血脉素用于低血容量休克病人的救治

血脉素用于３２例低血容量性休克病人的术前救治，并监测输注前后血压、心率、ＳＰＯ２和尿量的变化。发现血脉素用于各种原因引起的低血容量性休克，具有升压效果好，逆转化克症状迅速，维持时间长，使用简单方便，副作用注等优点。对低血容量休克病人，可部分甚至全部代替输全血。     

上消化道和其他部位出血导致休克病人的心率变化研究

[目的]探讨上消化道大出血和其他部位大出血引起低血容量性休克时心率变化的不同及其原因。[方法]采用回顾性研究方法收集消化道大出血病人46例与其他部位大出血休克病人44例,在血压基本相同的情况下比较两组病人低血容量性休克时的心率变化。[结果]两组病人低血容量性休克时心率比较差异有统计学意义（P〈0.05）。[结论]上消化道大出血引起低血容量性休克时的心率变化低于其他部位大出血的心率变化。     

高渗盐水在低容量性休克中的应用

低血容量性休克包括失血性休克和创伤性休克两类。作为外科急症，其来势凶猛，如若抢救不及时，可危及生命。自1993年2月-1995年10月，我们用7．5％高渗盐水抢救低血容量性休克病人22例，均获成功，现报告如下。     

如何紧急诊治休克

休克可分为失血性休克、心源性休克、神经源性休克等。灾区伤员发生的休克大部分是低血容量性休克和神经源性休克，少部分为挤压后发生的感染中毒性休克和心源性休克。低血容量性休克多由大血管破裂、肝脾破裂、骨折等所致。神经源性休克系外伤、骨折、剧烈疼痛、精神创伤等所致。心源性休克主要因张力性气胸、心肌挫伤、心包填塞所致。     

休克与护理

休克是导致死亡的主要原因之一。休克的早期发现、及时对症治疗、挽救危重伤病员的生命,不仅是医生,更是护士的光荣职责。一般急诊常见休克有低血容量性休克,感染性休克,创伤性休克,心源性休克和过敏性休克,作为一名护士亦必须掌握其病因、先驱症状,临床表现及急诊处理方法。低血容量性休克急诊常见以低血容量性休克为多,其有关情况处理见表。     

休克病人的应急处置

作者论述了常见三种类型休克的特点、抢救和护理要点。尽管休克有多种原因 ,但病程大致相同 ,主要是导致有效循环血量降低和组织血液灌注不足 ,引发机体代偿机制 ,一旦没能及时补充氧气和有效循环液量就会导致病人机体失代偿 ,最后导致器官功能丧失和坏死。因此 ,迅速判断休克的类型 ,及时正确有效地抢救是使病人起死回生的关键。低血容量性休克　低血容量性休克是最常见的一种。由于软组织损伤、烧伤、呕吐、腹泻或失血 (包括胃肠道内出血 ) ,导致液体丢失 ,有效循环血量减少而引起低血容量性休克。因此 ,首先需给予心电监护和脉搏血氧计数…     

低血容量性休克增加家兔对内毒素作用的敏感性

目的：为阐明“二次打击”假说在创伤／休克后内源性感染发病中的病理意义，本研究探讨了低血容量性休克对轻度门静脉源性内素素血症的影响。方法：１８只动物分３组，即低血容量性休克组、脂多糖（ＬＰＳ）组和低血容量性休克＋ＬＰＳ组。结果：①输注完ＬＰＳ后，低血容量性休克＋ＬＰＳ组动物的血压持续下降，且明显低于单纯ＬＰＳ或单纯低血容量性休克组动物；而后两组动物的血压无明显变化。②休克后２４小时，低血容量性休克＋ＬＰＳ组动物全部死亡，而其余两组动物全部存活。③低血容量性休克＋ＬＰＳ组动物的血浆乳酸和β葡萄糖醛酸酶（βＧ）水平在输入ＬＰＳ后也显著升高，并明显高于单纯低血容量性休克组和单纯ＬＰＳ组。结论：低血容量性休克具有增加机体对内毒素敏感性的作用，继发于休克后的轻度内毒素血症在休克后器官功能损害中的作用不容忽视     

浅谈低血容量性休克护理观察

低血容量性休克包括失血性休克和创伤性休克，是外科最常见的休克，是导致病人死亡的重要原因之一。患者病情十分凶险、危急，需果断采取急救措施进行治疗。治疗主要是迅速补充血容量，迅速查明病因并制止继续出血或失液，根据病情决定是否使用升压药。对低血容量性休克患者的治疗与抢救，早期发现病情变化，及时给予处理，对抢救患者的生命，有着非常重要的意义。     

按照发病学，休克分哪4类？

答：按照发病学休克分4类。 （1）根据休克过程中血容量丢失的程度分为：低血容量性休克，正血容量性休克，共2类。 （2）根据休克时外周血管阻力的变化，可分为：高阻力型休克，低阻力型休克，共2类。     

低血容量性休克的诊断和治疗

各种不同类型的休克,如常见的失血性休克、创伤性休克、脓毒性休克皆可导致不同程度的血容量减少,而出现低血容量性休克。但失血性休克,因其直接的原因是由于急性大出血所致,故必然急剧地发生低血容量性休克。由于失血致静脉的回心血量减少,同时导致心肌的收缩力减弱,造成血流量下降,血流缓慢郁积,继而出现微循环障碍,微血管的灌流量大大     

Vasoactive intestinal peptide down-regulates the intrahepatic renin-angiotensin system in the anaesthetized rat.

Gastric sodium loading results in an increase in the portal venous concentration of vasoactive intestinal peptide (VIP) and down-regulation of both the intrahepatic and circulating renin-angiotensin systems. In the present study we sought to determine whether an increase in the concentration of VIP in the portal circulation might act to down-regulate the intrahepatic and/or circulating renin-angiotensin systems. Male Sprague-Dawley rats were infused intraportally with haemaccel vehicle or VIP in haemaccel for 60 min. Livers were harvested and blood was sampled. Angiotensin-converting enzyme (ACE) activity and angiotensinogen, angiotensin I, angiotensin II and renin concentrations were measured. VIP infusion decreased hepatic ACE activity (P < 0.05), the hepatic angiotensinogen concentration (P < 0.001) and the hepatic angiotensin I concentration (P < 0.05). The plasma angiotensinogen concentration and serum ACE activity were also decreased by intraportal VIP infusion (P < 0.05 for each). Plasma renin, angiotensin I and angiotensin II concentrations were unchanged by VIP infusion. We conclude that an increase in the portal venous VIP concentration down-regulates the intrahepatic renin-angiotensin system. These changes are similar to those reported after gastric sodium loading, and we suggest, therefore, that the increase in portal venous VIP that occurs after gastric sodium is the means by which the gastric sodium sensor signals the liver to effect these changes in the renin-angiotensin system.     

婴儿肠套叠整复术后并发感染性休克的护理

目的:分析婴儿肠套叠整复术后并发感染性休克的护理。方法:选取我院2010年10月~2013年10月收治的肠套叠整复术后并发感染性休克的患儿24例,对其进行针对于感染性休克的完善护理,比较护理前后婴儿的生命体征变化情况。结果:护理前后婴儿的心率、血压、血乳酸浓度比较差异均有统计学意义(P0.05)。结论:完善的护理措施可以对肠套叠整复术后并发感染性休克的婴儿起到很好的恢复作用,能够让婴儿恢复生命体征的正常,避免感染性休克危及婴儿生命。     

The value of immune modulating parameters in predicting the progression from peritonitis to septic shock

Intra-abdominal infection is one of the major causes of septic shock and multiple organ failure. To date, what causes the disease's progression remains unclear and therefore the relevance of immune modulating therapies remains speculative. The primary outcome measure of this study was to investigate immune modulating mediators at the onset of peritonitis before the development of subsequent septic shock. The secondary outcome measure was to investigate the usefulness of these immune parameters in predicting progression from peritonitis to septic shock. Fifty-eight peritonitis patients were included in this study: 14 patients subsequently developed septic shock. All patients were examined on "diagnosis of peritonitis" (<4 h within establishment of diagnosis), during "early septic shock" (<12 h following the onset of septic shock), and once again during "late septic shock" (within 72-98 h following the onset of septic shock). The immune modulating parameters tumor necrosis factor-alpha (TNF-alpha), the soluble TNF-alpha receptors I and II (sTNF-alpha RI and sTNF-alpha RII), interleukines (IL) -1beta, -6, -8, and -10, and the adhesions molecules endothelial-leukocyte-adhesion-molecule (E-Selectin), intercellular-adhesion-molecule-1 (ICAM-1), and vascular-adhesion-molecule-1 (VCAM-1), in addition to nitrate and nitrite, were determined. In the peritonitis group with subsequent septic shock, TNF-alpha, sTNF-alpha RI + RII IL-1beta, IL-8, IL-10, and nitrate were significantly increased before the onset of septic shock. TNF-alpha had an area under the receiver operating characteristics curve (AUC) of 0.84 and was reliable in predicting the progression from peritonitis to septic shock. The AUC of the other immune modulating parameters, despite being significantly elevated, ranged from 0.71 to 0.76. The AUC of the conventional laboratory markers such as leukocytes and C-reactive protein ranged from 0.64 to 0.68. In peritonitis that progressed to septic shock, an early immune response had already occurred before the onset of septic shock. The progression was best predicted by TNF-alpha. Therefore, mediator therapy might be considered in high-risk peritonitis patients who show an exaggerated immune response before the progression to septic shock.     

亚甲蓝对兔创伤性休克的干预作用

目的 观察亚甲蓝（MB）干预后，创伤性休克兔血浆一氧化氮（NO）、肿瘤坏死因子-α（TNF-α）、白细胞介素-6（IL-6）的变化和小肠、肝脏病理形态学改变，探讨MB对创伤性休克的作用机制。方法 18只大白兔随机分为假手术组、创伤性休克生理盐水复苏组（生理盐水复苏组）、创伤性休克MB处理组（MB处理组），每组6只。生理盐水复苏组及MB处理组记录休克前（T1）、休克末（T2）、复苏末（T3），复苏后0．5（T4）、2（T5）、4h（T6）血流动力学的动态变化，并测定血浆NO、TNF-α、IL-6水平，假手术组于相应时间点测定。实验结束后，3组动物均留取小肠、肝脏组织，观察病理形态学变化。结果 MB处理组血流动力学较生理盐水复苏组平稳（P〈0．05或P〈0．01）。创伤性休克后，血浆NO水平明显高于T1水平，生理盐水复苏组复苏后血浆NO进行性增高，于T4时达峰值水平，以后逐渐下降，但仍高于T1水平；MB处理组复苏后血浆NO明显降低；假手术组各时间点血浆NO无明显变化。创伤性休克后TNF-α及IL-6明显升高，而应用MB复苏后TNF-α及IL-6与T1时比较差异均无显著性，假手术组各时间点TNF-α及IL-6差异无显著性。生理盐水复苏组各脏器病理损害明显；MB处理组各脏器病理损害显著减轻；假手术组各脏器无明显病理损害。结论 NO、TNF-α及IL-6在创伤性休克的病理发展过程中起着重要作用，应用MB可降低血浆NO、TNF-α及IL-6的水平，明显改善创伤性休克血流动力学，保护重要脏器，有助于创伤性休克的改善。     

预处理对失血性休克大鼠肠系膜上动脉收缩反应性的影响

目的评价不同条件预处理对失血性休克血管功能的保护作用机制。方法采用大鼠失血性休克模型，观察不同条件预处理（失血预处理及吡哪地尔预处理）对由激动剂[去甲肾上腺素（NE）]诱导在体大鼠肠系膜上动脉（SMA）收缩反应性的影响。结果5％～10％失血预处理对休克大鼠存活率无显著改善，而吡哪地尔可明显改善休克后120min的大鼠存活率。5％失血预处理30min可上调大鼠休克后0min使用NE前后的股动脉压变化，而预处理24h可降低大鼠休克前股动脉压变化，但对休克后使用NE前后的股动脉压变化无明显影响；吡哪地尔预处理1h可降低大鼠休克前使用NE前后的股动脉压变化，而预处理24h对大鼠休克后的股动脉压变化均无影响。5％失血预处理24h可改善休克后120min大鼠SMA对NE的收缩反应性，使用NE后的管径变化显著增加（P〈0．01）；吡哪地尔预处理1h和24h可明显降低大鼠休克前SMA对NE的收缩反应性，使用NE后的管径变化显著降低（P均〈0．05），但吡哪地尔预处理（1h和24h）均可改善休克后120min大鼠SMA对NE的收缩反应性，使用NE后的管径变化显著增加（P均〈0．05）；而格列苯脲可部分取消吡哪地尔的这一作用。结论吡哪地尔预处理24h可降低休克前大鼠SMA对NE的收缩反应性，并可改善休克后120min大鼠SMA对NE的收缩反应性，且使休克大鼠存活率明显提高。吡哪地尔预处理24h对失血性休克大鼠血管功能的保护作用可能与ATP敏感性钾通道有关。     

Prevention of experimental endotoxin shock by a monocyte activator.

In patients with polytrauma or major surgery, severe bacterial infections leading to septic shock and multiorgan failure are still a major cause of death. Prevention of septic shock in patients at risk would be an alternative to treatment of patients with overt septic shock. We therefore conducted a trial with the monocyte activator muramyl tripeptide phosphatidylethanolamine (MTP-PE) in an experimental pig model. Liposome encapsulated MTP-PE (50 micrograms/kg of body weight) or liposomes alone were given intravenously at 72 or 24 h before endotoxemia was induced by lipopolysaccharide (LPS), simultaneously with the induction of endotoxin shock, or 1 h thereafter. Pretreatment with MTP-PE at 72 and 24 h before endotoxemia was induced resulted in a reduction of endotoxin shock-induced mortality from 81.8% (9 of 11 animals) in the control group to 8.3% (1 of 12 animals) of the MTP-PE-pretreated animals (P < 0.001). The administration of MTP-PE 24 h before the induction of endotoxin shock was more effective (P < 0.01) than administration of MTP-PE 72 h before endotoxemia was induced (P = 0.05). The pretreated animals did not develop fever or cardiovascular complications, and pulmonary function was significantly improved. Furthermore, the alpha-form of the soluble CD14 LPS receptor in pig serum showed a marked decrease in LPS-treated animals, and this decrease was reduced by MTP-PE pretreatment at 24 h before endotoxemia was induced. When MTP-PE was given simultaneously with the induction of septic shock or 1 h thereafter, it did not influence either mortality or morbidity. In conclusion, pretreatment of pigs with MTP-PE improves several parameters of endotoxin shock and it reduces mortality. Patients with high risk of developing septic complications might benefit from a pretreatment with this monocyte-activating substance.     

Volume replacement with Ringer-lactate is detrimental in severe hemorrhagic shock but protective in moderate hemorrhagic shock: studies in a rat model

Introduction

To date, there are insufficient data demonstrating the benefits of preclinically administered Ringer-lactate (RL) for the treatment of hemorrhagic shock following trauma. Recent animal experiments have shown that lactate tends to have toxic effects in severe hemorrhagic shock. This study aimed to compare the effects of RL administered in a rat model of severe hemorrhagic shock (mean arterial blood pressure (MAP): 25 to 30 mmHg) and moderate hemorrhagic shock (MAP: 40 to 45 mmHg).

Methods

Four experimental groups of eight male Wistar rats each (moderate shock with Ringer-saline (RS), moderate shock with RL, severe shock with RS, severe shock with RL) were established. After achieving the specified depth of shock, animals were maintained under the shock conditions for 60 minutes. Subsequently, reperfusion with RS or RL was performed for 30 minutes, and the animals were observed for an additional 150 minutes.

Results

All animals with moderate shock that received RL survived the entire study period, while six animals with moderate shock that received RS died before the end of the experiment. Furthermore, animals with moderate shock that received RL exhibited considerable improvements in their acid-base parameters and reduced organ damage.In contrast, in animals with severe shock, only two of the animals receiving RS survived but all of the animals receiving RL died early, before the end of the study period. Moreover, the severe shock animals that were treated with RL exhibited considerably worsened acid-base and metabolic parameters.

Conclusions

The preclinical use of RL for volume replacement has different effects depending on the severity of hemorrhagic shock. RL exhibits detrimental effects in cases of severe shock, whereas it has pronounced protective effects in cases of moderate shock.     

感染性休克集束治疗对病死率影响的前瞻性临床研究

目的 探讨集束治疗对感染性休克患者病死率的影响.方法 采用前瞻性研究方法,将2007年1月-2008年6月重症加强治疗病房(ICU)收治的成人感染性休克患者分为培训前(2007年1-9月)和培训后(2007年10月-2008年6月)两个阶段进行感染性休克集束治疗.分析6 h及24 h感染性休克集柬治疗各指标与预后的关系;采用多元回归分析方法,筛选出集束治疗对感染性休克预后影响的独立相关因素,并研究两个阶段感染性休克集束治疗的依从性、机械通气时间、ICU住院时间以及28 d病死率.结果 研究期间共收治符合条件的感染性休克患者100例,其中培训前51例,培训后49例;存活36例,死亡64例.多元回归分析显示,6 h早期目标导向治疗(EGDT)、24 h EGDT是与感染性休克28 d病死率相关的两个独立保护因素,优势比(OR)分别为0.046和0.120(P均<0.01).培训后集束治疗依从性均有明显提高,其中6 h EGDT和24 h EGDT分别从19.6%、35.3%提升至55.1%、65.3%(P均<0.01).培训后机械通气时间[(166.6±156.4)h比(113.6±73.6)h3、ICU住院时间[(9.4±7.6)d比(6.0±3.9)d]及28 d病死率(72.5%比55.1%)较培训前明显缩短(P<0.05或P<0.01).结论 继续教育培训可提高医务人员对感染性休克集束治疗的依从性,降低感染性休克患者的病死率.     

丹宁酸预处理对失血性休克大鼠心血管功能的影响

目的 探讨丹宁酸预处理对失血性休克大鼠心血管功能的影响.方法 SD大鼠随机分为休克组和丹宁酸预处理组.①在体实验:于放血前10 min静脉注射丹宁酸5 mg/kg,放血至平均动脉压(MAP)达40 mm Hg(1 mm Hg=0.133 kPa)维持120 min造成失血性休克模型,观察两组大鼠休克前及休克180 min内MAP及心肌收缩功能;另外选择大鼠于制模后回血60、120、180 min时静脉给予去甲肾上腺素(NE),观察血管反应性的变化.②离体实验:休克后取心脏,固定于离体心脏灌流系统,维持灌注压在100 mm Hg,观察丹宁酸预处理对失血性休克大鼠心肌收缩功能的作用.结果 ①在体实验显示,与休克组比较,丹宁酸预处理组MAP于60 min和150 min、左心室收缩压(LVSP)于60 min时显著升高;心率(HR)于120 min时明显减慢,左心室舒张期末压(LVEDP)于休克时明显下降,血管反应性于120 min时显著改善(P均<0.05).②离体实验显示,与休克组比较,丹宁酸预处理组HR于90 min时显著减慢,左室内压上升最大速率(+dp/dt max)于10 min和20 min时、左室内压下降最大速率(-dp/dt max)于10 min时明显增加(P均<0.05).结论 丹宁酸预处理对失血性休克大鼠心血管功能有一定程度的改善作用.     

氨基胍对创伤性休克血浆内皮素的影响

目的探讨氨基胍（AG）对创伤性休克大鼠各时间段血浆内皮素（ET）浓度的影响。方法复制SD大鼠创伤性休克模型，将大鼠分为处理组与休克组，处理组在休克末给予AG。测定大鼠在休克末和复苏后1h、3h、5h各时间段血浆ET的浓度。结果创伤性休克大鼠休克末和复苏后各时间段血浆ET浓度显著升高（P〈0．05）。而处理组大鼠由于补充外源性氨基胍，在一定程度上抑制了血浆内皮素ET浓度的升高，改善了创伤性休克的预后。结论休克后血浆ET值显著升高，参与了休克的病理生理损害过程，是有可能造成休克后期机体死亡的原因之一。