失血性休克延迟复苏对犬血流动力学和内脏灌流的影响

目的 研究延迟补液对失血性休克血流动力学和内脏灌流的影响.方法 Beagle犬14只,先期无菌手术行颈动脉、静脉置管,24 h后从颈动脉放血造成失血性休克,总失血量为全身血容量的42%.随机(随机数字法)分为延迟补液组(n=8)和立即补液组(n=6).失血后第1个24小时延迟补液组无治疗,立即补液组静脉输入3倍失血量的葡萄糖-电解质溶液.失血后24 h起2组犬均实施静脉补液.测定犬失血前和失血后2,4,8,24,48和72 h非麻醉状态下的循环血流动力学和肠道组织灌流指标,并记录失血后72 h病死率.结果 与失血前相比,两组犬平均动脉压、心排指数、全身血管阻力指数、左室内压最大变化速率、尿量以及肠黏膜血流量在失血后均大幅降低(P＜0.05),而全身血管阻力显著升高.从失血后4 h起,立即补液组上述指标逐渐恢复,失血后72 h除全身血管阻力和肠黏膜血流量外均恢复至失血前水平.延迟补液组上述指标则持续恶化,8例中有5例无尿,失血后4 h起各时间点平均动脉压、心输出量、尿量以及肠黏膜血流量均显著低于立即补液组(P＜0.05).失血后72 h病死率延迟补液组为5/8(62.5%),立即补液组为0.结论 延迟补液显著加重失血性休克犬血流动力学紊乱、延迟脏器组织灌流恢复,增加早期病死率.     

限制与积极液体复苏法救治创伤失血性休克的疗效比较

目的比较限制液体复苏与积极液体复苏救治创伤失血性休克的临床效果,以提高治愈率。方法将符合创伤失血性休克患者随机分为限制液体复苏组和积极液体复苏组,对其临床资料和实验室指标进行统计学分析。结果限制性液体复苏组与积极液体复苏组比较,收缩压差异无显著性(院前51±19 mmHg vs 50±21 mmHg,术前74±27 mmHg vs 82±28 mmHg,P>0.05),输液量显著降低(院前232±215 mL vs 830±542 mL,术前328±309 mL vs 1905±1340 mL,P<0.01),死亡率降低(13.3%vs 27.8%,P<0.05),术前血红蛋白升高(94±21 g/L vs 85±23 g/L,P<0.05),术前凝血指标好转〔血小板计数(268±94)×109/L vs(233±91)×109/L,P<0.05;凝血酶原时间12.3±1.7 s vs 14.5±1.9 s,P<0.01;部分凝血酶原时间36.5±14.1 s vs 41.8±18.5 s,P<0.05〕。结论救治创伤失血性休克限制液体复苏法可能优于积极液体复苏法。     

Detrimental effects of rapid fluid resuscitation on hepatocellular function and survival after hemorrhagic shock

Because end-organ injury can occur with reperfusion following hemorrhage or ischemia, we hypothesized that aggressive intravenous fluid resuscitation would aggravate tissue injury in a fixed-volume model of hemorrhagic shock. Unanesthetized chronically prepared male rats were hemorrhaged 33-36 mL/kg for 2.5 h. Then Lactated Ringers Solution (3x hemorrhage volume) was infused over 5 min (FAST), 20 min (MEDIUM), 180 min (SLOW), or not at all (NO RESUS). Plasma ornithine carbamoyltransferase (OCT), lactate, and creatinine were measured as indices of hepatocellular injury, anaerobic metabolism, and renal function, respectively. At 1 h post-resuscitation (PR), MAP was greater after SLOW and MEDIUM treatment (tx) than after other txs (P < 0.05). OCT increased earliest after FAST tx to values greater than those after other txs from 30 min to 24 h PR (P < 0.01). Plasma lactate was elevated immediately before resuscitation in all groups (P < 0.01) and returned to baseline at 3 h PR after SLOW tx compared to 5 h PR after FAST tx (P < 0.05). Creatinine at 5 h PR was less in the groups treated with intravenous fluid compared to the NO RESUS group, P < 0.05. Survival at 72 h was reduced in the FAST (57%) and NO RESUS (58%) groups compared to the SLOW (87%) and MEDIUM (85%) groups (P < 0.05). Thus, overly aggressive fluid tx accelerates hepatocellular injury, is no better than lesser rates of resuscitation at correcting plasma lactate and preserving renal function, and provides no overall survival benefit.     

Low dose nitrite enhances perfusion after fluid resuscitation from hemorrhagic shock

This study determines the systemic and microvascular hemodynamic consequences of administering a low dose sodium nitrite after fluid resuscitation from hemorrhagic shock. Hemodynamic responses to hemorrhagic shock and resuscitation were studied in the hamster window chamber model. Moderated hemorrhage was induced by arterial controlled bleeding of 50% of the blood volume (BV) and the hypovolemic state was maintained for 1 h. Volume restitution was performed by infusion of 25% of BV using Hextend^® (6% Hetastarch 670 kDa in lactated electrolyte solution) 10 min after fluid resuscitation 100 μl of specific concentrations of sodium nitrite were infused. The experimental groups were named based on the nitrite concentration used, namely: 0 μM, 10 μM and 50 μM. Systemic parameters, microvascular hemodynamics and capillary perfusion (functional capillary density, FCD) were followed during entire protocol. Exogenous 10 μM nitrite maintained systemic and microhemodynamic conditions post fluid resuscitation from hemorrhagic shock, compared to 50 μM or no nitrite. A moderated increase in plasma nitrite during the early phase of resuscitation reversed arteriolar vasoconstriction and increased capillary perfusion and venous return, improving central cardiac function. Nitrite effects on resistance vessels, directly influenced intravascular pressure redistribution, sustained blood flow, and prevented tissue ischemia. In conclusion, increasing nitrite plasma bioavailability after fluid resuscitation from hemorrhagic shock can be a potential therapy to enhance microvascular perfusion and to improve overall outcome.     

Hyperoxic ventilation reduces six-hour mortality after partial fluid resuscitation from hemorrhagic shock

Ventilation with 100% oxygen (Fio(2) 1.0; hyperoxic ventilation; HV) as an alternative to red blood cell transfusion enables survival in otherwise lethal normovolemic anemia. The aim of the present study was to investigate whether HV as a supplement to fluid infusion therapy could also restore adequate tissue oxygenation and prevent death in otherwise lethal hemorrhagic shock. In 14 anesthetized pigs ventilated on room air (Fio(2) 0.21), hemorrhagic shock was induced by controlled withdrawal of blood (target mean arterial pressure 35-40 mmHg) and maintained for 1 h. Subsequently, the animals were partially fluid-resuscitated (i.e., replacement of lost plasma volume) either with hydroxyethyl starch (6% HES, 200/0.5) alone (G 0.21) or with HES supplemented by HV (G 1.0). After completion of partial fluid resuscitation, all animals were followed up for the next 6 h. Five of seven animals of G 0.21 died within the 6-h observation period (i.e., 6-h mortality 71%). Death was preceded by a continuous increase of the serum concentrations of arterial lactate and persistent tissue hypoxia. In contrast to that, all animals of G 1.0 survived the 6-h observation period without lactic acidosis and with improved tissue oxygenation (i.e., 6-h mortality 0%; G 0.21 versus G 1.0 P < 0.05). In anesthetized pigs submitted to lethal hemorrhagic shock, the supplementation of partial fluid resuscitation with HV improved tissue oxygenation and enabled survival for 6 h.     

活动性出血休克家兔的限制性液体复苏

目的 探讨有活动性出血的失血性休克家兔对不同剂量平衡盐溶液复苏的疗效.方法 用股动脉放血方法复制活动性出血的家兔休克模型,40只成年家兔随机分成5组(n=8):不输液对照组(N4组),大剂量液体复苏组(125 mL/kg,N3组),中剂量液体复苏组(92mL/kg,N2组),小剂量液体复苏组(57 mL/kg,N1组),假手术对照组(N5组).抽血使各实验组动物平均动脉压降至40mmHg,并维持30 min,然后用不同剂量平衡盐溶液复苏,再观察动物120 min或直至动物死亡,记录各组动物活动性出血量、死亡数、血细胞比容(Hct)、平均动脉压(MAP)的变化以及肾脏皮质SOD活性.数据分析采用SNK-q检验和秩和检验.结果 N5组的各项指标均优于N1,N2,N3组(P<0.01);N4组的各项指标均劣于N1,N2,N3组(P<0.01);N3组的出血量、死亡数明显高于N1,N2组(P<0.01).N3组的SOD明显低于N1和N2组(P<0.01).随着复苏液体量的增加,Hct逐渐减小,观察期内N2,N3,N4组MAP逐渐下降,死亡数增加.结论 对有活动性出血的失血性休克机体,应行限制性液体复苏(57～92 mL/kg).     

未控制出血性休克与TNF—a的关联性及不同液体复苏的作用

目的 研究未控制出血性休克时不同液体复苏的作用以及，INF—a的变化规律，以期阐明限制性液体复苏降低未控制出血性休克的死亡率和改善预后的相关机制。方法采用改良后的Krausz方法建立重度脾创伤未控制出血性休克大鼠模型。采用随机分组的原则将大鼠分为假处理组、限制输液组、常规输液组、不输液组。观察各组动物的出血量、输液量、存活率、存活时间及各时间点的血压、血细胞比容（Hct）和TNF—a的变化情况。结果①限制输液组的输液量明显少于常规输液组（P〈0．05），出血量也明显少于常规输液组（P〈0．05）。②限制输液组Hct明显高于常规输液组（P〈0．05）。②限制输液组的存活时间比常规输液组及不输液组明显延长（P均〈0．05）。限制输液组在72h内的存活率明显高于常规输液组和不输液组。但低于假处理组（P均〈0．1）。④除假处理组外其余各组在伤后90min和180min血TNF—a水平均较伤前均有明显升高（P均〈0．05）；常规输液组，TNF—a水平明显高于限制输液组（P〈0．05）。⑤死亡者TNF—a水平明显高于生存者。结论本研究结果表明，在重度未控制出血条件下，限制性液体复苏可明显降低出血量，提高存活率。未控制性出血休克时的TNF—a水平与预后密切相关，TNF—a高预后不良，而限制性液体复苏时TNF—a水平明显降低。     

未控制出血性休克早期液体复苏的实验研究

目的探讨未控制出血性休克限制性液体复苏的效果.方法Wistar大鼠60只,采用Krausz标准脾脏损伤+切断脾中部一动脉分支制作重度未控制出血性休克模型后,随机分为6组(n=10)未输液复苏组(NF组)及平均动脉压维持在6.67 kPa(1 kPa=7.5 mmHg)组(NS50组)、8.00 kPa组(NS60组)、10.70 kPa组(NS80组)、13.30 kPa组(NS100组)和结扎止血后使平均动脉压维持在13.30 kPa组(止血输液组).各输液组在平均动脉压降至5.33 kPa时开始用平衡盐液复苏,使血压分别维持在各相应水平,观察各组动物的出血量、输液量、存活率、存活时间及各时间点的血压、血乳酸、碱缺失和血细胞比容(Hct)的变化情况.结果NS50组的出血量、输液量明显低于NS80、NS100组(P均<0.05),存活率明显高于NS80、NS100组和未输液组(P均<0.05),存活时间比未输液组、NS80和NS100组明显延长(P均<0.05);随着维持血压的增高,Hct逐渐降低,伤后120分钟NS50组明显高于NS60组、NS80组和NS100组(P均<0.05);在各时间点,血乳酸和碱缺失随着复苏血压的增高而逐渐降低,伤后60分钟,NS50组明显高于NS60组、NS80组、NS100组和止血输液组(P均<0.05).结扎止血组各项指标优于其它各组,与NS50组无显著性差异.结论在重度未控制出血条件下,应限制性液体复苏,止血前仅输入少量液体以维持生命的基本需要,止血后再进行充分的液体复苏,可明显提高存活率,降低出血量.     

Small-volume resuscitation from hemorrhagic shock in dogs: effects on systemic hemodynamics and systemic blood flow.

BACKGROUND AND METHODS: This study compared canine systemic hemodynamics and organ blood flow (radioactive microsphere technique) after resuscitation with 0.8% saline (Na+ 137 mEq/L), 7.2% hypertonic saline (Na+ 1233 mEq/L), 20% hydroxyethyl starch in 0.8% saline, or 20% hydroxyethyl starch in 7.2% saline, each in a volume approximating 15% of shed blood volume. Twenty-four endotracheally intubated mongrel dogs (18 to 24 kg) underwent a 30-min period of hemorrhagic shock, from time 0 to 30 min into the shock period, followed by fluid resuscitation. Data were collected at baseline, 15 min into the shock period, immediately after fluid infusion, 5 min after the beginning of resuscitation, and at 60-min intervals for 2 hr, (65 min after the beginning of resuscitation, and 125 min after the beginning of resuscitation). The animals received one of four randomly assigned iv resuscitation fluids: saline (54 mL/kg), hypertonic saline (6.0 mL/kg), hydroxyethel starch (6.0 mL/kg) or hypertonic saline/hydroxyethyl starch (6.0 mL/kg). RESULTS: Mean arterial pressure increased in all groups after resuscitation. Cardiac output increased with resuscitation in all groups, exceeding baseline in the saline and hypertonic saline/hydroxyethyl starch groups (p less than .05 compared with hypertonic saline or hydroxyethyl starch). Sixty-five minutes after the beginning of resuscitation, cardiac output was significantly (p less than .05) greater in either of the two colloid-containing groups than in the hypertonic saline group. After resuscitation, hypertonic saline and hydroxyethyl starch produced minimal improvements in hepatic arterial flow, hypertonic saline/hydroxyethyl starch increased hepatic arterial flow to near baseline levels, and saline markedly increased hepatic arterial flow to levels exceeding baseline (p less than .05, saline vs. hydroxyethyl starch). One hundred twenty-five minutes after the beginning of resuscitation, hepatic arterial flow had decreased in all groups; hepatic arterial flow in the hypertonic saline group had decreased to levels comparable with those during shock. Myocardial, renal, and brain blood flow were not significantly different between groups. CONCLUSIONS: Small-volume resuscitation with the combination of hypertonic saline/hydroxyethyl starch is comparable with much larger volumes of 0.8% saline, and is equal to hypertonic saline or hydroxyethyl starch in the ability to restore and sustain BP and improve organ blood flow after resuscitation from hemorrhagic shock.     

创伤失血性休克限制性液体复苏的研究进展

目的 探讨限制性液体复苏用于创伤失血性休克的研究进展,从而掌握最新标准,科学地指导临床工作.方法 应用CNKI、Medline和ScienceDirect等数据库,查阅近年来相关文献,总结限制性液体复苏在动物实验与临床实践中的实施方法与临床效果.结果 限制性液体复苏在临床应用已非常广泛,国内外学者进行了大量研究和报道,虽然在适用条件、液体选择及监测指标等方面已达成一定共识,但有些结论还需要临床验证,并且需要不断的深入研究.结论 限制性液体复苏在实际应用中,虽然取得了很大突破,但至今仍没有统一的复苏指南,要选择最佳方案和取得最好效果,还需要今后不断地摸索.     

The effect of vigorous fluid resuscitation in uncontrolled hemorrhagic shock after massive splenic injury

OBJECTIVE: Using a standardized massive splenic injury model of uncontrolled hemorrhagic shock, we studied the effect of vigorous fluid resuscitation on the hemodynamic response and survival time in rats. DESIGN: Randomized, controlled study. Duration of follow-up was 4 hrs. SETTING: University research laboratory. SUBJECTS: Adult male Sprague-Dawley rats, weighing 240-430 g. INTERVENTIONS: Standardized massive splenic injury was induced by two transverse incisions in the rat's spleen. The animals were randomized into four groups: group 1 (n = 8) underwent sham operation; in group 2 (n = 15), massive splenic injury was untreated; in group 3 (n = 15), massive splenic injury was treated with 41.5 mL/kg 0.9% sodium chloride (large-volume normal saline); and in group 4 (n = 15), massive splenic injury was treated with 5 mL/kg 7.5% sodium chloride (hypertonic saline). MEASUREMENTS AND MAIN RESULTS: The hemodynamic and metabolic variables in the sham-operated group 1 were stable throughout the experiment. Mean arterial pressure in group 2 decreased from 86.5 +/- 4.0 to 50.3 +/- 6.3 mm Hg (p < .001) in the first 15 mins after massive splenic injury. Mean survival time in group 2 was 127.5 +/- 17.0 mins; total blood loss was 33.8% +/-2.6% of blood volume; and the mortality rate at 1 hr was 13.3%. Bolus infusion of large-volume normal saline after 15 mins resulted in an early increase in mean arterial pressure from 48.6 +/-7.4 to 83.3 +/- 7.2 mm Hg (p < .01); it then rapidly decreased to 24.6 +/- 8.6 mm Hg (p < .001) after 60 mins. The mean survival time (95.3 +/- 16.4 mins) was significantly lower than in group 2 (p < .01); total blood loss (48.0% +/- 4.3%) was significantly higher than in group 2 (p < .01); and mortality rate in the first hour was 33.3% (p < .05). Bolus infusion of hypertonic saline also decreased survival time to 93.3 +/- 20.3 mins (p < .01), but total blood loss was 35.2% +/- 3.0%, which was not significantly different from the blood loss in group 2. The mortality rate in the first hour (60.0%) was significantly higher than in group 2 (p < .005). CONCLUSIONS: Vigorous infusion of normal saline after massive splenic injury resulted in a significant increase in intra-abdominal bleeding and decreased survival time. The hemodynamic response to crystalloid infusion in blunt abdominal trauma is primarily dependent on the severity of injury and the rate of blood loss.     

失血性休克患者的液体复苏策略分析

失血性休克是临床上最常见的一种休克类型,通常由于大失血引起机体循环血量骤减而发生,大多继发于创伤或其他疾病。对于失血性休克患者,传统复苏方法往往要求：快速、充分、正压、复温、复苏,即主张在失血性休克发生后快速给予大量液体,恢复有效血容量,并使用正性肌力或血管活性药物以尽快恢复血压,维持血压在正常水平,保证器官组织灌注,保持机体正常体温,防止休克的进一步发展。但是,目前医学界对液体复苏时机、采用何种液体复苏、复苏原则等问题,均存在较大争议。为此,本文对失血性休克患者的液体复苏策略进行简略的分析。     

创伤非控制失血性休克大鼠限制性液体复苏的实验研究

目的 探讨创伤非控制失血性休克早期限制性液体复苏的效果及适宜的血压范围.方法 采用修订的Capone等方法 制备创伤非控制失血性体克模型.60只SD(Sprague-Dawley,SD)大鼠随机分为6组:NC组,正常对照组;NF组,休克不复苏组;NS40、NS60(限制性液体复苏组)、NS80、NS100组(大量液体复苏组).备液体复苏组在大鼠的平均动脉压(MAP)降至35～40mmHg时分刺给予生理盐水输注,使血压维持在各相应水平.输液1h后,备液体复苏组均给予手术止血、回输血液及给予足量的液体输注,保持大鼠的MAP≥90mmHg.监测出血量、输液量、存活时间、存活率、碱缺失、红细胞比客、心、脑、肾功能指标的变化.结果 创伤失血性休克早期在出血未控的制的情况下,大量液体复苏组(NS80、NS100组)、出血量和输液量明显大于限制性液体复苏组(NS40、NS60组)(P<0.05).NS60组有9/10只大鼠存活超过72h,NS40组3/10只存活起过72h,而NF组与NS80、NS100组无1只存活超过72h.NS40、NS60组大鼠的心、脑、肾病理学损害明显轻于大量液体复苏组.NS40组心、脑、肾病理学改变较NS60组明昱.结论 在有活动性出血的创伤失血性休克早期应给予限制性液体复苏,大鼠早期限制性液体复苏较为适宜的血压范围是MAP保持在55-65mmHg左右(平均60mmHg).     

未控制出血性休克与TNF-α的关联性及不同液体复苏的作用

目的研究未控制出血性休克时不同液体复苏的作用以及TNF-α的变化规律,以期阐明限制性液体复苏降低未控制出血性休克的死亡率和改善预后的相关机制.方法采用改良后的Krausz方法建立重度脾创伤未控制出血性休克大鼠模型.采用随机分组的原则将大鼠分为假处理组、限制输液组、常规输液组、不输液组.观察各组动物的出血量、输液量、存活率、存活时间及各时间点的血压、血细胞比容(Hct)和TNF-α的变化情况.结果①限制输液组的输液量明显少于常规输液组(P＜0.05),出血量也明显少于常规输液组(P＜0.05).②限制输液组Hct明显高于常规输液组(P＜0.05).③限制输液组的存活时间比常规输液组及不输液组明显延长(P均＜0.05).限制输液组在72 h内的存活率明显高于常规输液组和不输液组,但低于假处理组(P均＜0.1).④除假处理组外其余各组在伤后90 min和180 min血TNF-α水平均较伤前均有明显升高(P均＜0.05);常规输液组TNF-α水平明显高于限制输液组(P＜0.05).⑤死亡者TNF-α水平明显高于生存者.结论本研究结果表明,在重度未控制出血条件下,限制性液体复苏可明显降低出血量,提高存活率.未控制性出血休克时的TNF-α水平与预后密切相关,TNF-α高预后不良,而限制性液体复苏时TNF-α水平明显降低.     

腹腔复苏对失血性休克大鼠肺损伤的保护作用

目的探讨腹腔复苏对失血性休克大鼠肺损伤的保护作用。方法健康雄性SD大鼠40只,随机分成假手术组(Ⅰ组)、失血性休克组(Ⅱ组)、静脉复苏组(Ⅲ组)、PD-2液腹腔复苏加静脉复苏组(Ⅳ组)。Ⅰ组依次行右颈总动脉、右股静脉、左股动脉插管及全身肝素化;Ⅱ组在Ⅰ组基础上制备失血性休克大鼠模型;Ⅲ组在Ⅱ组基础上于造模后经右股静脉补入放出的血量及2倍量林格氏液进行静脉复苏;Ⅳ组在Ⅲ组基础上同时腹腔内注入30 mL2.5%PD-2液。各组分别于T0、T1、T2进行PaO2/FiO2值血气分析;T2时测定肺组织W/D比值,TNF-α、IL-1β、IL-10的含量,观察肺组织病理学结果。结果与Ⅰ组比较,Ⅱ组PaO2/FiO2值明显降低,Ⅲ组于T0、T2时下降明显,Ⅳ组T0时下降明显;与Ⅰ组比较,Ⅱ组、Ⅲ组、Ⅳ组肺组织TNF-α、IL-1β、IL-10的含量和W/D比值均升高(P<0.01),与Ⅱ组比较,Ⅲ组和Ⅳ组降低,Ⅳ组肺组织IL-10含量升高(P<0.05或P<0.01)。与Ⅳ组比较Ⅲ组肺组织IL-10含量降低;肺组织病理学比较,Ⅱ组较Ⅰ组有明显损伤,Ⅳ组病理损伤最轻。结论 PD-2液腹腔复苏能够减轻失血性休克大鼠肺组织损害的程度,降低炎症反应,对肺损伤具有保护作用。     

限制性液体复苏抢救非控制性失血性休克临床观察

目的探讨限制性液体复苏在抢救创伤非控制性失血性休克中的价值。方法创伤非控制性失血性休克患者114例随机分为限制性液体复苏组（观察组）和积极液体复苏组（对照组）各57例,比较2组术前输液量、病死率、血红蛋白、血小板计数、凝血酶原时间、血气剩余碱及并发症发生率。结果对照组病死率（15．79％）高于观察组（10．53％）（P〈O．05）,并发症发生率（29．17％）高于观察组（21．57％）（P〈0．05）;术前剩余碱对照组（（215±87）mmol／L）较观察组（（272±93）mmol／L）减少（P〈0．05）,对照组凝血酶原时间（（14．5±1．8）s）较观察组（（12．3±1．7）s）延长（P〈0．05）。结论术前急救采用限制性液体复苏可维持重要器官血流灌注,降低早期大量输液导致的并发症,降低病死率。     

限制性液体复苏救治创伤性失血性休克临床应用研究

目的探讨限制性液体复苏方法对创伤性失血性休克（HTS）的救治效果。方法用限制性液体复苏及常规液体复苏方法救治HTS患者68例,随机分为限制性液体复苏组（36例）,常规液体复苏组（32例）,对两组患者复苏前后血流动力学指标、输入液体量、血清乳酸值、血气碱剩余值进行统计学分析,并比较两组住院期间ARDS、ARF的发生率和死亡率。结果限制性液体复苏组液体输入量为（1966±348）ml,常规液体复苏组液体输入量为（3604±456）ml,两组比较差异有统计学意义（P〈0．05）;限制性液体复苏组、常规液体复苏组复苏前血乳酸值及碱剩余值比较差异无统计学意义（P〉0．05）,复苏12、24h后血乳酸值及碱剩余值比较差异有统计学意义（P〈0．05）;本研究治愈57例（83．8％）,死亡11例（16．2％）,发生ARDS14例,ARF7例,二组治愈率、死亡率、ARDS发生率比较差异有统计学意义。结论本组研究表明：采用限制性液体复苏在救治创伤性失血性休克患者方面,能有效地改善组织器官血液灌注,提高治愈率,降低死亡率,治疗效果优于常规液体复苏方法。     

Low-volume resuscitation cocktail extends survival after severe hemorrhagic shock

After severe hemorrhage, low-volume resuscitation with hypertonic fluids is increasingly preferred to more aggressive resuscitation strategies. Oxygen delivery to the tissues may be improved by augmentation with hemoglobin [Hb]-based oxygen-carrying compounds (HBOCs); however, previous studies have reported negative outcomes presumably related to extravasation of tetrameric Hb. The purpose of this study was to evaluate a novel large molecular weight polymer of cross-linked bovine Hb (OxyVita; OXYVITA Inc, New Windsor, NY) in a cocktail of hypertonic saline and Hextend (HX; HBOC-C) as an alternative to standard small-volume resuscitation using Hextend (HX) only. Outcomes were survival to 3 h and duration of MAP support more than 60 mmHg without additional fluid support. Conscious male Long-Evans rats were hemorrhaged to 60% total blood volume over 40 min. There were 4 groups: HBOC-C administered in a pressure-titrated infusion, HX titration, HBOC-C administered as a bolus, and HX bolus. Cardiovascular parameters, arterial gases, acid-base status, metabolites, electrolytes, Hb level, and oxygen saturation were measured at baseline, during each 20% hemorrhage increment, and 1, 2, and 3 h after the initiation of hemorrhage. Small-volume resuscitation with HBOC-C significantly improved survival to 3 h and improved MAP support times regardless of method of administration. However, physiological status at the end of hemorrhage significantly influenced survival regardless of resuscitation treatment. These results suggest that HBOC-augmented hypertonic cocktails are of promise in improving survival and providing target MAP support during small-volume resuscitation. Experimental evaluation of any resuscitation therapy should account for the degree of preexisting physiological compromise before therapy is initiated.     

液体复苏对初进高海拔地区重度失血性休克犬血流动力学的影响

目的 探讨液体复苏对初进高海拔地区重度失血性休克犬血流动力学的影响.方法 13只成年杂种犬由海拔1510 m地区用l d时间运至3780 m的高海拔地区,随机分为三组(n=13).每只犬麻醉后经颈静脉放置漂浮导管,开放股动、静脉通道,经股动脉放血,使MAP维持在(35±5)mmHg,建立重度失血性休克模型.对照组(n=3):休克模型复制后1 h不进行液体复苏;LR组(n=5):休克1 h后输入1.5倍失血量的LR;6%HES组:休克1 h后输入等失血量的6%HES(n=5):三组犬休克模型复制后每小时以5 mL/ks的速度输注LR作为维持量,观察血流动力学变化.结果 对照组犬在休克模型复制后2 h内全部死亡,较休克1h差异具有统计学意义(P<0.05).其他两组液体复苏后2 h时:LR组MAP,CO,PAWP,CVP,LVSWI,RVSWI较休克1 h显著升高(P<0.05),而HR,SVR,PvR较休克l h显著降低(P<0.05);6%HES组CO,PAP,PAWP,CVP.SVR,PVR较休克1 h显著升高(P<0.05),而MAP,HR,CI,LVSWI,RVSWI较休克1 h差异无统计学意义(P>0.05).,结论 初进高海拔地区的重度失血性休克犬,如果不进行有效的液体复苏,死亡均为(3/3);输入1.5倍失血最的TJR是安全有效的;输入等失血量的6%HKS容易导敛心力衰竭.