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.     

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…

探讨头部亚低温对心脏聚停犬超氧化物歧化酶和脂质过氧化物的影响。为脑复苏过程中开展亚低温治疗提供依据。采用放射免疫分析法和硫代巴比妥酸法分别测定犬心脏聚停前苏后常温及头部亚低情况下血清及脑脊液ＳＯＤ和ＬＰＯ水平。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。     

心脏骤停复苏后低温林格氏液诱导亚低温治疗的实施与护理探讨

目的 探讨低温林格氏液对心脏骤停复苏后患者进行亚低温治疗的效果及安全性.方法 选取2011年1月至2014年12月本院急诊科心脏骤停复苏后患者36例,按照随机数字排列表进行随机分组,分别为对照组和观察组.对照组采用常规冰帽方法降温,观察组采用林格液诱导亚低温,比较两组患者各项基本生命体征、降温成功率、IH-TT及三个月随访的脑功能.结果 观察组的SpQ2高于对照组;降温成功率(94.44%)高于对照组(33.33%);IH-TT值低于对照组,脑功能恢复较好(44.44%)的患者多于对照组(27.78%),且P<0.05,差异具有统计学意义.结论 静脉输注低温林格液诱导亚低温对患者进行脑组织保护治疗安全有效,是心脏骤停后心肺复苏的重要措施.而密切观察患者生命体征、预防肺水肿,降温过程中防治寒颤、缓慢复温是保证治疗实施的护理重点.     

亚低温治疗在急诊心脏骤停患者复苏后优化治疗中应用观察

目的:观察分析亚低温治疗在急诊心脏骤停患者复苏后优化治疗中的应用.方法:选取2018年12月～2019年12月急救收治的急诊心脏骤停患者98例为研究对象,按随机数字表法分成观察组与对照组,各49例.两组均实施急救后,对照组给予常规头部冰帽降温,观察组给予亚低温治疗.比较两组患者脑功能分级、急性生理与慢性健康状况评分Ⅱ评...     

代谢组学的进展及肝脏代谢组学

代谢组学是一门新兴的学科,最早来源于代谢轮廓分析,随着基因组学的提出和迅速发展,代谢组学将基因产物和基因关联起来,实现基因功能的鉴定,成为功能基因组学研究的有力工具。代谢组学是研究生物体系(细胞、组织或生物体)受外部刺激所产生的所有代谢产物的变化的科学,关注的对象是分子量1000以下的小分子化合物。在临床上,它是以组群特征分析为基础,以高通量分离、检测和数据处理为手段,主要应用包括发现疾病机理,开发新的更加准确的疾病诊断方法,发现跟疾病相关的生物标志物等。代谢组学有以下优点:①检测更容易;②不需要特征化的数据库;③种类少;④代谢产物具有通用性。     

代谢组学与运动疗法的研究策略

代谢组学包括组织细胞代谢组(metabolome)和系统整体代谢组(metabonomel)，是自人类基因组计划(human genome pmiect，HGP)以来迅速发展起来的以组群指标分析为基础、以高通量(high-throughputl检测和数据处理为手段、以信息建模与系统整合为目标的系统生物学(system biologyl的新兴学科。运动疗法研究热点之一是代谢调节，     

偏头痛大鼠的尿液代谢组学研究

目的:通过代谢组学方法,观察大鼠尿液中的代谢物的变化,探讨偏头痛可能的发病机制。方法:实验选用SPF级Wistar大鼠20只,体重(200±20)g左右,随机分为空白组和模型组,每组10只。采用改进的Christina Tassorelli方法复制偏头痛模型,采用代谢笼法,收集大鼠造模后6 h尿液。采用超高效液相色谱和高分辨率质谱联用(UPLC-Q-TOF/MS)技术对偏头痛大鼠尿样进行代谢图谱检测。结果:与空白组的尿液相比,模型组的代谢图谱中出峰量明显增加。空白组样本和模型组样本具有一定的聚类作用,分类运动的趋势明显。从总体趋势来看,相对于空白组,模型组的代谢特征有逐渐向右运动的趋势。对模型组样本与空白组样本所得的荷载图进行分析,发现尿中5-羟吲哚乙酸、1,3-二硝酸甘油、顺乌头酸、苹果酸明显增多。结论:尿中5-羟吲哚乙酸、1,3-二硝酸甘油、顺乌头酸、苹果酸可以作为偏头痛潜在的生物标志物。     

一例严重哮喘致心脏骤停行亚低温脑复苏的护理

严重哮喘可致呼吸衰竭,患者在送往医院救治途中即可出现心脏骤停。随着心肺脑复苏技术的发展,心脏骤停后心肺脑复苏技术水平已有明显提高,但复苏过程中脑保护问题仍未彻底解决。本文报道一例在抢救重度哮喘所致心脏骤停患者时,应用经股静脉置入双腔导管体行外循环亚低温治疗措施,成功地进行了脑保护,疗效满意。     

1例心搏骤停复苏后患者的人工亚低温循证治疗

目的为1例心搏骤停复苏后昏迷患者制定人工亚低温循证治疗方案。方法针对提出的临床问题，检索Medline（1981—2006年）和Cochrane图书馆（2006年第2期）。结果检索发现，关于心搏骤停复苏后人工亚低温治疗RCT3篇和SR1篇，通过分析检索结果、结合临床医生经验及患者实际情况，为患者制定了循证治疗方案，通过6个月随访发现证实，该方案适合患者。结论对心搏骤停复苏后昏迷者，采用人工亚低温治疗可改善患者的预后。     

Influence of mild therapeutic hypothermia on the inflammatory response after successful resuscitation from cardiac arrest

Purpose

Although animal studies document conflicting data on the influence of hypothermia on cytokine release in various settings, no data exist if hypothermia affects the inflammatory response after successful cardiopulmonary resuscitation.

Materials and Methods

Arrest- and treatment-related variables of 71 patients were documented, and serum samples were analyzed for levels of interleukin 6, tumor necrosis factor-α, C-reactive protein, and procalcitonin immediately after hospital admission and after 6, 24, and 120 hours. At day 14, patients were dichotomized in those with good and bad neurological outcome.

Results

Regardless of outcomes, interleukin 6 levels were significantly elevated by the use of hypothermia (n = 39). The rate of bacterial colonization was significantly higher in hypothermic patients (64.1 vs 12.5 %; P < .001). On the contrary, procalcitonin levels were, independent of the use of hypothermia, only significantly elevated in patients with bad neurological outcome. Hypothermic patients showed a strong trend to reduced mortality. However, there was no influence on neurological recovery.

Conclusions

In this observational study, hypothermia influenced the inflammatory response after cardiopulmonary resuscitation and lead to a higher rate of bacterial colonization without altering ultimate neurologic recovery.     

不同降温方法对大鼠心肺脑复苏的作用

目的研究亚低温脑复苏时不同降温方法的效果及对大鼠脑的保护作用。方法建立心肺复苏模型，SD大鼠45只，分成对照组、常温复苏组及低温复苏A组（体表降温）、低温复苏B组（0．5ml·kg^-1·min^-1静注4℃ NS）、低温复苏C组（0．5ml·kg^-1·min^-1静注4℃NS结合体表降温）、低温复苏D组（1ml·kg^-1·min^-1静注4℃NS）和低温复苏E组（1ml·kg-^1·min^-1静注4℃NS结合体表降温），分别观察各组血清及大脑皮质SOD、MDA、NO、Na^＋ K^＋ -ATP酶及P53、Bax、Bcl-2表达和脑组织含水量比。结果低温复苏各组均能达到亚低温状态，特别是低温复苏D、E组达到亚低温状态仅需（26．71±4．65）min及（10．00±2．52）min。低温复苏D组脑组织含水量比、MDA、NO、P53和Bax光密度值分别为（79．58±0．40）％、（14．16±2．36）nmol／gprot、（35．28±4．94）μmol／gprot、（0．0136±0．0001）和（0．0304±0．0019），低温复苏E组分别为（79．46±0．30）％、（10．30±3．16）nmol／gprot、（33．18±4．93）μmol／gpmt、（0．0134±0．0040）和（0．0323±0．0029）．均较常温复苏组明显下降（P〈0．05）。低温复苏D组脑组织SOD、Na^＋ K^＋ -ATP酶分别为（114．45±3．07）U／mgprot、（30．50±2．06）μmolpi／（mgpnt·hour），低温复苏E组分别为（114．45±8．11）U／mgprot、（28．10±5．67）μmolpi／（mgpnt·hour），均较常温复苏组明显升高（P〈0．05）。结论静脉快速灌注冷生理盐水或同时结合体表降温均能在较短的时间内达到理想的亚低温状态并产生良好的脑保护效果。     

亚低温对家兔心搏骤停复苏前后脑内兴奋性氨基酸水平的影响

目的：检测亚低温对家兔心搏骤停心肺复苏前后脑内兴奋性氨基酸水平的影响。方法：采用家兔室颤致心搏骤停5min再复苏模型,观察2h.18只家兔随机分为3组：A组为正常对照组（n=6),B组为常温复苏组（n=6),C组为亚低温复苏组（n=6)采用腹腔冷灌注法。结果：与A组相比,B、C两组脑内兴奋性氨基酸水平有非常显著的升高（P＜0．01）;C组与B线相比,脑内兴奋性氨基酸水平有显著降低（P＜0．05）。结论：亚低温能显著降低心搏骤停后脑内兴奋性氨基酸水平,是亚低温脑保护的重要机制之一。     

亚低温对心脏外科术后低心排的治疗评价

目的 探讨亚低温对心脏外科术后低心排的治疗价值及其疗效.方法 选择2009年5月至2011年2月本院心脏外科术后应用大剂量血管活性药物及主动脉内球囊反搏术(IABP)治疗仍存在低心排,而给予亚低温治疗的患者12例.监测患者亚低温治疗前后心排血指数(Cl)、混合静脉血氧饱和度(S-vO2)、尿量的变化等.结 果在应用亚低温治疗过程中,将患者膀胱温度降至33～ 35℃以降低组织的氧需求.与治疗前比较,经亚低温治疗后患者CI(ml·s-1·m-2)明显增加(38.34±5.00比30.01±5.00),S-vO2明显升高(0.64±0.07比0.54±0.08),尿量(ml·kg-1·h-1)明显增加(3.0±2.1比1.5±1.1,均P＜0.05);而心率、平均动脉压、动脉血氧分压则无明显改变.结论 亚低温治疗可有效改善心脏外科术后低心排患者循环功能,且操作简单.     

Minimal effects on ex vivo coagulation during mild therapeutic hypothermia in post cardiac arrest patients

Objectives

Mild therapeutic hypothermia (MTH) is being used to improve neurological outcome and survival in patients successfully resuscitated after cardiac arrest. The impact on coagulation may be difficult to assess since most coagulation parameters are measured at 37 °C and not at actual body core temperature. Therefore we investigated the effects of MTH both at body core (target) temperature of 32 °C and at 37 °C.

Methods

Patients admitted at the ICU after cardiac arrest treated with MTH. Baseline blood samples, measured at 37 °C were taken directly at arrival. The second and third samples were drawn within 1 h and 24 h after reaching target temperature and were measured at 32 °C and 37 °C. A final sample was drawn when the patient returned to normotemperature (measured at 37 °C). Clotting time (CT) and maximum clotting formation (MCF) were measured with thromboelastometry.

Results

Upon reaching target temperature (32 °C) Extem and Intem CT were increased compared to baseline with 57 s (49–75) to 65 s (59–72) and 165 s (144–183) to 193 s (167–212) respectively (median with IQR; P < 0.05), with a further significant increase after 24 h of hypothermia with 68 s (57–80) and 221 s (196–266). Samples analyzed at 32 °C showed a significant longer CT of 12 s in Extem and 33 s in Intem compared to 37 °C. MCF was not affected by MTH or adjustment of temperature.

Conclusion

The mild effect of MTH on coagulation parameters remains unidentified when measured at 37 °C. Although measurements at 32 °C differ from those at 37 °C, this does not appear to be of clinical relevance as all values were still within the reference range.     

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     

Effects of adenosine monophosphate on induction of therapeutic hypothermia and neuronal damage after cardiopulmonary resuscitation in rats

Background

Animal studies and pathophysiological considerations suggest that therapeutic hypothermia after cardiopulmonary resuscitation is the more effective the earlier it is induced. Therefore this study is sought to examine whether pharmacological facilitated hypothermia by administration of 5′-adenosine monophosphate (AMP) is neuroprotective in a rat model of cardiac arrest (CA) and resuscitation.

Methods

Sixty-one rats were subjected to CA. After 6 min of ventricular fibrillation advanced cardiac life support was started. After successful return of spontaneous circulation (ROSC, n = 40), animals were randomized either to placebo group (n = 14) or AMP group (800 mg/kg body weight, n = 14). Animals were kept at an ambient temperature of 18 °C for 12 h after ROSC and core body temperature was measured using a telemetry temperature probe. Neuronal damage was analyzed by counting Nissl-positive (i.e. viable) neurons and TUNEL-positive (i.e. apoptotic) cells in coronal brain sections 7 days after ROSC. Functional status evaluated on days 1, 3 and 7 after ROSC by a tape removal test.

Results

Time until core body temperature dropped to <34.0 °C was 31 min [28; 45] in AMP-treated animals and 125 min [90; 180] in the control group (p = 0.003). Survival until 7 days after ROSC was comparable in both groups. Also number of Nissl-positive cells (AMP: 1 [1; 7] vs. placebo: 2 [1; 3] per 100 pixel; p = 0.66) and TUNEL-positive cells (AMP: 56 [44; 72] vs. placebo: 53 [41; 67] per 100 pixel; p = 0.70) did not differ. Neither did AMP affect functional neurological outcome up to 7 days after ROSC. Mean arterial pressure 20 min after ROSC was 49 [45; 55] mmHg in the AMP group in comparison to 91 [83; 95] mmHg in the control group (p < 0.001).

Conclusion

Although application of AMP reduced the time to reach a core body temperature of <34 °C neither survival was improved nor neuronal damage attenuated. Reason for this is probably induction of marked hypotension as an adverse reaction to AMP treatment.     

Therapeutic hypothermia after cardiopulmonary resuscitation

Full cerebral recovery after cardiopulmonary resuscitation is still a rare event. Unfortunately, up to now, no specific and outcome-improving therapy was available after such events. From several cases it is known that low body and brain temperature during a cardiocirculatory arrest improves the neurological outcome following these events. As it is not possible in acute events to induce hypothermia beforehand, whether cooling after the insult could also be protective was evaluated. After animal studies in the 1990s and first clinical pilot trials of mild therapeutic and induced hypothermia, two randomized trials of hypothermic therapy after successful resuscitation after cardiac arrest were conducted. These studies demonstrated that hypothermia after cardiac arrest could improve neurological outcome as well as overall mortality.