麻醉对猪失血性休克模型血流动力学及氧动力学的影响

目的 探讨麻醉对猪失血性休克血流动力学及氧动力学的影响.方法 巴马香猪16头随机分为:麻醉休克组和清醒休克组,每组8头.按30 mL/kg放血建立失血性休克模型,记录建模前及建模后4 h内不同时点的核心体温、心率(HR)、平均动脉压(MAP)、肺动脉压(PAP)、肺动脉楔压(PAWP)、中心静脉压(CVP)、心输出量(CO)、血红蛋白(Hb)、混合静脉血氧饱和度(SvO2)及血气分析变化,并计算氧摄取率(O2ER)、氧供指数(DO2I)和氧耗指数(VO2I).结果 模型建立后清醒组动物核心体温略有下降,但麻醉组动物核心体温下降更加明显.两组的HR、MAP、PaO2、PaCO2及pH值未表现出明显差异,但清醒组乳酸水平明显高于麻醉组.尽管模型建立后两组的DO2I和VO2I都出现了相同幅度的下降,但清醒组的DO2I、VO2I和O2ER在模型建立前后都显著高于麻醉组.结论 麻醉可以减轻失血性休克后的氧代谢紊乱,麻醉引起的诱导性低温可能是造成这种现象的原因.     

异氟烷麻醉对失血性休克血液循环和氧代谢的影响

目的 研究异氟烷麻醉对失血性休克(HS)血液循环和氧代谢的影响.方法 巴马小型猪16只,随机分为两组(n=8):清醒对照组(C组)和麻醉实验组(A组).两组猪分别于清醒和异氟烷麻醉两种状态下在15 min内按全身血容量的40%(即按30 mL/kg计算)匀速放血制备休克模型,监测放血前和放血后4 h内不同时间点的肺动脉温度(TP)、心率(HR)、平均动脉压(MAP)、中心静脉压(CVP)、平均肺动脉压(MPAP)、肺动脉楔压(PAWP)、心输出量(CO)、混合静脉血氧饱和度(SmvO2)及血气指标;计算每搏输出量(SV)、体循环阻力(SVR)、氧摄取量(Ca-vO2)、氧供(DO2)、氧耗(VO2)和氧摄取率(O2ER);记录每头猪的生存时间.结果 HS发生后,C组和A组HR分别增快至(193±19)次/min和(126±16)次/min,其后C组逐渐下降,A组变化较小;C组MAP和CO下降后回升较快、幅度较大,于HS 90 min分别回升至80 mm Hg和1.5 L/min以上,而A组回升不明显;但两组SVR增加较一致,且A组MPAP降低后回升较明显.HS导致两组DO2和VO2均分别降低至200 mL/min和150 mL/min以下,但A组下降并维持在更低水平,其O2ER、Ca-vO2和乳酸(LA)依然较低,SmvO2较高;两组猪在4 h内均存活.结论 异氟烷麻醉下,HS机体血流动力学应激代偿反应明显减弱,心血管系统受抑明显,氧供减少,但氧耗降低更显著,氧动力学失衡明显减轻.     

酚妥拉明对失血性休克家兔微循环血流动力学…

本研究旨在探讨酚妥拉明对失血性休克微循环灌流的作用，两组家兔－－生理盐水对照组和酚妥拉明治疗组，麻醉后放血至血压为５．３３￣６．００ｋＰａ，以造成重度失血性休克，维持６０ｍｉｎ后将５ｍｇ酚妥拉明加入２５ｍｌ生理盐水中静脉滴注，同时将放出的人武部血液回输。观察休克及用药前后平均动脉血压，心率和肠系膜微循环变化。用显微电视录像静像步进技术测定毛细血管口径、血流速度及血流量。酚妥拉明滴注后，心率略加快。     

四种溶液对失血性休克犬血流动力学的影响

目的探讨四种不同溶液(高渗盐水、高渗盐水羟乙基淀粉溶液、生理盐水及羟乙基淀粉)对失血性休克犬复苏早期血流动力学、氧代谢动力学的影响。方法杂种犬32只制备成失血性休克模型,并随机分为4组。分别以6 ml/kg高渗盐水溶液(HS)与6 ml/kg高渗盐水羟乙基淀粉溶液(HSS)对两组失血性休克模型进行容量复苏,而以3倍失血量生理盐水(NS)及等失血容量羟乙基淀粉(HES)对其他两组复苏作对照,观察复苏早期血流动力学、氧代谢动力学指标的变化。结果四种溶液均能改善失血性休克犬复苏的早期血流动力学、氧代谢动力学及组织灌流,但在30 min后HS、HSS及NS容量指标下降,血流动力学及氧代谢动力学下降,其中HS及NS下降最为明显,其次HSS,而HES能保持相对稳定。结论小容量高渗盐水在失血性休克模型中复苏有效,其作用与生理盐水类似;小容量高渗盐水加胶体溶液较优于单纯高渗盐水;羟乙基淀粉溶液复苏效果最好且持续长久。     

血必净注射液对脓毒性休克患者血流动力学和氧代谢的影响

脓毒性休克具有高排低阻的血流动力学特点，是导致脓毒症患者死亡的主要原因。研究表明，中药血必净注射液具有强效拮抗内毒索，抑制炎症介质肿瘤坏死因子-α（TNF-α）释放，拮抗白细胞介素-1（IL-1）、IL-6、IL-8的作用，可使多器官功能障碍综合征（MODS）人白细胞DR抗原（HLA—DR）的表达明显增强，恢复患者的免疫功能，有效降低脓毒症患者的病死率。本研究旨在探讨早期目标指导治疗原则联合血必净注射液治疗对脓毒性休克患者血流动力学和氧代谢的影响。     

抑制鸟苷酸环化酶对感染性休克犬血流动力学和氧代谢的影响

感染性休克是细菌内毒素通过一氧化氮(N0)等共同介质和作用途径诱导损伤的结果。但阻断NO的作用。不能逆转感染性休克^[1]。本研究用鸟苷酸环化酶抑制剂——亚甲蓝(methvlene blue，MB)阻断NO的后续作用，显示了良好的治疗效果。     

高渗高张液对失血性休克病人血流动力学的影响

关于高渗高张液 (ＨＳＤ)在国外已有较多研究 ,这里我们用其治疗 18例失血性休克病人 ,取得较为显著的效果 ,现报告如下。1　资料与方法1.1　一般资料　 18例成年患者 ,男 13例 ,女 5例 ,年龄 19～46岁 ,均为多发性创伤。入手术室时所有病人的收缩压 <10 6 7ｋＰａ ,麻醉选用咪唑安定 10ｍｇ ,芬太尼 0 .1～ 0 .2ｍｇ ,万可松 4～ 6ｍｇ快速诱导后作气管插管 (血气胸者先作闭式引流 ) ,用异丙酚、万可松和吸入安氟醚复合维持麻醉。1.2　方法　麻醉后作桡动脉穿刺持续测量ＭＡＰ ,作右颈内静脉穿刺用Ｓｗａｍ -Ｇａｎｚ漂浮导管热稀释法ＣＯ…     

不同时相应用高张盐对失血性休克犬血流动力学参数的影响

目的 比较不同时相应用高张盐对失血性休克犬血流动力学参数的影响。方法 采用修订的Wiggers法复制犬失血性休克模型后,将实验动物随机分为两组,分别于休克后10min（组1）、70min（组2）给予6ml/kg 7.5%NaCl右旋糖酐溶液（HSD）静推,5min内输完。分别在基础期、休克期及复苏后测定血流动力学参数的变化。结果 应用高张盐复苏后,组1犬各参数较组2改善明显（P＜0．01）,且在上升速度和维持时间上显优于组2,尤以每搏指数（SI）、平均动脉压（MAP）、左室每搏作功指数（LVSWI）等值改善明显。结论 早期应用高张盐,可通过加强左室心肌收缩力、扩张全身血管、降低外周阻力,达到改善休克的目的。用液越早,疗效越好,维持时间越长。     

海水浸泡对枪弹伤合并失血性休克大鼠血流动力学的影响及机制探讨

目的　研究海水浸泡对枪弹伤合并失血性休克大鼠血流动力学、心肌细胞线粒体功能及一些生化指标的影响 ,探讨海水浸泡对心肌功能的影响及可能的机制。方法　健康Wistar雄性大鼠 2 0只 ,右侧大腿肌肉丰满处应用射钉枪造成贯通伤 ,包扎伤口。右侧颈总动脉插管至左心室 ,接四道生理记录仪 ,记录心肌力学的改变。左侧股动脉快速放血使血压降至 50mmHg(1mmHg =0 .1 33kPa) ,维持低血压 1h后 ,随机分为 2组 :海水浸泡组和陆地对照组 ,测定海水浸泡 5h大鼠平均动脉压 (MAP)、心率 (HR)、左室内压最大变化速率 (±dp·dt- 1 ·max- 1 )、左室收缩压 (LVSP)、心肌细胞线粒体呼吸功能、膜流动性 ,心肌组织Na+ -K+ -ATP酶活性、丙二醛 (MDA)含量及血浆乳酸脱氢酶 (LDH)。结果　海水浸泡 5h ,枪弹伤合并失血性休克大鼠MAP、HR、±dp·dt- 1 ·max- 1 、LVSP显著低于陆地对照组 ,心肌细胞线粒体呼吸控制率 (RCR)显著下降 ,膜脂区微黏度显著升高 ,心肌组织Na+ -K+ -ATP酶活性显著下降 ,心肌MDA含量和血浆LDH活力显著升高。结论　海水浸泡可以严重影响枪弹伤合并失血性休克大鼠血流动力学状态 ,加重其心肌的损伤     

乌司他丁对脓毒症休克犬血流动力学、氧代谢及组织灌注的影响

目的:探讨乌司他丁对脓毒症休克犬血流动力学、氧代谢及组织灌注指标的影响.方法:健康雄性杂种狗14只,内毒素静脉注射复制犬脓毒症休克模型,随机分为对照组(n=7)和治疗组(n=7).对照组只接受林格液复苏.治疗组另外给予首剂乌司他丁1万U/kg,然后持续泵入0.1 7万U/(kg·h).直至12 h后实验结束.脓毒症休克模型稳定后记为0 h,此后每4小时收集血流动力学、氧代谢及组织灌注指标.结果:(1)血流动力学指标:休克后中心静脉压、肺动脉嵌压、右室每搏功指数、肺循环血管阻力指数明显上升(P<0.05),治疗组逐渐回落,8 h后两组比较差异有显著性(P<0.05),治疗组血压在第8小时有明显回升(P<0.05),对照组血压无此趋势,两组比较差异有显著性(P<0.05).复苏后两组的心指数均有上升(P<0.05),治疗组表现尤为明显,但两组差异无显著性(P>0.05).心搏指数、左室每搏功指数休克后明显下降,但两组均迅速回复到基线水平,两组差异无显著性(P>0.05).休克后体循环血管指数明显下降(P<0.05),治疗组逐渐上升,8 h后两组比较差异有显著性(Jp<0.05).(2)氧代谢及组织灌注指标:犬脓毒症休克模型建立后,氧输送、氧消耗、混合静脉血氧饱和度(SVO2)、尿量明显下降(P<0.05),血乳酸、胃黏膜PHi、胃-动脉-PCO2 差上升(P<0.05).治疗组氧输送、SVO2、尿量、胃黏膜PHi逐渐回升,第8小时与对照组比较有明显差异(P<0.05),治疗组氧消耗也有增加趋势,但与对照组比较无明显差异(p>0.05).治疗组血乳酸水平、胃-动脉PCO2差逐渐下降,8 h后与对照组比较差异有显著性(P<0.05).结论:乌司他丁能够明显改善脓毒症休克动物的血流动力学、氧代谢及组织灌注指标.     

创伤失血性休克控制性低温的研究进展

创伤后低体温显著增加患者的死亡率,但控制性低温可能改善患者的预后.临床前期研究显示,控制性低温在能量代谢、炎症免疫反应、缺血-再灌注损伤、脏器保护和降低死亡率方面有保护作用,其机制可能与低温降低细胞能量消耗有关.控制性低温有不同的控温方法,并有一定的副作用,在应用时需要加以选择和重视.本文回顾了低温的相关知识及介绍近年来控制性低温对失血性休克的研究进展.     

溶液温度对失血性休克兔循环功能的影响

目的探讨不同温度液体复苏对失血性休克兔循环功能的影响,以筛选较为适宜的抗休克补液温度.方法将实验兔(n=30)以随机的方法分为假手术组(n=7)、温热组(n=8)、常温组(n=7)、低温组(n=8).选择休克前(t1)、休克模型形成后30min(t2)、液体复苏后1h(t3)、2h(t4)、4h(t5),观察心率、平均动脉压、中心静脉压和休克指数的变化.结果温热组失血性休克兔在液体复苏后心率稳定,而常温及低温组心率明显下降.液体复苏后4 h,温热组与常温组、低温组之间比较有统计学差异.温热组平均动脉压升高平稳,常温及低温组曲线有一定波动.液体复苏后4h,低温组平均动脉压较低,与其他3组比较有统计学差异.中心静脉压、休克指数组间比较无统计学差异.结论温热液体复苏使休克兔心率、平均动脉压、中心静脉压较为平稳,有助于改善休克兔循环功能.     

常用呼吸方式对血液动力学和氧代谢的影响

目的本文对８例危重症患者行Ａ／Ｃ、ＳＩＭＶ和ＰＳＶ呼吸支持,探讨三种方式对血液动力学和氧代谢的影响。方法呼吸支持最初阶段采用Ａ／Ｃ方式,并逐渐改为ＳＩＭＶ和ＰＳＶ方式,每种方式持续３０ｍｉｎ,ＳＩＭＶ频率为Ａ／Ｃ的７５％,ＰＳＶ设置在能够达到呼出气潮气量相同于Ａ／Ｃ的水平,三种方式吸入氧浓度不变,利用Ｓｗａｎ－Ｇａｎｚ导管获得血液动力学和氧代谢参数。结果与Ａ／Ｃ相比,ＳＩＭＶ和ＰＳＶ有一个低的ＰＩＰ增加的ＰａＯ２,与Ａ／Ｃ相比,ＳＩＭＶ可进一步增加ＣＩ和ＤＯ２、ＰｖＯ２。结论与Ａ／Ｃ相比,ＳＩＭＶ和ＰＳＶ对胸内压和血液动力学影响较小,ＳＩＭＶ可进一步增加组织的氧利用率。     

Effects of arterial oxygen content on oxidative stress during resuscitation in a rat hemorrhagic shock model

Objective

To examine whether reactive oxygen species (ROS) production is affected by arterial oxygen content (CaO₂) in attempted resuscitation to restore blood pressure from hemorrhagic shock (HS) or not.

Methods

Under light anesthesia and spontaneous beating, 16 rats underwent HS for 80 min, during which 3.0 mL/100 g of blood was withdrawn, followed by resuscitation attempt for 70 min. At 80 min, rats were randomized into a high-CaO₂ group (Group 1, transfusion under fractional inspired oxygen (F_IO₂) of 1.0, n = 8) or a low-CaO₂ group (Group 2, fluid administration under F_IO₂ of 0.21, n = 8). In each group, either blood or lactate Ringer's (LR) solution was infused to maintain mean arterial pressure ≥75 mmHg under each F_IO₂ concentration. CaO₂, O₂ utilization coefficient (UC) and plasma %CoQ9 were compared between groups.

Results

Mean infused volume for attempted resuscitation was 7.6 ± 1.0 mL of blood in Group 1, and 31.4 ± 5.5 mL of LR solution in Group 2. At the end of resuscitation, CaO₂ was 18.5 ± 1.2 vol% in Group 1, almost double the 9.1 ± 0.8 vol% in Group 2 (P < 0.01). O₂ UC and %CoQ9 in all rats increased from baselines of 0.25 ± 0.12 and 7.6 ± 1.8% to 0.44 ± 0.13 and 9.7 ± 1.8% after resuscitation, respectively (P < 0.05 vs. baseline for each), but did not differ significantly between the groups.

Conclusion

In a rat HS model, attempted resuscitation to restore blood pressure increased O₂ UC as well as %CoQ9. However, the magnitude of %CoQ9 increase that represents ROS production is not affected by CaO₂ during resuscitation from HS.     

不同镇静药物对机械通气患者血流动力学及氧代谢的影响

目的探讨丙泊酚、咪达唑仑及右美托咪定对机械通气患者血流动力学及氧代谢的影响。方法将60例机械通气患者分为丙泊酚组（P组）、咪达唑仑组（M组）及右美托咪定组（D组）,每组各20例。对每组镇静前后及不同组间镇静后血流动力学及氧代谢指标变化进行比较。结果三组患者镇静后心率、平均动脉压、心排量、心指数及氧供均有不同程度下降,中心静脉血氧饱和度（ScvO2）均有不同程度上升,而全身血管阻力指数（SVRD、全心舒张末期容积指数（GEDVI）仅在D组镇静后有所下降（P均〈0．05）。镇静后三组患者的心率、平均动脉压、SVRI、GEDVI、心排量、心指数、氧供及ScvO2比较,差异均有统计学意义（P均〈0．05）。进一步两两比较,心率、平均动脉压及ScvO2在M组与D组比较时有统计学意义（P=0．003、0．006、0．000）,SVRI水平在D组与P组及M组比较时均有统计学意义（P=0．001、0．015）,而GEDVI、心排量、心指数仅在D组与P组比较时有统计学意义（P=0．015、0．011、0．002）。结论三种药物均能达到减少氧耗作用且镇静效果确切,但使用右美托咪定镇静时需注意药物所致心动过缓及低血压的风险,而使用丙泊酚镇静时需注意药物对心功能的抑制。     

猪创伤失血性休克模型凝血功能的变化

目的 创伤引起的凝血功能障碍是死亡的重要原因.本研究主要观察猪创伤失血性休克后凝血功能的变化.方法 12只家猪随机(随机数字法)分为对照组(CG,n=6)和实验组(EG,n=6).实验组先受到胸部钝性伤,然后放全血的35％左右,维持平均动脉压(MAP)在(40±3) mmHg(1 mmHg=0.133 kPa)2 h,随后进行复苏.对照组没有创伤、失血及复苏.分别在实验开始时(H0)、创伤失血后15 min (H1)、1 h(H2)、2 h(H3)以及复苏后15 min (R1)、2h (R2)、6 h(R3)、24h (R4)采血,进行血气分析、血常规(Plt)、凝血试验(PT、APTT、Fib)和血栓弹力图(TEG)检测.结果 实验组动物Plt持续下降,复苏后各时间点与对照组差异均有统计学意义(P ＜0.05);Fib创伤放血后15 min开始显著下降直至复苏后2h,期间各时间点均低于对照组(P＜0.05),复苏后24 h显著高于对照组(P＜0.05);PT在创伤放血后15 min显著缩短(P=0.001),之后逐渐延长,复苏后6h开始缩短,放血后2h至复苏后6h期间各时间点与对照组比较,差异有统计学意义(P＜0.05);APTT在创伤放血后15 min显著缩短(P=0.024),后显著延长直至复苏后6h,各时间点差异有统计学意义(P＜0.05).实验组TEG的R值在创伤放血后15 min显著缩短(P＜0.05),复苏后24h较对照组显著延长(P =0.022);K值在创伤放血后15 min显著缩短(P=0.001);MA值在创伤放血后2h显著低于对照组(』P=0.004).结论 创伤失血性休克早期存在一过性高凝状态,表现为PT、APTT、R值和K值的缩短,随后转变为低凝状态,表现为PT、APTT的延长和Fib、MA值的下降.复苏期仍处于低凝状态,早期表现为PT、APTT的延长和Plt、Fib的下降,晚期表现为R值的延长和Plt的下降.     

Effects of various concentrations of inhaled oxygen on tissue dysoxia,oxidative stress,and survival in a rat hemorrhagic shock model

Objective

To test the hypothesis that a fractional inspired oxygen (F_IO₂) of 1.0 compared to 0.4 during hemorrhagic shock (HS) and fluid resuscitation (FR): mitigates tissue dysoxia; however, enhances the oxidative stress; therefore, offsets the benefit on survival.

Methods

Thirty rats underwent: HS for 75 min, during which 3.0 mL/100 g of blood was withdrawn, followed by FR for 75 min, during which 1.0 mL/100 g of shed blood and 3.0 mL/100 g of crystalloid solution were infused. Ten rats were randomized into one of three F_IO₂ (0.21 vs. 0.4 vs. 1.0) groups, and observed for survival until 72 h in each group. Hemodynamics, liver tissue PO₂ (P_TO₂), and, plasma antioxidants levels were also monitored.

Results

Oxygen inhalation increased mean arterial pressure (MAP) and decreased heart rate (HR) during HS and FR. Liver P_TO₂ was less than 10 Torr in all groups throughout HS; while it increased to average 26–35 Torr in oxygen groups during FR, it remained at 10 Torr with F_IO₂ 0.21 (P < 0.01). MAP, HR, and P_TO₂ did not differ significantly between oxygen groups. Plasma antioxidants levels did not differ among the three groups. All rats treated with oxygen, but eight of 10 rats with F_IO₂ 0.21 survived up to 72 h (NS).

Conclusions

Supplemental oxygen does not mitigate tissue dysoxia during HS, but does reduce tissue dysoxia without enhancing oxidative stress during subsequent FR. Increased F_IO₂ appears to prolong survival. These beneficial effects of supplemental oxygen do not differ between an F_IO₂ of 0.4 and 1.0.     

失血性休克时大鼠全身氧供给与氧消耗关系的变化

目的　研究失血性休克时全身氧供给 (DO2 )与氧消耗 (VO2 )关系的变化。方法　按 4ml/kg、每隔 0 5小时分次从静脉放血 ,观察大鼠休克过程中DO2 、VO2 、氧摄取率(ExtO2 )等变化。结果　失血 2 0小时平均动脉压开始明显下降 (P <0 0 1)。在休克早期 ,DO2随进行性下降 ,ExtO2 出现代偿升高、VO2 维持相对不变 ,呈非氧供依赖关系 ;当DO2 降至2 7 6 4ml·min- 1 ·kg- 1 后、VO2 随DO2 线性降低 (r=0 788,P <0 0 1) ,即呈氧供依赖关系 ,并伴血乳酸浓度升高。结论　失血性休克时DO2 与VO2 间呈双相变化关系 ,氧供依赖关系出现反映了全身组织缺氧的存在     

Effects of environmental hypothermia on hemodynamics and oxygen dynamics in a conscious swine model of hemorrhagic shock

BACKGROUND:

Hypothermia is associated with poor outcome in trauma patients; however, hemorrhagic shock (HS) model with anesthetized swine was different from that of clinical reality. To identify the effects of environmental hypothermia on HS, we investigated hemodynamics and oxygen dynamics in an unanesthetized swine model of HS under simulating hypothermia environment.

METHODS:

Totally 16 Bama pigs were randomly divided into ambient temperature group (group A) and low temperature group (group B), 8 pigs in each group. Venous blood (30 mL/kg) was continuously withdrawn for more than 15 minutes in conscious swine to establish a hemorrhagic shock model. Pulmonary arterial temperature (Tp), heart rate (HR), mean arterial pressure (MAP), pulmonary arterial pressure (PAP), pulmonary arterial wedge pressure (PAWP), central venous pressure (CVP), cardiac output (CO), hemoglobin (Hb), saturation of mixed venous blood (SvO₂) and blood gas analysis were recorded at the baseline and different hemorrhagic shock time (HST). The whole body oxygen delivery indices, DO₂I and VO₂I, and the O₂ extraction ratio (O₂ER) were calculated.

RESULTS:

Core body temperature in group A decreased slightly after the hemorrhagic shock model was established, and environmental hypothermia decreased in core body temperature. The mortality rate was significantly higher in group B (50%) than in group A (0%). DO₂I and VO₂I decreased significantly after hemorrhage. No difference was found in hemodynamics, DO₂I and VO₂I between group A and group B, but the difference in pH, lactic acid and O₂ER was significant between the two groups.

CONCLUSION:

Environmental hypothermia aggravated the disorder of oxygen metabolism after hemorrhagic shock, which was associated with poor prognosis.KEY WORDS: Hemorrhagic shock, Environmental hypothermia, Hemodynamics, Oxygen dynamics     

Effects of hypothermia on the liver in a swine model of cardiopulmonary resuscitation

BACKGROUND:

The study aimed to explore the effects of hypothermia state induced by 4 ºC normal saline (NS) on liver biochemistry, enzymology and morphology after restoration of spontaneous circulation (ROSC) by cardiopulmonary resuscitation (CPR) in swine.

METHODS:

After 4 minutes of ventricular fibrillation (VF), standard CPR was carried out. Then the survivors were divided into two groups: low temperature group and normal temperature group. The low temperature (LT) group (n=5) received continuously 4 ºC NS at the speed of 1.33 mL/kg per minute for 22 minutes, then at the speed lowering to 10 mL/kg per hour. The normal temperature (NT) group (n=5) received NS with normal room temperature at the same speed of the LT group. Hemodynamic status and oxygen metabolism were monitored and the levels of serum alanine aminotransferase (ALT), aspartate aminotransferase (AST) and lactate dehydrogenase (LDH) were measured in blood samples obtained at baseline and at 10 minutes, 2 hours and 4 hours after ROSC. At 24 hours after ROSC, the animals were killed and the liver was removed to determine the Na⁺-K⁺-ATPase and Ca²⁺-ATPase enzyme activities and histological changes under a light or electron microscope.

RESULTS:

Core temperature was decreased in the LT group (P<0.05), while HR, MAP and CPP were not significantly decreased (P>0.05) compared with the NT group (P>0.05). The oxygen extraction ratio was lower in the LT group than in the NT group (P<0.05). The serum levels of ALT, AST and LDH increased in both groups but not significantly in the LT group. The enzyme activity of liver ATP was much higher in the LT group (Na⁺-K⁺-ATP enzyme: 8.64±3.32 U vs. 3.28±0.71 U; Ca²⁺-ATP enzyme: 10.92±2.12 U vs. 2.75±0.78 U, P<0.05). The LT group showed less cellular edema, inflammation and few damaged mitochondria as compared with the NT group.

CONCLUSION:

These data suggested that infusing 4 ºC NS continuously after ROSC could quickly lower the core body temperature, while maintaining a stable hemodynamic state and balancing oxygen metabolism, which protect the liver in terms of biochemistry, enzymology and histology after CPR.KEY WORDS: Therapeutic hypothermia, Cardiac arrest, Liver, Hemodynamics