低温闭胸心肺转流复苏后心肺脑组织的电镜改变

目的　观察狗心脏停搏 15min后 ,用浅低温和深低温闭胸心肺转流 (CPB)复苏后心肺脑组织的电镜改变。方法　 13只实验狗分三组 ,浅低温组 (33～ 34℃ ) (n =5 ) ,深低温组 (2 6～ 2 7℃ ) (n =5 ) ,狗心脏停搏 15min后行闭胸CPB ,维持平均动脉压大于 80mmHg ,3h后取心、肺和海马组织 ,对照组 (n =3)停搏 15min后立即取组织。结果　浅低温组海马组织的神经元数为 (4 6± 0 9)个 ,明显少于深低温组 (13 6± 5 2 )个 (P <0 0 5 )和对照组 (8 3± 4 7)个 ;少突胶质细胞核平均直径为 (5 86± 0 80 ) μm ,显著大于深低温组 (3 94± 0 90 ) μm(P <0 0 1)和对照组 (4 5 6± 1 0 35 ) μm(P <0 0 5 ) ,细胞膜破损明显 ;肺表面活性物质减少 ,毛细血管内皮细胞连接松弛。深低温组心肌肌原纤维变细、变稀 ,部分断裂 ,明显受损。结论　狗心脏停搏 15min后 ,浅低温闭胸CPB结合头部深低温或深低温闭胸CPB结合心肌保护治疗 ,可能更有益于心肺脑复苏     

心肺转流行心肺复苏的实验研究

观察狗心脏停搏30分钟后的心肺复苏效果,以10%氯化钾溶液静脉注射使实验狗心脏停搏、呼吸停止30分钟后,分两组进行心肺复苏实验研究.实验狗每组5只.第一组采用常规法;第二组采用心肺转流(cardiopul-monary bypass,CPB)法.实验期间,定时对心电图、动脉压、静脉压、动脉血气和瞳孔进行监测.心肺骤停后60分钟检查最终复苏效果.结果第一组仅1只狗(20%)于第15分钟后恢复自主循环,瞳孔开始缩小,其余4只狗均未获复苏;第二组于2—3分钟后全部恢复自主循环(100%),瞳孔缩小.复苏30分钟后,其平均动脉压为8—14.0kPa,明显高于第一组(0—12.0kPa)(P<0.05),其静脉压为0.09—0.12kPa,明显低于第一组(0.14—0.24kPa)(P<0.01),PaCO_2为2.06—5.73kPa,明显低于第一组7.22—11.90kPa;PaO_2为21.70一59.81kPa,明显高于第一组(5.88—14.56kPa)(P<0.01).上述实验结果表明,心搏呼吸骤停30分钟后,以心肺转流法进行复苏可有效地恢复自主循环,并可能有益于脑复苏.从少量实验动物复苏效果提示,CPB法明显优于常规法.     

心肺转流行心肺复苏的实验研究

观察狗心脏停搏３０分钟后的心肺复苏效果，以１０％氯化钾溶液静脉注射使实验狗心脏停搏、呼吸停止３０分钟后，分两组进行心肺苏实验研究。实验狗每组５只，第一组采用常规法，第二组采用心肺转流法。实验期间，定时对心电图、动脉压、静脉压、动脉血气和瞳孔进行监测。心脏骤停后６０分钟检查最终复苏效果。结果第一组仅１只狗于１５分钟后恢复自主循环，瞳孔开始缩小，其余４只狗均未获复苏，第二组于２－３分钟后全部恢复自主循     

低温闭胸心肺转流对狗心肺复苏后脑损伤的保护作用

目的　观察闭胸低温心肺转流 (CPB)对狗心肺复苏后脑损伤的保护作用。方法制作狗心搏骤停模型 ,停搏 15min后行浅低温 (33～ 34℃ ) (n =5 )和深低温 (2 6～ 2 7℃ ) (n=5 )闭胸CPB复苏。于停搏前、停搏后 15min、CPB开始后 1h、 3h抽血 ,于 3h取大脑皮层 ,测定血浆和脑组织肌酸磷酸激酶 BB (CK BB)浓度。另设 5只为缺血对照组。结果　CPB开始后3h ,浅低温组和深低温组血浆CK BB浓度明显高于停搏前 (P <0 0 5 ) ,深低温组大脑皮层中CK BB浓度明显低于浅低温组 (P <0 0 5 )。结论　狗心脏停搏 15min后行深低温闭胸CPB复苏对大脑皮层的损伤较轻 ,有一定保护作用     

低温闭胸心肺转流对缺血再灌注损伤血浆和组织中 SOD、 MDA、 NO的影响

目的:了解狗心脏停搏15分钟后,用浅低温和深低温闭胸心肺转流(CPB)时,对血浆和组织中超氧化物歧化酶(SOD)、丙二醛(MDA)和一氧化氮(NO)的影响。方法:10只实验狗,用10％氯化钾静注致心脏停搏15分钟后,行闭胸CPB复苏,浅低温组(33℃～34℃)(N=5),深低温组(26℃～27℃)(N=5),15分钟后复温。于停搏前、停搏15分钟、CPB开始后1小时、3小时抽血,并于3小时取心、肺、脑组织,行血浆和组织SOD、MDA和NO测定。结果:在停搏15分钟时,两组血浆SOD活性均明显高于停搏前;CPB后1小时,二组均明显低于停搏前(P<0.05),但至3小时,二组均上升接近停搏前水平(P>0.05)。两组血浆MDA和NO含量于停搏15分钟和CPB后1小时、3小时均明显低于停搏前(P<0.05)。浅低温组脑组织和肺组织中SOD明显低于深低温组(P<0.05),MDA明显高于深低温组(P<0.05);而心肌组织中NO含量明显低于深低温组(P<0.05),MDA也明显低于深低温组(P<0.05)。结论:狗心脏停搏15分钟后,用低温闭胸CPB复苏,血浆SOD代偿性升高,MDA和NO下降,即低温复苏有助于减轻氧自由基和NO造成的再灌注损伤。组织中的指标测定,表明深低温闭胸CPB复苏对脑和肺的再灌注损伤较轻,浅低温闭胸CPB复苏则对心肌的再灌注损伤较轻。     

延迟使用升压素与肾上腺素在窒息家兔心肺复苏中的疗效比较

目的 观察心肺复苏时延迟使用升压素或肾上腺素对自主循环恢复率的影响，比较两者对窒息性心跳停搏家兔心肺复苏的疗效。方法 62只家兔均在呼气末夹闭气管8min，造成窒息性心脏停搏模型后，开始人工胸外心脏按压及机械通气，期间不用任何药物，复苏5min内恢复自主循环的家兔定义为常规心肺复苏成功，对5min内复苏不成功者，再随机分为两组，分别给予升压素（0．8IU／kg）或肾上腺素（0．2mg／kg）静脉注射，并继续常规心肺复苏：结果 常规心肺复苏的自主循环恢复率为24．19％（15／62），加用升压素和肾上腺素后总的自主循环恢复率提高到48．39％（30／62）。其中升压素组23只家兔中2只复苏成功（8．70％），肾上腺素组24只家兔中13只复苏成功（54．16％），肾上腺素组复苏成功率明显高于升压素组（P=0．001）。结论 对窒息性心脏停搏的家兔心肺复苏时应用升压素或肾上腺素可提高自主循环恢复率。肾上腺素在提高窒息家兔冠脉灌注压及复苏成功率方面明显优于升压素。     

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.     

犬心肺复苏前后红细胞流变学变化的特征

目的:从非失血因素导致的心跳骤停复苏前后红细胞流变学变化入手,对影响后期脑复苏及重要器官保护的其中一个因素进行研究。方法:实验选用健康杂种家犬8只,体质量11～20.5kg。将狗麻醉后,于右胸及左心尖的皮下电极以交流电(50～80V)刺激,诱发室颤至循环停止。8min后开始机械通气及心肺复苏,复苏成功行常规后续支持治疗。心跳骤停前5min,心跳骤停中第5秒,心肺复苏后30,60,90,120min于股静脉采集血液标本测定红细胞聚集指数(RBCaggregationindex,RAI),红细胞变形指数(RBCdeformationindex,RDI),红细胞刚性指数(RBCrigidityindex,RRI),全血高切黏度(high-shearbloodviscosity,HBV),全血低切黏度(low-shearbloodviscosity,LBV),卡松黏度,卡松屈服应力(Cassonyieldstress,CYS)。结果:心跳骤停中5min,复苏后30min与复苏前RAI比较,差异无显著性意义(P>0.05);复苏后60min,90min与复苏前比较,差异有显著性意义(t=2.97,2.42,P<0.05);复苏后120min与复苏前比较,差异有非常显著性意义(t=3.46,P<0.01)。心跳骤停中5min与复苏后120minRDI(0.96±0.09,0.91±0.13)和复苏前(0.88±0.07)比较,差异无显著性意义(P>0.05);复苏后90min(1.01±0.12)与复苏前比较,差异有显著性意义(t=2.57,P<0.05);复苏后30min(1.05±0.13),60m     

心肺复苏时联合使用血管加压素、肾上腺素、盐酸纳洛酮的临床观察

目的　研究心肺复苏时联合使用血管加压素、肾上腺素、盐酸纳洛酮的疗效。方法　 5 6例呼吸心跳骤停的患者随机分为两组。肾上腺素标准剂量组 (对照组 ) 2 6例 ,联合使用血管加压素、肾上腺素、盐酸纳洛酮 (治疗组 ) 30例 ,各组分别观察自主循环、呼吸恢复率 ;2 4小时存活率及出院存活率 ;自主循环、呼吸恢复时间。结果　对照组、治疗组自主循环恢复率分别为 2 3.1%、6 6 .7% ;自主呼吸恢复率分别为 11.5 %、5 0 % ;自主循环恢复时间分别为 (18.5±2 .5 )min、(7.5± 2 .2 )min ;自主呼吸恢复时间分别为 (12 0± 11.2 )min、(5 0± 8.5 )min ;2 4小时存活率分别为 11.5 %、4 3.3% ;出院存活率分别为 7.7%、33.3%。治疗组的自主循环、呼吸恢复率、2 4小时存活率、出院存活率明显高于对照组 ,治疗组的自主循环、呼吸恢复时间明显短于对照组。结论　心肺复苏期间 ,联合应用血管加压素、肾上腺素、盐酸纳洛酮比单独使用标准剂量的肾上腺素能显著提高自主循环、呼吸恢复率、2 4小时存活率、出院存活率、缩短自主循环、呼吸恢复时间     

儿童心肺复苏的治疗进展

积极正确的复苏,尤其是提供有效的通气和供氧,防止心脏停搏;一旦心脏停搏及时给予有效的心脏按压极为重要[1]。持续性自主循环恢复指自主循环恢复时间达20 min以上,只有持续性自主循环恢复才可认为心肺复苏初步成功。呼吸心搏停止经复苏自主循环恢复后,如仍无自主呼吸或自主呼吸不规则,呼吸功     

Rapid induction of hypothermia with a small volume aortic flush during cardiac arrest in pigs

Purpose

The induction of deep cerebral hypothermia (15°C) via large-volume cold (4°C) saline aortic flush during cardiac arrest and resuscitation with cardiopulmonary bypass improves neurologic outcome in pigs. We hypothesized that induction of mild cerebral hypothermia (33°C) via smaller volume and resuscitation without bypass will improve survival and neurologic outcome after 15 minutes of cardiac arrest as compared with conventional resuscitation attempts.

Basic Procedures

Twenty-four pigs (29-38 kg) underwent ventricular fibrillation cardiac arrest for 15 minutes. Conventional resuscitation (n = 8) was compared with hypothermic (4°C, n = 8) and normothermic (38.5°C, n = 8) aortic flush (30 mL/kg) at the beginning of resuscitation efforts, with defibrillation attempts 2 minutes later. Outcomes after 9 days were compared.

Main Findings

In the hypothermic flush group, brain temperature decreased from 38.3°C ± 0.5°C to 33°C ± 0.5°C within 277 ± 112 seconds. We observed considerably higher mean coronary perfusion pressures in the normothermic and hypothermic flush groups (hypothermic vs conventional, P = .023; normothermic vs conventional, P = .041). Three animals of each flush group, compared with none of the conventional group, achieved restoration of spontaneous circulation (P = .2); and 3 pigs of the hypothermic flush group and 2 pigs of the normothermic flush group survived to 9 days without differences in neurologic outcome.

Principal Conclusion

A smaller volume, cold saline aortic flush during prolonged cardiac arrest rapidly induces mild cerebral hypothermia to 33°C and improves coronary perfusion pressure but does not result in a significant improvement in outcome as compared with conventional resuscitation attempts.     

搏动性导管泵在绵羊心脏复苏中的应用

目的探讨搏动性导管(pulsatile catheter, PUCA)泵在心脏复苏中的应用,为临床抢救心跳骤停的患者提供一种新的思路.方法健康绵羊11只,致室颤心脏停跳行心脏复苏,根据有无PUCA泵辅助及辅助是否及时分三组无辅助(n=3)、延迟辅助(n=2)和即时辅助(n=6),记录并比较3组复苏所持续时间和成败率.分别于复苏后5 min、60 min和180 min监测并记录血流动力学参数.结果无辅助、延迟辅助和即时辅助复苏持续时间分别为(38.3±5.8) min、(43.5±9.2) min和(48.7±23.8) min,3组比较差异无显著性(P＞0.05);3组成败比分别为0/3、0/2和5/1,差异有显著性(P＜0.05).复苏成功的5只绵羊在支持期间血流动力学逐步恢复并趋向稳定,血压在辅助180 min与5 min相比有明显的统计学意义(P＜0.05).结论心跳骤停中,在PUCA泵即时辅助下行心脏复苏明显提高复苏成功率,并能恢复和稳定复苏动物的血流动力学;该结果可望拓展PUCA泵在临床上新的应用.     

急诊体外循环动脉灌注管位置对心肺复苏效果的影响

目的 探讨急诊体外循环（ECPB）动脉灌注管位置对肺门部火器伤后心脏骤停犬心肺复苏（CPR）的影响。方法 杂种犬14只随机均分为两组,麻醉后用小口径步枪射击犬右肺门区,心脏骤停后10min开始复苏。A、B两组分别采用股动脉、颈动脉插管建立ECPB,同时给予人工呼吸、胸内心脏按压、静注肾上腺素治疗。观察动物CPR情况。结果 A、B两组动物均全部复苏成功,B组恢复自主循环时间明显短于A组（P＜0．05）;复苏1min时B组平均动脉压（MAP）显著高于A组（P＜0．05）,PaO2显著高于A组（P＜0．01）,PaO2显著低于A组（P＜0．05）;复苏3min时B组PaO2显著高于A组（P＜0．05）,PaCO2显著低于A组（P＜0．05）。自主循环恢复后10min两组间MAP、PaO2、PaCO2均无统计学差异。辅助循环停止后,两组动物自主循环基本保持稳定。结论 ECPB能有效地应用于心脏骤停的CPR,动脉灌注管靠近升主动脉根部有助于提高急诊体外循环心肺复苏的治疗效果。     

Mild hypothermia during prolonged cardiopulmonary cerebral resuscitation increases conscious survival in dogs

OBJECTIVE: Therapeutic hypothermia during cardiac arrest and after restoration of spontaneous circulation enables intact survival after prolonged cardiopulmonary cerebral resuscitation (CPCR). The effect of cooling during CPCR is not known. We hypothesized that mild to moderate hypothermia during CPCR would increase the rate of neurologically intact survival after prolonged cardiac arrest in dogs. DESIGN: Randomized, controlled study using a clinically relevant cardiac arrest outcome model in dogs. SETTING: University research laboratory. SUBJECTS: Twenty-seven custom-bred hunting dogs (19-29 kg; three were excluded from outcome evaluation). INTERVENTIONS: Dogs were subjected to cardiac arrest no-flow of 3 mins, followed by 7 mins of basic life support and 10 mins of simulated unsuccessful advanced life support attempts. Another 20 mins of advanced life support continued with four treatments: In control group 1 (n = 7), CPCR was with normothermia; in group 2 (n = 6, 1 of 7 excluded), with moderate hypothermia via venovenous extracorporeal shunt cooling to tympanic temperature 27 degrees C; in group 3 (n = 6, 2 of 8 excluded), the same as group 2 but with mild hypothermia, that is, tympanic temperature 34 degrees C; and in group 4 (n = 5), with normothermic venovenous shunt. After 40 mins of ventricular fibrillation, reperfusion was with cardiopulmonary bypass for 4 hrs, including defibrillation to achieve spontaneous circulation. All dogs were maintained at mild hypothermia (tympanic temperature 34 degrees C) to 12 hrs. Intensive care was to 96 hrs. MEASUREMENTS AND MAIN RESULTS: Overall performance categories and neurologic deficit scores were assessed from 24 to 96 hrs. Regional and total brain histologic damage scores and extracerebral organ damage were assessed at 96 hrs.In normothermic groups 1 and 4, all 12 dogs achieved spontaneous circulation but remained comatose and (except one) died within 58 hrs with multiple organ failure. In hypothermia groups 2 and 3, all 12 dogs survived to 96 hrs without gross extracerebral organ damage (p < .0001). In group 2, all but one dog achieved overall performance category 1 (normal); four of six dogs had no neurologic deficit and normal brain histology. In group 3, all dogs achieved good functional outcome with normal or near-normal brain histology. Myocardial damage scores were worse in the normothermic groups compared with both hypothermic groups (p < .01). CONCLUSION: Mild or moderate hypothermia during prolonged CPCR in dogs preserves viability of extracerebral organs and improves outcome.     

头部亚低温对心脏骤停犬血清及脑脊液中超氧化物歧化酶和脂质过氧化物的影响

目的：探讨头部亚低温对心脏骤停犬超氧化物歧化酶（ＳＯＤ）和脂质过氧化物（ＬＰＯ）的影响，为临床脑复苏过程中开展亚低温治疗提供依据。方法：采用放射免疫分析法和硫代巴比妥酸法分别测定犬心脏骤停前及复苏后常温及头部亚低温情况下血清及脑脊液ＳＯＤ和ＬＰＯ水平。结果：复苏后血清及脑脊液ＳＯＤ水平较心脏骤停前明显降低，而ＬＰＯ水平则明显升高；亚低温组脑脊液中ＳＯＤ水平较常温组高，ＬＰＯ水平则较低，但血清中ＳＯＤ及ＬＰＯ水平无明显差异。结论：氧自由基（ＯＦＲ）在心脏骤停所致的脑缺血缺氧性损害中起重要作用，头部亚低温可通过减少脑组织ＯＦＲ生成而起到保护脑的作用。     

Mild hypothermia in improving multiple organ dysfunction after cardiac arrest

BACKGROUND:

Resuscitation after cardiac arrest (CA) with a whole-body ischemia–reperfusion injury causes brain injury and multiple organ dysfunction (MODS). This study aimed to determine whether mild systemic hypothermia could decrease multiple organ dysfunctions after resuscitation from cardiac arrest.

METHODS:

The patients who had been resuscitated after cardiac arrest were reviewed. During the resuscitation they had been assigned to undergo therapeutic hypothermia (target temperature, 32°C to 34°C, measured in the rectum) over a period of 24 to 36 hours or to receive standard treatment with normothermia. Markers of different organ injury were evaluated for the first 72 hours after recovery of spontaneous circulation (ROSC).

RESULTS:

At 72 hours after ROSC, 23 patients in the hypothermia group for whom data were available had favorable neurologic, myocardial, hepatic and pulmonic outcomes as compared with 26 patients in the normothermia group. The values of renal function were not significantly different between the two groups. However, blood coagulation function was badly injured in the hypothermia group.

CONCLUSION:

In the patients who have been successfully resuscitated after cardiac arrest, therapeutic mild hypothermia can alleviate dysfunction after resuscitation from cardiac arrest.KEY WORDS: Cardiac arrest, Ischemia reperfusion injury, Mild hypothermia, Multiple organ dysfunction     

亚低温治疗及选择时机对窒息大鼠心肺复苏后的脑保护作用

【目的】探讨亚低温治疗及选择时机对窒息大鼠心肺复苏后的脑保护作用。【方法】36只成年 SD 大鼠随机分为假手术组(6只,A 组)、常温组(6只,B 组)和亚低温治疗组(24只,C 组),C 组随机分为 C1、C2、C3和 C4组四个亚组,每组6只。A 组仅进行麻醉、气管切开及血管穿刺操作,不进行心肺复苏;B 组不行低温治疗;C1~4组分别于心脏骤停后2、4、6、8 min 立即实施心肺复苏。统计各组复苏成功率;免疫组化法检测皮质及海马组织 Nrf2及 HO-1蛋白表达;按 Elliott 法计算脑组织百分水含量。【结果】C 组皮质、海马组织 Nrf2及 HO-1蛋白表达水平均显著高于 A 组和 B 组(P <0.05);C1、C2、C3和 C4四个亚组比较差异无统计学意义(P >0.05)。B 组和 C 组脑组织含水量均显著高于 A 组(P <0.05),但 B 组和 C 组比较差异无统计学意义(P >0.05),C1、C2、C3和 C4四个亚组比较差异也无统计学意义(P >0.05)。【结论】亚低温干预对心肺复苏大鼠的脑保护作用可能是通过激活 Nrf2-ARE 信号通路,上调 Nrf2及其下游基因 HO-1表达实现的,对窒息性心脏骤停心肺复苏后应早期进行亚低温治疗以减轻脑损伤,提高心肺复苏的成功率。     

延迟性低温对沙土鼠全脑缺血再灌注损伤的影响

目的研究全脑缺血后30 min开始的低温对沙土鼠行为学和组织病理学的影响,并与脑缺血后即刻低温进行比较.方法采用沙土鼠全脑缺血模型,缺血时间10 min.动物随机分为4组假手术组、常温组、延迟性低温组和即刻低温组,每组7只.于脑缺血后第5天行开阔法行为学检查,第7天行海马CA1区组织病理学检查.结果常温组10 min爬过的格子数(651±108)较假手术组(278±67)、延迟性低温组(478±89)、即刻低温组(368±46)有明显增多(t=7.76,2.21,6.37,P＜0.01～0.05).延迟性低温组较假手术组和即刻低温组增多(t=4.75,2.90,P＜0.01～0.05).海马CA1区内侧神经元数(以正常海马成活神经元的百分数表示,即各组成活神经元数与假手术组之比)延迟性低温组[(42±7)%]较常温缺血组[(5±1)%]多(t=13.00,P＜0.01),不及即刻低温组[(66±10)%](t=5.20,P＜0.01).海马CA1区中间神经元计数延迟性低温组[(60±9)%]较常温缺血组[(10±4)%]多(t=13.20,P＜0.01),不及即刻低温组[(77±16)%]多(t=2.45,P＜0.05).海马CA1区外侧成活神经元计数延迟性低温[(71±13)%]和即刻低温组[(80±14)%]之间无差别(t=1.25,P＞0.05),均较常温组[(23±5)%]多(t=9.14,t=10.14,P均＜0.01).结论延迟性低温可以减轻全脑缺血后神经功能障碍和海马神经元坏死,但作用不及即刻低温.     

亚低温技术和常温技术对脑功能保护的比较与评估

背景亚低温对缺血性损害的脑细胞有显著的保护作用,对脑复苏后的脑功能是否也具有保护作用?目的比较采用亚低温技术和常温技术评估脑复苏3个月时患者神经功能结局评分与生活自理能力评分的差异.设计随机对照实验.单位南京大学医学院附属鼓楼医院急诊中心.对象选择南京鼓楼医院2002-02/10在急诊抢救室经心肺复苏术抢救的患者16例,均为内科系统病变及中毒患者,在院内突发心跳与呼吸停止而进行心肺复苏术.其中男10例,女6例;年龄27～57岁;根据是否采用亚低温技术,将16例患者随机分为两组常温组与亚低温组,每组8例.方法心肺复苏后亚低温组患者立即采用药物+头部冰帽+电子冰毯方法做降温处理,使其脑部温度控制在32～34℃,维持72 h后复温;常温组患者在室温下对症处理.主要观察指标①两组患者复苏后第3,7天的血氧饱和度,血酸碱度,体温,颅内压,平均动脉压和格拉斯格昏迷评分.②复苏后3个月的格拉斯格神经功能结局评分(功能独立为85～100分,中度残疾为74～84分,严重残疾为10～50分,植物状态为＜10分)和生活自理能力评分(采用Bathel指数进行评价,共10项,每项0～15分不等,满分100分,＜60分为不能自理).结果16例患者均进入结果分析.①第3天时亚低温组平均脑温和颅内压均低于常温组[(33.1±0.26)℃,(37.4±18)℃;15.7 mm Hg,19.1 mm Hg,P=-0.027,0.043].血氧饱和度,血酸碱度,平均动脉压和格拉斯格昏迷评分两组基本接近(P＞0.05).②第7天亚低温组的格拉斯格昏迷评分明显高于常温组[(9.1±1.4),(11.2±1.6)分,P=0.032].③3个月后亚低温组格拉斯哥预后量表评分和Barthel指数明显高于常温组[(12.9±1.75),(9.9±1.9)分;(86±6),(52±12)分,P＜0.05～0.01].结论亚低温对早期脑复苏时的颅内压减低有效,尤其对复苏远期神经功能和日常生活活动能力恢复具有良好效果,具有显著的脑功能保护作用.     

Plasma epinephrine levels in resuscitation with cardiopulmonary bypass

Since the highest plasma epinephrine levels have been recorded during resuscitation, we evaluated the isolated effect of cardiac arrest upon adrenomedullary secretion. We determined plasma epinephrine in dogs resuscitated with cardiopulmonary bypass (CPB) after cardiac arrest periods of 12 (CPB-12; n = 4) or 16 min (CPB-16; n = 5). Through 2 h of CPB and the following 6 h of critical care, there was no difference between CPB-12 and CPB-16 regarding most cardiopulmonary functional variables. Plasma epinephrine was markedly elevated immediately after initiation of CPB (p less than .01 at 1 min CPB vs. basal) and returned rapidly to basal concentrations. Comparison of plasma epinephrine levels between CPB and standard CPR groups showed that responses to cardiac arrest were similar (p greater than .05 at 1 min CPB vs. 11.5 min CPR). We conclude that cardiac arrest is the main or sole determinant of the plasma epinephrine elevation of resuscitation.