDA及24h脑匀浆MDA无作用。结论静脉注射10%高渗盐能减轻大鼠心搏骤停复苏后脑组织损伤,改善脑功能。     

低温疗法在心肺脑复苏中的研究进展

目的 探讨低温对心搏骤停复苏成功后血清炎症因子、肺组织酶学及形态学的影响.方法 对10只猪诱导心室纤颤(室颤)4 min后给予标准心肺复苏,待自主循环恢复(ROSC)后按随机数字表法均分为两组.低温组立即给予4℃的生理盐水以1.33 ml·kg~(-1)·min~(-1)补液22 min,继之以10ml·kg~(-1)·h~(-1)补液4 h;常温组采用室温生理盐水按相同用量和速度输入.实时监测血流动力学指标;分别于室颤前、ROSC后10 min、2 h、4 h检测血清肿瘤坏死因子-α(TNF-α)和白细胞介素-6(IL-6)含量;于ROSC后24 h取肺组织检测ATP酶活性,同时行普通病理和超微结构观察.结果 与常温组比较,低温组除可降低体温外,余血流动力学指标均无明显差异.低温组ROSC后10 min、2 h、4 h血清TNF-α[(15.55±1.65)、(17.06±0.86)、(12.52±1.82)ng/L]和IL-6[(173.80±15.01)、(184.09±13.44)、(73.17±6.95)ng/L]均较常温组(TNF-α:(20.09±1.32)、(26.18±1.16)、(29.18±1.20)ng/L,IL-6:(176.92±16.68)、(239.17±13.18)、(405.48±55.49)ng/L]显著降低(P＜0.05或P＜0.01).低温组较常温组能显著降低细胞膜Na~+-K~+-ATP酶活性[(3.78±1.14)U/L比(6.22±1.23)U/L,P＜0.01].低温组肺组织病理变化较常温组损伤轻.结论 4℃生理盐水诱导的低温疗法能减少猪心搏骤停模型中炎症介质的释放,抑制肺泡细胞膜ATP酶的活性,并对肺组织形态学有一定的保护作用.     

弥散加权成像观察去甲肾上腺素诱导的高血压灌注对心搏骤停猪脑功能的影响

目的 观察高血压灌注心搏骤停猪自主循环恢复(ROSC)后脑功能的变化.方法 采用电刺激建立猪心室纤颤(室颤)模型,室颤4 min后给予标准心肺复苏(CPR),将ROSC猪按随机数字表法分为两组,每组5只.高血压灌注组立即给予去甲肾上腺素(NE)使平均动脉压(MAP)维持在室颤前血压的130％;正常灌注组给予NE维持MAP为室颤前水平;两组均监测4h观察血流动力学变化;于室颤前及ROSC后1h、3h用弥散加权成像(DWI)技术扫描大脑顶叶皮质,观察脑功能成像的动态变化;于复苏后24 h制备脑组织切片,观察顶叶的病理学变化.结果 与正常灌注组比较,高血压灌注组于ROSC后不同时间点心率(HR,次/min)、MAP(mm Hg,1 mm Hg=0.133 kPa)、心排血量(CO,L/min)、冠状动脉灌注压(CPP,mm Hg)均出现升高趋势(ROSC 30 min HR:167±8比140±15,ROSC 1 h MAP:131 ±9比108±10,ROSC 1 h CO:4.9±0.1比3.4±0.5,ROSC 2 h CPP:118±12比88±1,P＜0.05或P＜0.01).两组复苏前后DWI未见明显异常;复苏后大脑皮质表观弥散系数(ADC)均呈下降趋势,正常灌注组下降趋势较高血压灌注组明显.光镜下观察高血压灌注对脑的保护作用优于正常灌注组.结论 高血压灌注可引起心搏骤停猪复苏后血流动力学的改变,增加脑血流量,对脑具有保护作用,有利于促进神经功能的恢复.