Dobutamine compensates deleterious hemodynamic and metabolic effects of vasopressin in the splanchnic region in endotoxin shock

BACKGROUND: Vasopressin is a potent vasopressor in septic shock, but it may impair splanchnic perfusion. We compared the effects of vasopressin alone and in combination with dobutamine on systemic and splanchnic circulation and metabolism in porcine endotoxin shock. METHODS: Twelve pigs were randomized to receive either vasopressin (VASO, n = 6) or vasopressin in combination with dobutamine (DOBU, n = 6) during endotoxin shock (E. coli endotoxin infusion). Endotoxin infusion rate was increased to induce hypotension after which vasoactive drugs were started. We aimed to keep systemic mean arterial pressure (MAP) >70 mmHg by vasopressin; the goal of dobutamine infusion was to prevent decrease in cardiac output often associated with vasopressin infusion. Regional blood flows, oxygen delivery and consumption, arterial and regional lactate concentrations were measured. RESULTS: Mean arterial pressure >70 mmHg was achieved in both the VASO and DOBU groups. After the primary decrease of cardiac output by vasopressin, systemic blood flow remained stable in vasopressin-treated animals. However, vasopressin as a monotherapy decreased portal venous blood flow. This was prevented by dobutamine. Vasopressin also induced splanchnic lactate release and arterial hyperlactatemia, which were not observed when dobutamine was combined with vasopressin. CONCLUSION: Dobutamine prevents adverse hemodynamic and metabolic effects of vasopressin in septic shock.     

低压复苏对非控制性出血性休克的作用

目前国内外的动物实验和部分临床研究结果显示，低压复苏是治疗非控制性出血性休克较为合理的方案，但还没有人从增加血容量，减少应激反应引起的血管收缩、改善组织微循环氧供方面进行研究。本研究拟观察低压及低压扩容复苏对腹腔实质脏器损伤非控制性出血性休克的治疗效果。     

外伤性肝脾破裂致失血性休克早期液体复苏的诊治探讨

目的观察外伤性肝脾破裂致失血性休克早期限制性液体复苏和常规正压液体复苏的疗效对比。方法将81例外伤性肝脾破裂致失血性休克患者按随机原则分为限制性液体复苏组(41例,快速输入2∶1的平衡液和贺斯进行液体复苏,使平均动脉压(MAP)维持在50~70 mmHg(1 mmHg=0.133 kPa))和常规正压液体复苏组(40例,维持MAP在70~90mm Hg)。比较两组患者的输液量、凝血酶原时间(PT),ARDS,MODS及治愈率。结果与常规正压液体复苏组比较,限制性液体复苏组输液量明显减少[(1240±243)ml比(2850±520)ml],PT明显缩短[(11.2±1.5)s比(15.9±1.7)s],治愈率明显升高(87.8%比62.5%),差异均有统计学意义(均P0.05)。结论限制性液体复苏能降低未控制出血的患者的死亡率,能减少MODS和ARDS的发生率,提高其治愈率。     

Arginine vasopressin: a promising rescue drug in the treatment of uncontrolled haemorrhagic shock

Haemorrhagic shock is one of the most frequent types of shock. If haemorrhage cannot be controlled and fluid resuscitation as well as catecholamines are insufficient to stabilize cardiovascular function, uncontrolled haemorrhagic shock occurs. Several approaches have been suggested as promising alternatives to volume resuscitation. The rationale for the use of arginine vasopressin (AVP) is the pharmacologic amplification of the neuroendocrine stress response. AVP-mediated vasoconstriction is the first physiologic step to haemostasis and shifts blood away from the bleeding site towards the heart, lungs and brain. Particularly, when uncontrolled haemorrhage is accompanied by traumatic brain injury this may help to reduce secondary neurological damage. Since AVP can prevent acute death only transiently, it must comprehensively be combined with rapid hospital admission, immediate control of haemorrhage followed by aggressive fluid resuscitation and blood transfusion. This review article summarizes current experimental and clinical evidence on the use of AVP in uncontrolled haemorrhagic shock.     

Glucose infusion arrests the decompensatory phase of hemorrhagic shock

Waning of hyperglycemia has been shown to be closely associated with the deterioration of mechanisms supporting homeostasis during hemorrhagic shock. However, the mechanisms which link plasma glucose levels to maintenance of homeostasis during hemorrhagic shock are not clear. The goal of the present study was to evaluate the importance of glucose to maintenance of compensatory mechanisms. This was undertaken by maintaining plasma glucose levels through infusion of hypertonic glucose (2-3 M) starting at the onset of decompensation during persisting hypovolemia. Administration of glucose at a rate of between 60 and 80 mumoles/min X kg arrested the fall in glucose concentration and significantly slowed or arrested the decompensatory phase. All of the saline infused control animals (n = 6) died within 3 hours after reaching their maximum shed blood volume, averaging 145 +/- 25 minutes, while two of the eight animals in the glucose infusion group died less than 4 hours after reaching the maximum shed blood volume. The remaining six animals were sacrificed between 270 and 397 minutes (average, 340 +/- 22 minutes) after reaching the maximum shed blood volume since decompensation was arrested. Compared to the saline-infused control group, animals receiving glucose infusion exhibited a more moderate acidosis, and the hemoconcentration which normally accompanies decompensation was also prevented. Since the increase in plasma osmolality and the fraction of the total osmolality change accounted for by glucose was less in the glucose-infused animals, these results suggest that the effect is not mediated through a glucose-related maintenance of a transcapillary osmotic gradient.(ABSTRACT TRUNCATED AT 250 WORDS)     

Employing vasopressin as an adjunct vasopressor in uncontrolled traumatic hemorrhagic shock

Resuscitation of patients in hemorrhagic shock remains one of the most challenging aspects of trauma care. We showed in experimental studies that vasopressin, but not fluid resuscitation, enabled short-term and long-term survival in a porcine model of uncontrolled hemorrhagic shock after penetrating liver trauma. In this case report, we present two cases with temporarily successful cardiopulmonary resuscitation (CPR) using vasopressin and catecholamines in uncontrolled hemorrhagic shock with subsequent cardiac arrest that was refractory to catecholamines and fluid replacement. In a third patient, an infusion of vasopressin was started before cardiac arrest occurred; in this case, we were able to stabilize blood pressure thus allowing further therapy. The patient underwent multiple surgical procedures, developed multi-organ failure, but was finally discharged from the critical care unit without neurological damage.     

限制性液体复苏治疗失血性休克的临床研究

目的 探讨失血性休克早期限制性液体复苏的临床意义.方法 分析我院60例未控制失血性休克的液体复苏方法,比较常规液体组(n=30)与限制性液体复苏组(n=30)两种方法的治愈率、病死率及实验室指标血红蛋白(HBG)、红细胞压积(HCT)、血小板(PLT)、凝血酶原时间(PT)的结果.结果 常规组输液量(2 980±564)ml,治愈率66.7%、病死率33.3%,限制性组输液量(1980±302)ml,治愈率90.0%、病死率10.0%,两组间差异有统计学意义(P＜0.05),HBG、HCT、PLT、PT的比较,两组间差异有统计学意义(P＜0.01).结论 高渗液早期限制性液体复苏可提高治愈率,降低病死率,与常规复苏组比较不致于扰乱机体代偿机制及内环境.     

小剂量血管加压素在感染性休克中的应用进展

血管加压素应用于感染性休克可以改善组织灌注,稳定血流动力学.它的主要作用机制是在感染性休克状态下,血浆血管加压素水平的相对性缺乏与血管对血管加压素的敏感性增强.目前研究主张小剂量血管加压素与其他血管活性药物联合使用治疗感染性休克,由于缺乏临床多中心随机对照研究,血管加压素仍是感染性休克的二线升压药.     

损伤控制性复苏用于失血性休克救治的研究进展

背景 失血性休克(hemorrhagic shock,HS)是导致人类死亡和致残的重要原因,与患者转归密切相关,目前尚缺乏理想的复苏方案.目的 综述损伤控制性复苏(damage control resuscitation,DCR)研究进展.内容 DCR是较新的整合性复苏策略,已被广泛应用于创伤急救、心脏外科、妇产科等多个手术领域.由于凝血机制的破坏,HS患者常伴有创伤性凝血病、低体温和酸中毒.DCR推荐对HS患者进行允许性低压复苏、止血复苏和损伤控制性手术的处理.DCR不仅可以提高复苏效果,还能减少休克相关并发症.趋向 DCR在HS处理中有良好应用前景,然而尚需进一步研究使其完善.     

小剂量精氨酸加压素在血管扩张性休克病人中的应用

目的观察小剂量精氨酸加压素(arginine vasopressin,AVP)在血管扩张性休克病人治疗中的作用及其并发症。方法对17例血管扩张性休克病人进行了研究。病人均予儿茶酚胺类药物治疗,在充分容量治疗后加用小剂量AVP(<0.04U/min),在维持MAP≥65mmHg的基础上逐步调整儿茶酚胺类药物的剂量。记录AVP治疗前后的血流动力学参数、肾功能、儿茶酚胺类药物的用量、并发症及病人的预后。结果予小剂量AVP治疗后,病人HR和儿茶酚胺类药物的剂量均显著下降(P<0.01),MAP显著升高(P<0.05),心脏指数(CI)显著下降(P<0.01),每搏量指数(SVI)和周身血管阻力指数(SVRI)均显著升高(P<0.05),尿量显著增加(P<0.01),血肌酐(Cr)显著下降(P<0.01),肌酐清除率(CL)显著升高(P<0.01)。结论加用小剂量AVP治疗可明显改善血管扩张性休克病人的血流动力学,可减少儿茶酚胺类药物的需要量,并改善肾功能。     

失血性休克后液体复苏的研究进展

背景 失血性休克是外伤死亡的主要原因.在重危病例的急救和围手术期的处理中,液体复苏起着关键性的治疗作用. 目的 就重度失血性休克后液体治疗方案的研究进展作一综述. 内容 除了传统的晶体液,近年来开发了诸多新品种的液体用于复苏,如丙酮酸钠溶液等.复苏方式的研究也在静脉复苏的基础上拓展到了腹腔复苏. 趋向 丙酮酸钠溶液以及腹腔复苏是近年来研究提出的新的复苏液体和复苏方案,通过已有的研究已经证实其积极的治疗作用.其应用于失血性休克的方法、时间、疗效等仍需更进一步研究.     

Arginine vasopressin vs. terlipressin in the treatment of shock states

The synthetic vasopressin analogue, terlipressin, is being increasingly used to treat catecholamine-resistant hypotension in septic shock and other conditions. While terlipressin holds some theoretical and anecdotal advantages over vasopressin, this has not been formally tested in prospective randomised trials. This review analyses the published literature and makes comparisons, where possible, between vasopressin and terlipressin.     

减阻剂用于出血性休克复苏的实验研究

Drag reducing polymers （DRPs） provide large drag reductions iu turbulent flow at nanomolar concentrations of linear macropolymers,as polyethylene glycol, aloe vera polymer. DRPs have been shown to significantly enhance hemodynamics and improve microcirculation, make the red blood cells work harder and increase blood pressure , improve survival in hemorrhagie shock.     

Vasopressin analogues in the treatment of shock states: potential pitfalls

Vasopressin analogues are increasingly used for haemodynamic support of catecholamine-refractory, hyperdynamic septic shock. Arginine vasopressin (AVP) and terlipressin (TP) effectively increase mean arterial pressure and reduce catecholamine requirements in this condition. However, the use of either of the drugs may be linked to relevant haemodynamic side effects, including reductions in cardiac output, oxygen delivery and mixed-venous oxygen saturation. These alterations may result in impaired tissue perfusion and foster the genesis of ischemic tissue injury. In addition, decreases in platelet count and increases in aminotransferases activity and bilirubin concentration have been reported with the use of V1 agonists. However, it remains unclear whether these changes are of clinical relevance. This review article summarizes the previous data on adverse effects related to the therapy with vasopressin analogues and discusses potential options to prevent such adverse events. In summary, continuous TP infusion appears to be superior to bolus infusion. Maximum doses of 0.03 (-0.067) U min(-1) of AVP or 2 microg kg(-1) h(-1) of TP, respectively, should not be exceeded. Aggressive fluid therapy may prevent adverse haemodynamic effects linked to infusion of either AVP or TP. Finally, platelet count, surrogate variables of hepatic dysfunction, electrolytes and osmolality should be strictly monitored in patients treated with vasopressin analogues.     

Hypertonic saline prevents early bacterial translocation in hemorrhagic shock

The most appropriate solution for volume replacement in hemorrhagic shock is controversial; however, hypertonic saline (HTS) solutions have recently gained widespread acceptance. In this study, various solutions were used to resuscitate rats in hemorrhagic shock, and their impact on the extent of bacterial translocation was investigated. Rats were bled to a mean arterial blood pressure of about 35 mmHg which was maintained for 30 min. They were then randomized into six groups. Blood pressure was found to be regulated by blood + lactated Ringer's solution (LR) and HTS+LR, but no significant improvement was observed in the control and LR groups. Groups II (7.5% HTS+60 ml/kg LR) and IV (60 ml/kg LR + autologous blood) had a significantly better result than groups I (7.5% HTS), III (60 ml/kg LR), and IV (P<0.05), among which no statistically different results were seen (P>0.05). While no organisms were isolated from the mesenteric lymph nodes in the sham group, the rates of positive culture were 12.5%, 12.5%, 50%, 62.5%, and 62.5% in groups I, II, III, and the control group, respectively.Escherichia coli was the most commonly isolated organism. HTS+LR was demonstrated to be effective for decreasing the rate of early bacterial translocation to mesenteric lymph nodes and also for restoring the mean arterial pressure.     

Impact of alcohol intoxication on hemodynamic, metabolic, and cytokine responses to hemorrhagic shock

BACKGROUND: Alcohol intoxication is associated with a high incidence of traumatic injury, particularly in the young healthy population. The impact of alcohol intoxication on the immediate pathophysiologic response to injury has not been closely examined. We hypothesized that acute alcohol intoxication would aggravate the immediate outcome from hemorrhagic shock by impairing homeostatic counterregulation to blood loss. METHODS: Chronically catheterized male Sprague-Dawley rats were randomized to receive an intragastric infusion of ethyl alcohol (1.75 g/kg followed by 250-300 mg/kg/h) or isocaloric dextrose (3-mL bolus + 0.375 mL/h) for 15 hours. Before initiating fixed-pressure hemorrhage followed by fluid resuscitation, an additional intragastric bolus of ethyl alcohol (1.75 g/kg) was administered. Hemodynamic, metabolic, cytokine, and acid-base parameters were assessed during the hemorrhage period and at completion of resuscitation. Lungs were obtained for cytokine determinations. RESULTS: Basal mean arterial pressure was significantly lower in alcohol-intoxicated (blood-alcohol concentration, 135 +/- 12 mg/dL) animals than in controls during baseline (20%) and after the initial fluid resuscitation period (30%). Hemorrhage decreased arterial HCO3 and Pco2, and increased Po2 without significant alteration in arterial blood pH. Alcohol intoxication blunted the decrease in Pco2 and increase in Po2 and decreased blood pH during baseline and throughout the course of the hemorrhage period. Hemorrhage produced marked and progressive elevations in plasma glucose and lactate levels in controls, and this was inhibited by alcohol intoxication. Hemorrhage elevated plasma tumor necrosis factor-alpha (TNF-alpha) (686 +/- 252 pg/mL) and interleukin (IL)-10 (178 +/- 25 pg/mL), and did not alter IL-6 and IL-1 levels. Alcohol blunted the hemorrhage-induced rise in plasma TNF-alpha (142 +/- 48 pg/mL) and enhanced the hemorrhage-induced increase in IL-10 (678 +/- 187 pg/mL). Hemorrhage produced a two- to threefold increase in lung content of TNF-alpha, IL-1alpha, and IL-6 without significantly altering lung IL-10. Alcohol exacerbated the hemorrhage-induced increase in lung TNF-alpha, and did not alter the IL-1alpha, IL-6, and IL-10 lung responses. CONCLUSION: These results indicate marked alterations in the hemodynamic and metabolic responses to hemorrhagic shock by alcohol intoxication. Furthermore, our findings suggest that alcohol modulates the early proinflammatory responses to hemorrhagic shock. Taken together, these alterations in metabolic and inflammatory responses to hemorrhage are likely to impair immediate outcome and predispose to tissue injury.     

丙酮酸腹膜透析液对大鼠失血性休克静脉液体复苏后腹腔脏器的保护作用

目的：研究丙酮酸腹腔透析液对大鼠失血性休克静脉液体复苏后腹腔脏器的保护作用。方法：雄性SD大鼠40只,随机分为4组（n=10）。大鼠按全身血容量的45％经股动脉放血制作失血性休克模型。单纯静脉复苏组（VR组）于休克1h后回输失血及2倍失血量的乳酸钠林格液行静脉复苏,其余3组在上述静脉复苏基础上,分别腹腔注射生理盐水（DPR组）、乳酸钠透析液（L组）、丙酮酸钠透析液（P组）20ml行腹腔复苏,时间30min。分别于休克前（O时）及休克后60（静脉复苏前）、180（腹腔复苏后1h）、360rain（腹腔复苏后4h）用PICCO心肺容量监测仪监测大鼠平均动脉压（MAP）;激光多普勒血流仪测定休克后180min和360min肝、肾和小肠黏膜血流量;生化法测定休克前及休克后180、360min血丙氨酸转氨酶（ALT）、二胺氧化酶（DAO）活性和肌酐（cr）水平;干／湿比重法测定休克后180、360min肝、肾、肠各组织含水率。结果：失血性休克后各组MAP骤降至（35±5）mmHg;休克后60min时,各组大鼠MAP无明显差异（P〉0．05）。腹腔复苏后,与VR组比较,L和P组均能显著提高失血性休克大鼠MAP（P〈0．05）,降低血ALT、Cr和DAO水平,减轻肝、肾、肠组织含水率,提高腹腔脏器血流量（P〈0．05或P〈0．01）,在失血后360min时,P组的上述变化较其余复苏组更为显著。结论：丙酮酸腹腔透析液对大鼠失血性休克静脉液体复苏后腹腔脏器具有保护作用。     

早期液体复苏对感染性休克患者血流动力学的影响

目的 分析早期液体复苏对感染性休克患者血流动力学的影响。方法 选取2011年1月至2012年4月我院ICU收治的26例感染性休克患者作为研究对象,随机分为对照组和试验组,各13例。两组患者均采用PICCO监测,并根据早期复苏目标导向疗法（early goal directed therapy,EGDT）进行早期液体复苏治疗。对照组和试验组复苏液分别为林格液和6%羟乙基淀粉130/0.4氯化钠溶液。分别于复苏开始时（0 h）、8 h和24 h收集患者的血流动力学参数。结果 试验组和对照组的CVP、CI、ITBVI及GEDVI水平均随着时间的增加上升（P＜0.05）,但EVLWI在对照组明显增加（P＜0.05）,而试验组无明显变化。除试验组EVLWI外,与开始复苏（0 h）相比较,试验组和对照组的CVP、CI、ITBVI、GEDVI及对照组的EVLWI与开始复苏（0 h）相比较均有明显差异（P＜0.05）。经重复测量资料的方差分析发现,试验组CVP和GEDVI较对照组上升水平明显,对照组EVLWI较试验组上升水平明显,差异均具有统计学意义（P＜0.05）。结论 感染性休克患者根据EGDT方案使用6%羟乙基淀粉130/0.4氯化钠溶液进行复苏,能更好地改善患者的血流动力学指标。     

限制性液体复苏对失血性休克大鼠网状内皮系统的影响

目的探讨限制性液体复苏对失血性休克大鼠网状内皮系统的影响。方法60只SD大鼠制成未控制性重度失血性休克模型,随机分成对照组、NF组(无液体复苏组)、NS40组(限制性液体复苏组)和NS80组(常规大量液体复苏组),检测和比较休克复苏后各组存活大鼠肝脏枯否细胞和腹腔巨噬细胞的吞噬功能。结果重度失血性休克大鼠失血后150min存活率NF组、NS40组和NS80组比对照组明显提高,NS40组较NS80组显著改善(P0.05);NS40组大鼠肝脏枯否细胞和腹腔巨噬细胞的吞噬功能较NS80组明显改善(P0.05)。结论限制性液体复苏可以显著改善失血性休克大鼠的网状内皮系统的吞噬功能,提高大鼠的免疫功能,降低死亡率。