近红外光谱技术在神经外科患者脑氧和血流动力学监测中的应用研究进展

神经外科患者,尤其是脑血流自动调节功能受损的重症患者,脑氧饱和度是反应患者脑组织氧代谢情况的重要指标,实时、准确的脑氧饱和度监测方法对于指导选择有效的治疗措施和判断患者预后具有重要价值。基于血红蛋白不同氧合状态,即氧合血红蛋白(oxyhemoglobin,Hb O2),还原血红蛋白(deoxygenated hemoglobin,Hb)具有的差异性分子光谱,近红外光谱技术near infrared spectroscopy,NIRS)可监测人体局部组织氧饱和度。由于近红外射线能穿透颅骨直接获得脑组织内平均氧饱和度的特性,可协助临床实现无创持续监测脑氧饱和度的目的,近年来该技术在神经外科领域的应用研究获得了迅速发展,在颅脑创伤和其它神经外科疾病的应用研究中均取得了显著的进展,本文将对最新研究结果及其意义和未来发展方向进行综述。     

不同温度“钾维普”停搏对幼大鼠心功能的影响

目的:探讨未成熟缺血心脏钾维普停搏保护的适宜温度。方法:离体幼大鼠心脏Langendorff法灌流,分5组(n=6～8)。对照组:36℃正常灌流170 min;36℃(常温)组:正常灌流20 min,灌钾维普停搏液(KVP)3 min停灌87 min(常温停搏90 min),恢复正常灌流(复灌)60 min;32、28、24℃(低温)组:正常灌流15 min,5 min内分别降温至32、28、24℃,灌KVP3 min停灌87 min(低温停搏90 min),复灌60 min。实验过程实时监测心率(b/min)、心肌张力(g)、收缩力(g)、最大收缩速度(dT/dtmax)、最大舒张速度(-dT/dtmax)及冠脉流量(drop/min)反映心功能。结果:与对照组相比,各组KVP停搏50 min后心脏张力均增高;与低温停搏相比,常温停搏的心脏不良挛缩迟缓、复灌后心脏张力、心率、收缩力、冠脉流量恢复好(P<0.05)。结论:未成熟缺血心脏常温钾维普停搏保护效果优于低温停搏。     

缺血预处理合并低温及晶体停搏液对兔未成熟心肌的保护作用

本文拟探讨缺血预处理(ischemic preconditioning,IP)合并低温及晶体停搏液对幼兔的离体心脏是否具有心肌保护作用.采用Langendorff离体心脏灌注模型,灌注液为Krebs-Henseleit液(K-H液).取3～4周龄幼兔心脏,在第一部分实验中分为Con、IP1、IP2、IP3组(n=6),分别给予0、1、2、3次IP,其后各组心脏均在20℃低温下停灌2 h,37℃常温下再灌注30 min.在第二部分实验中分为SConI、SCon2、SCon3、SIPl、SIP2、SIP3组(n=8),其中SIPl、SIP2、SIP3组给予2次IP后灌注St.Tho-mas Ⅱ晶体停搏液(CCS)使心脏停搏,然后分别使心脏在32℃、25℃、20℃下停灌30、90和120min,其后各组均在37℃再灌注30 min.SConl,SCon2,SCon3三组则不给予IP,继续灌注20min后灌注CCS使心脏停搏,然后分别在32℃、25℃、20℃下停灌30、90和120 min,其后各组均在37℃再灌注30 min.以Maclab/4 s生理实验系统记录平衡末、缺血前、再灌注后1、3、5、10、20、30 min时心率(HR)、左心室发展压(LVDP)以及左心室内压上升及下降最大速率(±dp/dtmax),测定再灌注末心肌组织中ATP和丙二醛(MDA)的含量,以及超氧化物歧化酶(SOD)的活性.在20℃低温停灌且停灌期间不给予CCS时,再灌注末IP2组LVDP×HR、+dp/dtmax和-dp/dtmax的恢复率分别为96%±21%、101%±19%和84%±15%,显著高于Con组和IP3组(P＜0.01,P＜0.05);心肌组织的ATP含量亦高于Con组(P＜0.01).在不同低温停灌且停灌期间给予CCS时,再灌注末SIP1、SIP2组的LVDP×HR、+dp/dtmax分别恢复到87%±14%、99%±26%(P＜0.05,vs SConl group)和87%±16%、102%±20%(P＜0.05,vs SCon2 group);心肌组织的ATP含量均分别显著高于SCon1组和SCon2组(P＜0.05),心肌组织MDA含量亦分别低于SCon1组和SCon2组(P＜0.05).上述结果提示,IP对在20℃低温停灌的兔未成熟心脏具有一定的心肌保护作用,2次IP的保护效应优于1次或3次IP.在停灌期间应用CCS,IP的心肌保护作用随停灌期间低温程度的升高而减弱.     

重症患者急救插管预氧合的临床研究

目的:观察预氧合在ICU重症患者急救插管中的效果并探讨预氧合的最佳方式。方法:选择ICU内低氧血症成年危重患者28例,按入ICU顺序随机分为3组:A组(对照组,n=10),B组(气囊-面罩预氧合组,n=9)和C组(麻醉机-面罩预氧合组,n=9)。A组入室后即行快速气管插管,B组气囊-面罩预氧合5 min后行气管插管,氧流量为15 L/min。C组麻醉机-面罩预氧合5 min后行气管插管,氧流量为4 L/min。观察指标:持续脉搏血氧饱和度(SpO2),动脉血气分析及相关并发症。结果:三组在预氧合之前,各项基本指标比较无统计学差异。在预氧合后,B、C组的SpO2明显高于A组(P0.05);在插管后即刻,B、C组的SpO2也显著高于A组(P0.05),同时C组SpO2高于B组(P0.05)。血气分析中,预氧合后,C组的PaO2和SaO2均高于A、B组(P0.05);在插管后即刻,C组PaO2和SaO2高于A组,同时C组SaO2高于B组(P0.05)。并发症的比较上,C组的腹胀发生率明显低于B组(P0.05)。结论:ICU内急救插管前的预氧合能显著提高患者的血氧水平,效果明显好于直接气管插管;在预氧合的方式中,麻醉机-面罩的预氧合效果要优于常规使用的气囊-面罩,且并发症也较少。     

血清神经功能指标及心肌酶谱在病毒性脑炎患儿中的变化研究

目的观察血清神经功能指标及心肌酶谱在病毒性脑炎患儿中的变化,分析其在病情判断中的意义。方法 2014年1月~2015年10月在我院就诊的病毒性脑炎患儿123例,根据临床病情的轻重分为轻症病脑组(n=87)和重症病脑组(n=36),并选取同时期健康儿童30例作为对照组,比较各组间血清神经功能指标及心肌酶谱水平差异。结果病毒性脑炎患儿血清神经功能相关指标S100B、NSE、MBP、NGF水平和心肌酶谱相关指标CK、CK-MB、AST、LDH水平显著高于对照组(均P0.05),而且重症病脑组患儿血清中神经功能相关指标S100B、NSE、MBP、NGF水平和血清心肌酶谱相关指标CK、CK-MB、AST、LDH水平均显著高于轻症病脑组(均P0.05)。经治疗后,患儿各指标水平均有下降,入院后第1、2周S100B、NSE、MBP、NGF水平均显著低于治疗前(均P0.05)。结论在病毒性脑炎的诊疗中,神经功能指标和心肌酶活性均能用作判断疾病严重程度及转归的重要指标。     

盐酸右美托咪定对快通道麻醉患儿血清CRP、PCT、LD、NSE的影响及脑保护作用研究

目的:研究盐酸右美托咪定对快通道麻醉患儿血清C反应蛋白(CRP)、降钙素原(PCT_)、血清乳酸(LD)、神经特性性元烯醇化酶(NSE)的影响及脑保护作用。方法:选择2016年4月至2017年4月在我院进行麻醉手术的61例患者,以抛硬币的方式将其均分为观察组(31例)和对照组(30例)。观察组患者给予盐酸右美托咪定(艾贝宁)行快通道麻醉,而对照组患者采用常规药物行快通道麻醉,比较两组患者治疗前后血清CRP、PCT_水平,T_0(术前1天)、T_1(术后1天)、T_2(术后2天)、T_3(术后3天)、T_4(术后4天)时点血清LD、NSE、脑动静脉血糖差(Ca-j)、乳酸差(AVDL)、脑氧摄取率(O_2Ext)、动脉颈静脉血氧浓度差(Ca-jvO_2)及动脉氧浓度(CaO_2)水平。结果:治疗后,观察组患者的血清CRP及PCT_水平明显低于对照组(P0.05)。在T_1-T_4各时点,观察组患者的血清LD水平显著低于对照组(P0.05);在T_3时,观察组患者的血清NSE水平、Ca-j及AVDL水平均显著低于对照组,而O_2Ext、Ca-jvO_2及CaO_2水平均显著高于对照组(P0.05)。结论:与常规药物进行快通道麻醉相比,艾贝宁快通道麻醉可显著降低患儿血清CRP、PCT_、LD及NSE水平,且能有效改善患儿的脑组织代谢。     

亚低温治疗对重型颅脑损伤患者颅内压、脑血流及氧代谢的影响

目的:探讨亚低温治疗对重症颅脑损伤(sTBI)患者颅内压(ICP)、脑血流及氧代谢的影响。方法:收集50例sTBI患者随机分为实验组和对照组,每组25例,均给予常规治疗,观察组在常规治疗基础上给予亚低温辅助治疗,检测患者治疗前、治疗第3、5、7天ICP动态变化以及治疗前和治疗7天后脑血流和氧代谢等指标变化。结果:治疗第3、5、7天ICP组间差异均具有统计学意义(P0.05),随着治疗时间增加两组ICP均逐渐降低,差异具有统计学意义(P0.05);治疗前Qmean、Vmean、Wv、DR等组间差异无统计学意义(P0.05),治疗7天后Qmean、Vmean均升高,Wv、DR均降低,差异具有统计学意义(P0.05);治疗前SjvO_2、CjvO_2、CaO_2、CERO_2组间差异无统计学意义(P0.05),治疗7天后SjvO_2、CjvO_2、CERO_2均升高,CaO_2降低,差异具有统计学意义(P0.05)。结论:亚低温治疗可以显著降低患者颅内压,改善脑血流和氧代谢水平。     

近红外光谱技术在猫脑射频热凝毁损中的应用研究

目的:探索近红外光谱(nears)技术用于立体定向靶点毁损术中实时监测的可行性。方法:利用猫脑建立体内不同毁损时间、温度下的毁损灶体积模型,通过病理检测及近红外光谱仪观察并记录脑组织靶点毁损时的NIRS尤其是优化散射系数()的变化情况。结果:不同温度、不同时间温度点下NIRS出现特征性变化曲线。并建立时间、温度及三维模型。结论:利用NIRS实时活体在位监测猫脑射频神经核团毁损术是科学、可行的,优化散射系数是监测的良好指标,比以往单凭经验的作法更科学、更准确。     

硬膜外局部低温与全身低温并发症的对比研究

目的:探讨硬膜外局部低温的并发症情况.方法:SD大鼠随机分为常温对照组(Nor组)、硬膜外局部低温组(LH组)和全身低温组(SH组),LH组以自制降温线圈贴附于一侧硬膜外实施局部低温,SH组以冰袋和酒精全身降温,两组均使脑温降至31.0-32.0℃并持续10小时.实验中观察大鼠寒战反应,监测脑温、肛温及呼吸、心率、血压变化,于降温末取血进行血气分析、电解质、血常规及血液流变学检测.结果:降温后,LH组和SH组脑温均下降到目标温度并维持稳定.降温过程中,SH组寒战发生率为57.1%,且出现心率下降,血小板降低,高切变率全血粘度和血浆粘度增高,LH组未观察到如上变化.结论:硬膜外局部降温可达到与全身降温一样的降温效果,而与全身低温相比,硬膜外局部低温并发症更少.     

低温对大鼠海马脑片缺氧无糖损伤的保护作用及其与Glu受体的关系

目的:探讨低温对离体大鼠海马脑片缺氧无糖(oxygen and glucose deprivation,OGD)损伤的保护作用及其机制.方法:①观察大鼠海马脑片在OGD条件下顺向群峰电位(orthodromic population spike,OPS)的变化及温度对它的影响.②观察谷氨酸(Glu)对海马脑片OPS的影响及低温的抗Glu毒性作用.并在人工脑脊液(ACSF)中分别加入GABA-R的特异性阻滞剂bicuculline(BMI)和NMDA-R的特异性阻滞剂D-(-)-2-Amino-5-phospho-nopentanoic Acid(AP5)或加入BMI和非NMDA-R阻滞剂6,7-Dinitroquinoxaline-2,3(1H,4H)-dione(CNQX)来观察低温对海马脑片OGD损伤保护作用的突触后受体机制.③观察OGD1h后海马CA1区锥体细胞超微结构的变化及低温对其的影响.结果:①OGD可以使海马脑片OPS迅速降低并很快消失,14 min后复氧供糖OPS极少恢复.低温(32℃、25℃)能使OPS消失时间明显延长,复氧供糖后OPS恢复良好.25℃其作用优于32℃.②2 mmol/LGlu使海马脑片OPS迅速消失,洗出后难以恢复.低温(3 2℃、25℃)能显著改善去Glu 1h后OPS的恢复.ACSF中加入BMI CNQX和BMI AP5均对25℃低温处理28min的脑保护作用没有影响.③OGD1h后CA1区锥体细胞水肿严重,胞浆内细胞器变性坏死脱失,线粒体肿胀,脊呈空泡状.低温(25℃)组细胞核膜规则,线粒体轻度肿胀.结论:低温有显著的抗脑OGD损伤作用,其作用机制可能与抗Glu的兴奋性毒性作用和维持细胞内ATP水平有关.而其抗兴奋性毒性作用可能既有NMDA-R又有非NMDA-R的参与.     

Alteration in the distribution of organ perfusion following profound hypothermia and circulatory arrest in the baboon.

The physiologic consequences of profound hypothermic circulatory arrest in infants are incompletely understood. Immature baboons underwent surface cooling, followed by core cooling using cardiopulmonary bypass, circulatory arrest for 30 min, and perfusion rewarming. Blood flow to and within organs was studied using the multiple-radionuclide-label microsphere technique. Marked redistribution of total and regional myocardial and cerebral flow occurred during cooling and rewarming.     

Inhaled carbon monoxide provides cerebral cytoprotection in pigs

Carbon monoxide (CO) at low concentrations imparts protective effects in numerous preclinical small animal models of brain injury. Evidence of protection in large animal models of cerebral injury, however, has not been tested. Neurologic deficits following open heart surgery are likely related in part to ischemia reperfusion injury that occurs during cardiopulmonary bypass surgery. Using a model of deep hypothermic circulatory arrest (DHCA) in piglets, we evaluated the effects of CO to reduce cerebral injury. DHCA and cardiopulmonary bypass (CPB) induced significant alterations in metabolic demands, including a decrease in the oxygen/glucose index (OGI), an increase in lactate/glucose index (LGI) and a rise in cerebral blood pressure that ultimately resulted in increased cell death in the neocortex and hippocampus that was completely abrogated in piglets preconditioned with a low, safe dose of CO. Moreover CO-treated animals maintained normal, pre-CPB OGI and LGI and corresponding cerebral sinus pressures with no change in systemic hemodynamics or metabolic intermediates. Collectively, our data demonstrate that inhaled CO may be beneficial in preventing cerebral injury resulting from DHCA and offer important therapeutic options in newborns undergoing DHCA for open heart surgery.     

Rewarming from severe accidental hypothermia with circulatory arrest

This case report demonstrates successful cardiopulmonary and cerebral resuscitation (CPCR) of a young male explored 15 hours following a suicide attempt (carbamazepine intoxication) in deep hypothermia (19 degrees C) with circulatory arrest. An extracorporeal circuit was used to rewarm the patient's blood. Weaning from extracorporeal circulation (ECC) was successful and without complications as was recovery from multiorgan dysfunction, severe rhabdomyolysis and carbamazepine intoxication. An excellent outcome was achieved without any neurological deficit at the time of discharge from the hospital.     

乌司他丁对体外循环法洛四联症患儿围心脏手术期循环和呼吸功能的影响

目的:探讨乌司他丁对体外循环法洛四联症患儿围心脏手术期循环和呼吸功能的影响。方法:选取我院于收治的60例法洛四联症婴幼儿参与研究,并将其随机分为对照组和试验组两组,每组患儿30例。其中试验组患儿在体外循环前以及患儿进行手术后的三天内每天均给予10000U/kg乌司他丁,而对照组患儿则在相应的时间点给予等量的生理盐水。分析比较两组患儿的体外循环时间、心脏停搏时间、手术时间、在监护室治疗的时间以及患儿术后住院时间和患儿肺部感染发生例数等临床病理情况。结果:所有入选患儿均痊愈出院,在两组患儿的手术操作情况和治疗效果对比中,对照组患儿的手术时间、体外循环时间和心脏停搏时间均显著低于试验组患儿,但重症监护时间及术后住院时间则高于试验组患儿;在两组患儿治疗后的循环功能指标比较中,试验组患儿超滤后CVP和血管活性药物均低于对照组患儿而超滤后MAP则显著高于对照组患儿;在两组患儿治疗后的呼吸功能指标的比较中,试验组患儿的动脉血氧分压明显高于对照组患儿以及试验组患儿的术后机械通气时间和肺部感染例数均低于对照组患儿,两组患儿的数据比较差异除手术时间、体外循环时间和心脏停搏时间外均具有统计学意义(均P0.05)。结论:乌司他丁对体外循环法洛四联症患儿围心脏手术期的循环和呼吸功能具有较好的保护作用,值得在临床上加以广泛推广和运用。     

Accidental deep hypothermia with cardiac arrest. Prompt complete recovery after rewarming by extracorporeal circulation. Case report

BACKGROUND: Deep accidental hypothermia (core temperature <28 degrees C) is an uncommon medical emergency requiring rapid active core rewarming. Extracorporeal circulation has become the treatment of choice for deep hypothermic patients with cardiac arrest. CASE REPORT: We report on a 30-year-old patient who suffered from deep accidental hypothermia (core temperature 24.8 degrees C) and cardiac arrest by prolonged exposure to a cold urban environment as a consequence of severe ethylalcohol intoxication. The rewarming with the aid of extracorporeal circulation was initiated shortly after his arrival at the hospital. External cardiac massage was maintained until full ECC fl ow was established. The patient was weaned from extracorporeal circulation after 157 min, awaked 4 hours later and consequently extubated within 16 hours after rewarming with no neurological impairment. At 3-week follow-up, the patient was fully re-integrated in his work and personal life. CONCLUSION: This case demonstrates the excellent prognosis of a young victim in the case of deep accidental hypothermia with cardiac arrest, provided that deep hypothermia precedes the cardiac arrest and rewarming by extracorporeal circulation is immediately applied. Simultaneous ethyl alcohol intoxication can be considered a protective factor improving the patient's outcome. Complete recovery was achieved within 24 hours after the accident.     

Perfusion cérébrale,non prévue,en cours de CEC dans les dissections aortiques

Acute aortic dissections constitute major cardiovascular emergencies. In 30% of patients, intimal tear stands on the aortic arch. The need for a partial or a total aortic arch replacement under circulatory arrest requires the use of cerebral protection i.e. deep hypothermia, retrograde cerebral perfusion via the superior vena cava, selective antegrade cerebral perfusion.In this situation, we consider selective antegrade cerebral perfusion under mild hypothermia (23-25 °C) because it provides good cerebral protection with a low incidence of neurologic complications (4% of transient accidents and 4% of fixed deficits), allows a safe circulatory arrest beyond 45 minutes and is also rather easy to perform especially if the location of the tear on the arch is an operative findings.Operative mortality for acute dissections remains high, 28% to 49% in literature data. Neurological complications may occur despite cerebral protection. These complications may influence both vital and functional prognosis.     

Effect of Mild Hypothermia on the Coagulation-Fibrinolysis System and Physiological Anticoagulants after Cardiopulmonary Resuscitation in a Porcine Model

The aim of this study was to evaluate the effect of mild hypothermia on the coagulation-fibrinolysis system and physiological anticoagulants after cardiopulmonary resuscitation (CPR). A total of 20 male Wuzhishan miniature pigs underwent 8 min of untreated ventricular fibrillation and CPR. Of these, 16 were successfully resuscitated and were randomized into the mild hypothermia group (MH, n = 8) or the control normothermia group (CN, n = 8). Mild hypothermia (33°C) was induced intravascularly, and this temperature was maintained for 12 h before pigs were actively rewarmed. The CN group received normothermic post-cardiac arrest (CA) care for 72 h. Four animals were in the sham operation group (SO). Blood samples were taken at baseline, and 0.5, 6, 12, 24, and 72 h after ROSC. Whole-body mild hypothermia impaired blood coagulation during cooling, but attenuated blood coagulation impairment at 72 h after ROSC. Mild hypothermia also increased serum levels of physiological anticoagulants, such as PRO C and AT-III during cooling and after rewarming, decreased EPCR and TFPI levels during cooling but not after rewarming, and inhibited fibrinolysis and platelet activation during cooling and after rewarming. Finally, mild hypothermia did not affect coagulation-fibrinolysis, physiological anticoagulants, or platelet activation during rewarming. Thus, our findings indicate that mild hypothermia exerted an anticoagulant effect during cooling, which may have inhibitory effects on microthrombus formation. Furthermore, mild hypothermia inhibited fibrinolysis and platelet activation during cooling and attenuated blood coagulation impairment after rewarming. Slow rewarming had no obvious adverse effects on blood coagulation.     

Differential cerebral hypothermia

Differential cerebral hypothermia was induced in these experiments by isolating the cerebral circulation in the halothane-anesthetized goat. The brain was perfused through isolated cerebral branches of the internal maxillary artery using a height-adjusted reservoir system which provided a constant inflow pressure. Cerebral blood flow (CBF) and cerebral O₂ metabolic rate (CMRO₂) were measured continuously as brain temperatures were decreased from 38 to 28, 18 and 8 °C and during rewarming. Arterial blood gases were maintained constant. During hypothermia CBF decreased at brain temperatures of 28 °C and did decrease further at 18 or 8 °C. CMRO₂ decreased linearly from 38 to 8 °C and was 7% control levels at 8 °C. CBF and CMRO₂ returned to control levels upon rewarming. Cerebral lactate metabolism did not change significantly during hypothermia or rewarming. Evoked cortical potentials were abolished at 8 °C but recovered upon rewarming. These results indicate that if adequate brain perfusion is maintained during hypothermia and rewarming, recovery of CBF, metabolism, and brain neural activity can be obtained.     

Recover of peripheral nerve function after prolong hypothermic cardiac arrest in a porcine model with extra corporeal life support

ObjectivesSurviving long lasting cardiac arrest following accidental hypothermia has been reported after treatment with extra corporeal life support (ECLS), but there is a risk of neurologic injury. Most surviving hypothermia patients have a prolonged stay in the intensive care unit, where most patients experience polyneuropathy. Theoretically, accidental hypothermic cardiac arrest may in itself contribute to polyneuropathy. This study was designed to examine the impact of three hours of cardiac arrest at a core temperature of 20 °C followed by reanimation of peripheral nerve function.MethodsSeven pigs were cannulated for ECLS and cooled to a core temperature of 20 °C followed by three hours of circulatory arrest where the extremities were packed with ice. After three hours, ECLS was started and rewarming was performed. During the process, neural testing of the ulnar nerve (a somatic nerve) and of the vagus nerve (an autonomic nerve) were performed and blood was drawn for analysis of p-potassium, serum-neuron-specific enolase, and S100b protein.ResultsThe ulnar nerve was cooled from 34.9±1.6 °C to 12.8±3.8 °C and the vagus nerve from 36.2±1.2 °C to 15.4±1.4 °C. Physiologic function of both somatic and autonomic nerves were strongly affected by cooling, but recovered to almost normal levels during rewarming, even after three hours of hypothermic cardiac arrest. P-potassium rose from 3.9 (3.6–4.6) mmol/l to 8.1 (7.2–9.1) mmol/l after three hours of cardiac arrest, but normalized after recirculation. There was no rise in serum-neuron-specific enolase, but a slight rise in S100b protein during three hours of hypothermic cardiac arrest was observed. All pigs obtained return of spontaneous circulation (ROSC).ConclusionsReanimation after three hours of hypothermic cardiac arrest using ECLS was possible with no or, if present, minor damage to the two nerves tested.     

Prolonged suspended animation in puppies

Three groups of a total of 26 puppies were subjected to surface-induced hypothermia with or without limited left-heart bypass to seek recovery after 2.5-hr total circulatory arrest. In spite of various protective measures, surface-induced hypothermia which was carried out until the effective circulation ceased, failed to protect the animal from 2.5-hr circulatory arrest. With a combination of limited leftheart bypass, the central nervous tissue tolerated the procedure better than expected. Metabolic derangements, although severe immediately after the procedure, were reversible. Respiratory distress was a serious problem, which was considerably alleviated in the 3rd group of 10 puppies by perfusion of the lung with a solution approximating the intracellular electrolyte composition. Six puppies of this group survived the procedure, 5 without any persistent disorders. These results indicate the possibility of 2.5-hr hypothermie circulatory arrest.