脂肪乳对局麻药中毒大鼠的作用研究

目的 研究布比卡因诱导的大鼠心跳骤停的模型中,脂肪乳复合肾上腺素心肺复苏的效果.方法 40只SD大鼠,随机分为两组,每组20只,A组:肾上腺素对照组,L组:肾上腺素联合脂肪乳组.将大鼠麻醉后静脉注射布比卡因20 mg/kg,心跳停搏后行心肺复苏(CPR).A组开始CPR时注入肾上腺素10 μg/kg,共3次,之后每5分钟注入肾上腺素10 μg/kg.同时注入0.9%氯化钠注射液5 ml/kg,然后0.9%氯化钠注射液1 ml·kg-1·min-1;L组肾上腺素的应用与A组相同,并且在注入肾上腺素后注入20%脂肪乳5 ml/kg,接着注入脂肪乳0.25 ml·kg-1·min-1.监测心率、血压和体温.在麻醉后、心肺复苏成功5 min、30 min测量动脉血气.记录大鼠CPR成功的时间、数量,肾上腺素的用量.结果 A组心肺复苏成功11只, 成功率为55%,L组复苏成功16只,成功率为80%,脂肪乳组成功率高(P<0.05).A组用的肾上腺素剂量比L组小(P<0.05).两组大鼠复苏后5 min、30 min心率正常.复苏后30 min,两组的收缩压均在正常范围,L组的收缩压比A组高.L组的PaO2比A组高(P<0.05).结论 布比卡因中毒心跳骤停的大鼠用脂肪乳联合肾上腺素比单纯肾上腺素心肺复苏效果好.     

脂肪乳对罗哌卡因致大鼠心脏停搏的复苏作用

目的探讨脂肪乳对罗哌卡因致大鼠心脏停搏的复苏作用。方法 44只大鼠随机分为2组,脂肪乳组(A组,n=22)和对照组(B组,n=22)。大鼠静脉注射罗哌卡因20mg/kg,观察到心跳停止1min时行胸外心脏按压,2min时静脉注射20%脂肪乳注射液5 mL/kg(A组)或生理盐水5 mL/kg(B组),复苏药物和肾上腺素20μg/kg,5%碳酸氢钠2 mL/kg,继续心脏按压,直到恢复自主心率,恢复自主循环。记录基础的心率、血压,大鼠恢复心跳的时间,大鼠恢复自主循环的时间。大鼠的复苏成功率。记录两组使用肾上腺素的剂量。结果实验组心脏停搏后30min有2只大鼠死亡,对照组有1只大鼠死亡。A组恢复自主循环时间是(258.3±11.5)s,B组恢复自主循环时间是(268.7±12.7)s。两组的差异无统计学意义。两组所用的肾上腺素的量无显著性差异。结论脂肪乳剂对罗哌卡因所致的心脏停跳无明显的复苏效果。     

呼气末二氧化碳分压在心肺复苏中的应用

目的：探讨呼气末二氧化碳分压（PETCO2）在心肺复苏（CPR）中的临床意义。方法：选取本院急诊科发生心跳骤停并符合入选标准患者54例,依据复苏是否恢复自主循环分为初始复苏成功组和失败组,监测CPR过程中PET-CO2的变化。结果：21例患者初始复苏成功;复苏成功组和失败组复苏即刻PETCO2水平差异无统计学意义（P〈0.05）。两组患者PETCO2水平在复苏开始后5、10min以及20min时比较,差异有统计学意义（P〈0.01）。结论：PETCO2水平与心跳骤停患者心肺复苏的预后相关。     

脂肪乳预处理对大鼠静脉注射布比卡因与罗哌卡因致心脏毒性的影响

目的：研究脂肪乳对布比卡因、罗哌卡因导致的大鼠心脏毒性的影响,并初步探讨其机制。方法：SD成年雄性大鼠72只,体重200～280g,随机分为5组,空白对照组（A组,n=8）、布比卡因对照组（B组）、布比卡因＋脂肪乳组（C组）、罗哌卡因对照组（D组）、罗哌卡因＋脂肪乳组（E组）,B、C、D、E每组再分为致死组（1组）和取材组（2组）（每组n=8）。A组经大鼠静脉泵入0.9%氯化钠溶液3ml/（kg·min）,6min后开胸取心,B、C、D、E组大鼠经静脉泵入0.9%氯化钠溶液或脂肪乳3ml/（kg·min）,共5min,再以2mg/（kg·min）速度泵入相应的局麻药,取材组泵入局麻药1min开胸取心肌,致死组泵入局麻药致心跳停搏。持续监测平均动脉压和心率,记录大鼠出现心律失常、心跳停止的时间及各对应时相局麻药的累积剂量,A组及取材组测心肌ATP含量。结果：C1组出现心律失常和心跳停止的时间比B1组明显延迟、布比卡因用量大于B1组,差异均有统计学意义（P〈0.001）,而D1组与E1组之间差异无统计学意义。各组心肌ATP酶含量比较,A组〉D2组〉C2组〉B2组,任意两组比较差异均有统计学意义（P〈0.001）,而D2、E2组之间差异无统计学意义。结论：脂肪乳能够减轻布比卡因的心脏毒性,其机制可能与增加心肌ATP含量有关,但脂肪乳对罗哌卡因的心脏毒性无明显作用。     

心肺复苏98例回顾性临床分析

心跳呼吸骤停是临床上最严重、最紧急的危重症,是意外死亡的主要原因.不管心脏骤停原因如何,一旦发生,应迅速积极抢救.抓住心跳骤停后5 min的黄金抢救时间是CPR的成功关键所在.为了总结CPR成功经验,本文回顾性分析了影响心肺复苏后存活率的相关因素.现对本院急诊内科和心内科98例心跳骤停患者的心肺复苏抢救资料进行回顾性临床分析,报告如下.     

急诊老年患者心肺复苏的影响因素分析

目的分析本院急诊科老年患者心跳呼吸骤停后心肺复苏(CPR)的影响因素,探讨如何进一步提高急诊复苏水平。方法对急诊科89例老年心肺复苏患者的临床资料进行回顾性分析。结果心跳呼吸骤停后5 min内CPR较10 min后CPR成功率明显提高,差异有统计学意义(P<0.05);病因分析中心血管疾病复苏成功率高于其他疾病;院内复苏成功率明显高于院前,二者比较差异有统计学意义(P<0.05)。可见CPR成功的影响因素与复苏开始时间、原发疾病、救治地点有明显关系。结论早期、高质量、有效的CPR及早期电除颤是复苏成功的关键,积极防治原发疾病、普及全民急救知识是复苏成功的保障。     

心肺脑复苏临床分析

目的探讨心跳呼吸骤停的救治经验,提高心肺脑复苏成功率。方法对我院2008年1月~2009年12月住院病例中29例心跳呼吸骤停患者进行回顾性多因素分析。结果29例心跳呼吸骤停者中,初步复苏成功25例,心肺脑复苏成功7例,康复出院5例,仍在康复中2例。结论心肺脑复苏成功与CPR的及时正确,尽早的电除颤和气管插管,脑复苏的措施及患者原发病密切相关     

肝素对心肺复苏大鼠神经细胞Bcl-2和Bax表达的影响及脑保护作用

目的观察肝素对大鼠心肺复苏后24h神经细胞Bcl-2、Bax表达的影响及保护作用。方法 30只雄性SD大鼠随机均分为单纯肾上腺素组(A组)、肝素组(H组)和假手术组(C组)。麻醉后行气管插管和动静脉置管,A组和H组建立窒息性心跳骤停模型。窒息8min后开始心肺复苏:A组给予肾上腺素0.01mg/kg+生理盐水,H组给予肾上腺素0.01mg/kg+肝素0.5mg/kg,C组不窒息。麻醉前、复苏后24h行神经功能损害(ND)评分,免疫组化方法检测复苏后24h大鼠大脑皮质和海马神经元Bcl-2、Bax的表达。结果与A组相比,H组ND评分降低(P<0.05);与C组相比,A组和H组Bcl-2和Bax表达均增加,H组Bcl-2增加更显著,A组Bax增加更显著(P<0.01)。结论肝素可通过增加Bcl-2表达、减少Bax表达而减轻脑损伤。     

Effect of heparin on expressions of cerebral Bcl-2 and Bax and its neuroprotective effect after cardiopulmonary resuscitation in rats

目的 观察肝素对大鼠心肺复苏后24 h神经细胞Bcl-2、Bax表达的影响及保护作用.方法 30只雄性SD大鼠随机均分为单纯肾上腺素组(A组)、肝素组(H组)和假手术组(C组).麻醉后行气管插管和动静脉置管,A组和H组建立窒息性心跳骤停模型.窒息8 min后开始心肺复苏:A组给予肾上腺素0.01 mg/kg+生理盐水,H组给予肾上腺素0.01 mg/kg+肝素0.5mg/kg,C组不窒息.麻醉前、复苏后24 h行神经功能损害(ND)评分,免疫组化方法检测复苏后24 h大鼠大脑皮质和海马神经元Bcl-2、Bax的表达.结果 与A组相比,H组ND评分降低(P＜0.05)；与C组相比,A组和H组Bcl-2和Bax表达均增加,H组Bcl-2增加更显著,A组Bax增加更显著(P＜0.01).结论 肝素可通过增加Bcl-2表达、减少Bax表达而减轻脑损伤.     

院前心肺复苏成功36例分析

目的　分析院前心肺复苏 (CPR)成功的因素。方法　院前急救中抢救心跳呼吸骤停患者 1 2 96例 ,心跳呼吸骤停主要由心脏疾患和颅脑损伤、重度创伤、中毒、过敏等病因所引起。抢救中最先均给予CPR、吸氧、畅通呼吸道、建立静脉通道、复苏药物的应用 ,部分患者进行了早期电除颤等复苏的常规方法。结果 :本组抢救心跳呼吸骤停患者 1 2 96例 ,成功3 6例 ,成功率占 2 77%。在复苏成功的 3 6例中小于4分钟开始复苏者 1 9例 ;早期进行除颤 1 9例全部获得成功 ;大剂量肾上腺素的应用 1 0例都能很快恢复自主循环。结果 :凡早期发现、早期复苏、采用CPR、开放气道、早期除颤、大剂量的肾上腺素的应用 ,可以提高复苏成功率。     

Pralidoxime administered during cardiopulmonary resuscitation facilitates successful resuscitation in a pig model of cardiac arrest

Pralidoxime is a common antidote for organophosphate poisoning; however, studies have also reported pralidoxime's pressor effect, which may facilitate the restoration of spontaneous circulation (ROSC) after cardiac arrest by improving coronary perfusion pressure (CPP). We investigated the immediate cardiovascular effects of pralidoxime in anaesthetised normal rats and the effects of pralidoxime administration during cardiopulmonary resuscitation (CPR) in a pig model of cardiac arrest. To evaluate the immediate cardiovascular effects of pralidoxime, seven anaesthetised normal rats received saline or pralidoxime (20 mg/kg) in a randomised crossover design, and the responses were determined using the conductance catheter technique. To evaluate the effects of pralidoxime administration during CPR, 22 pigs randomly received either 80 mg/kg of pralidoxime or an equivalent volume of saline during CPR. In the rats, pralidoxime significantly increased arterial pressure than saline (P = .044). The peak effect on arterial pressure was observed in the first minute. In a pig model of cardiac arrest, CPP during CPR was higher in the pralidoxime group than in the control group (P = .002). ROSC was attained in three animals (27.3%) in the control group and nine animals (81.8%) in the pralidoxime group (P = .010). Three animals (27.3%) in the control group and eight animals (72.2%) in the pralidoxime group survived the 6-hour period (P = .033). In conclusion, pralidoxime had a rapid onset of pressor effect. Pralidoxime administered during CPR led to significantly higher rates of ROSC and 6-hour survival by improving CPP in a pig model.     

Vasopressor effect of epinephrine with and without dopamine during cardiopulmonary resuscitation

We prospectively studied nine prehospital cardiac arrest patients (six M, three F; aged 60 +/- 8 yr) to determine the vasopressor response following incremental (1, 3, and 5 mg) doses of intravenous epinephrine given 5 minutes apart with or without dopamine 15 micrograms/kg/min. All patients were in ventricular fibrillation on arrival of the paramedics and were not resuscitated with standard advanced cardiac life support therapy. Cardiopulmonary resuscitation (CPR) was performed with a computerized Thumper at 60 compressions/min with a 50:50 downstroke-to-upstroke ratio. All patients were intubated and received 12 ventilations/min at a fraction of inspired oxygen of 80 percent. Radial artery pressure was monitored through a #20 gauge radial artery catheter inserted by cutdown within ten minutes after arrival at the emergency room. Five patients received epinephrine alone (group A) and four received epinephrine plus dopamine (group B). The patient's age, paramedic response time, arterial blood gases, and initial diastolic blood pressure (BP) did not differ significantly between treatment groups. Baseline systolic BP was significantly higher (p less than 0.01) in group B (68 +/- 10 mm Hg) than in group A (35 +/- 5 mm Hg). Epinephrine produced a dose-dependent vasopressor response in group A, but not in group B. In group A, peak systolic BP following epinephrine 1, 3, and 5 mg was 57 +/- 20, 69 +/- 23, and 76 +/- 27 mm Hg, respectively (p less than 0.05 for 5 mg vs. baseline). No statistically significant difference was observed among the respective values in group B (81 +/- 13, 80 +/- 18, and 78 +/- 19 mm Hg).(ABSTRACT TRUNCATED AT 250 WORDS)     

No antidotal effect of intravenous lipid emulsion in experimental amitriptyline intoxication despite significant entrapment of amitriptyline

Abstract: Intravenous lipid emulsion has been used in the resuscitative treatment of intoxications caused by local anaesthetics and tricyclic antidepressants with seemingly beneficial results. We studied the effect of intravenous lipid emulsion on the plasma concentration of amitriptyline and haemodynamic recovery in a pig model of amitriptyline intoxication. Twenty pigs were anaesthetized (1% isoflurane in 21% O₂) and given amitriptyline 15 mg/kg intravenously for 15 min. In random fashion immediately thereafter, either 20% lipid emulsion (ClinOleic^®, Lipid group) or Ringer’s acetate (Control group) was infused for 30 min.; first 1.5 ml/kg for 1 min., followed by 0.25 ml/kg/min. for 29 min. The amitriptyline concentration in total and lipid‐poor plasma and haemodynamic parameters were measured until 30 min. after the infusions. Lipid infusion prevented the decrease in plasma total amitriptyline concentration, resulting in a 90% higher (p < 0.001) total concentration and significantly (p = 0.014) lower free fraction of plasma amitriptyline in the Lipid group (1.1%) compared with the Control group (3.0%) at 30 min. Haemodynamic recovery from the intoxication as measured by heart rate, arterial pressure or cardiac output was similar in both groups. However, five pigs in the Lipid group and two pigs in the Control group died. In conclusion, a marked entrapment of amitriptyline by intravenous lipid emulsion was observed but this did not improve the pigs’ haemodynamic recovery from severe amitriptyline intoxication. Care should be exercised in the antidotal use of lipid emulsion until controlled human studies indicate its efficacy and safety.     

红花注射液对脑复苏大鼠神经元凋亡相关基因的影响

目的：观察红花在大鼠脑复苏时对海马CA1区神经细胞凋亡相关基因的影响。方法：将实验大鼠随机分为手术对照组,心肺复苏组,心肺复苏＋红花组。采用呼气末夹闭气管法造成大鼠窒息心跳停止,制备大鼠动物模型,利用免疫组化法、原位末端标记法检测大鼠脑复苏不同时间内Fas、p53蛋白表达的水平及凋亡细胞数的变化。结果：（1）脑复苏10min再灌注6h,海马CA1区有少量p53蛋白表达的阳性细胞,再灌注12h后增多。（2）脑复苏10min再灌注3h,Fas蛋白表达的阳性细胞,再灌注12h,Fas蛋白表达的阳性细胞达高峰,后下降。（3）神经细胞凋亡数随脑复苏时间延长而增加。（4）给予红花治疗后,上述变化均减轻。结论：红花注射液对脑复苏的作用机制之一可能是抑制或延迟脑缺血时细胞凋亡、调控基因Fas、p53的表达而起到脑保护作用。     

辐照对盐酸肾上腺素注射液含量的影响

目的建立测定盐酸肾上腺素注射液中盐酸肾上腺素含量的高效液相色谱法,考察盐酸肾上腺素注射液吸收不同强度的γ射线辐照后的含量变化。方法将同一批盐酸肾上腺素注射液放置于60Co-γ射线放射源中,一次性吸收1,2,4,8,16,25 kGy的辐照剂量。以0.14%庚烷磺酸钠溶液(磷酸调节pH=3.0)-甲醇(65∶35)为流动相,流速1.0 mL/min,检测波长280 nm,进样量20μL,测定盐酸肾上腺素注射液含量。结果含量测定方法质量浓度线性范围是2.5～12.5μg/mL(r=0.999 8),高、中、低3个质量浓度的平均回收率为96.11%,96.05%,98.46%,日间(n=5)及日内(n=3)精密度RSD均小于1%。盐酸肾上腺素注射液吸收1,2,4,8,16,25 kGy的辐照剂量后,外观及澄明度没有明显变化,含量随着辐照强度的增加呈下降趋势,且吸收16 kGy辐照剂量以上含量下降超出质量合格范围。结论所建立的方法可用于盐酸肾上腺素注射液的含量测定。超过一定辐照剂量对盐酸肾上腺素注射液的稳定性有影响。     

心肺复苏机与徒手心肺复苏抢救心脏骤停的临床效果比较

目的：比较心肺复苏机与徒手心肺复苏抢救心脏骤停患者的临床疗效,寻求有效的心脏骤停的抢救方法。方法回顾性分析100例心脏骤停患者临床资料。2011年1月至2012年1月收治的50例心脏骤停患者作为对照组,采取徒手心肺复苏进行抢救;2012年1月至2013年1月收治的50例心脏骤停患者作为观察组,采取心肺复苏机进行抢救。观察并比较两组患者术后的疗效。结果观察组心肺复苏后收缩压、SpO2及心率分别为（95．2±10．4） mmHg、（93．1±8．2）％、（89．6±5．7）次/min,均明显高于对照组的（71．8±6．7）mmHg、（78．7±5．5）％、（70．8±5．2）次/min,组间差异有统计学意义（t＝8．456、8．246、9．625,均P＜0．05）;两组呼吸频率差异无统计学意义（t＝0．955,P＞0．05）;观察组复苏成功率及存活率分别为72％、46％,均明显高于对照组（44％、22％）,观察组不良反应发生率为2％,低于对照组（18％）,组间差异均有统计学意义（χ2＝8．05、6．42、10．15,均P＜0．05）。心肺复苏后5 min两组患者动脉血气分析指标PaO2、PaCO2、SaO2差异均无统计学意义（ t＝0．868、0．922、0．747,均P＞0．05）;15 min、30 min后两组患者PaO2、PaCO2、SaO2等动脉血气分析指标差异均有统计学意义（ t＝5．984、4．673、4．685、9．647、8．356、5．534,均P＜0．05）。结论心肺复苏机较徒手心肺复苏在抢救心脏骤停患者中具有明显优势,可明显缩短自主循环时间,提高心肺复苏成功率,疗效确切,且不良反应较少,是一种简单、安全和有效的抢救方法,值得在临床广泛推广应用。     

丙泊酚对罗哌卡因中枢及心脏毒性的影响

目的探讨丙泊酚对罗哌卡因中枢及心脏毒性的影响。方法 30只雄性大鼠,随机分为3组(n=10),生理盐水组(A组)、丙泊酚Ⅰ组(B组)、丙泊酚Ⅱ组(C组)。实验前5min,A组大鼠股静脉注射生理盐水5mL/kg,B组大鼠股静脉注射0.5%丙泊酚5mL/kg,C组大鼠股静脉注射1%丙泊酚5mL/kg。所有实验动物股静脉置管泵注0.5%罗哌卡因,速度为2.5mL/(kg-min)并记录大鼠出现抽搐、心律失常和心跳停止的时间及罗哌卡因用量。结果 A组、B组、C组泵入罗哌卡因后均出现抽搐、室性心律失常及心跳停止的中枢及心脏毒性反应,预注丙泊酚B组、C组出现抽搐、心律失常及心跳停止时的中毒剂量明显大于预注生理盐水A组的动物(P<0.01),C组出现抽搐、心律失常及心跳停止的中毒剂量大于B组(P<0.01)。结论短时间内过量罗哌卡因引起大鼠的中枢及心脏毒性反应,预先给予丙泊酚可明显减轻罗哌卡因对大鼠的中枢及心脏毒性作用。