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。     

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。     

醋酸钠林格氏液对犬失血性休克复苏过程中血流动力学及血乳酸的影响

目的 比较醋酸钠林格氏液(AR)、乳酸林格氏液(LR)和生理盐水(NS)对失血性休克犬碱剩余(BE)、乳酸(LAC)水平及其血液动力学的影响.方法 将健康成年雄性犬15条随机分为3组:AR组、LR组和NS组,用放血法复制失血性休克模型.分别于放血前、复苏前和复苏后5、30、60 min检测血流动力学参数、动脉血气和血乳酸值.结果 平均动脉压(MAP)恢复至休克前的水平,AR组[(41.10±2.18) ml/kg、(28.15±0.29) min]较LR组[(54.17±2.97) ml/kg、(43.26±0.87) min]、NS组[(59.61±2.88) ml/kg、(48.19±1.23) min]所需输液量更少、时间更短,差异有统计学意义(P＜0.05);复苏30 min后,MAP AR组[(99.25±12.13) mmHg(1mmHg=0.133 kPa)]较LR组[(84.25±11.87)mm Hg]、NS组[(81.25±13.26) mm Hg]明显升高,且AR组较其他组血液pH值、BE及LAC水平显著改善,差异有统计学意义(P＜0.05).结论 醋酸钠林格液比乳酸林格氏液和生理盐水更适合失血性休克犬的早期紧急液体复苏治疗.     

高海拔地区失血性休克早期限制性液体复苏临床研究

目的探讨高海拔地区失血性休克早期限制性液体复苏的临床意义。方法2001年12月至2003年12月根据不同的复苏方式将41例失血性休克病人分为对照组和实验组,检测血红蛋白(HB)、血小板计数(PLT)、红细胞压积(HCT)、血清乳酸水平和失血量变化情况,比较限制性液体复苏与常规液体复苏对高海拔地区失血性休克病人的疗效。结果不同处置后12h两组HCT变化差异有显著性意义(P<0.05);12h及24h两组PLT变化差异有显著性意义(P<0.05);24h两组血清乳酸变化差异有显著性意义(P<0.05)。结论高海拔地区失血性休克病人早期液体复苏时,限制液体复苏相对于快速大量液体复苏不至于扰乱机体的代偿机制和内环境,且对改善细胞氧代谢更有利。     

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.     

气管夹闭窒息法家兔心脏骤停模型的研究

目的　用气管夹闭窒息法建立一种稳定的心肺复苏动物模型。方法　家兔呼气末夹闭气管窒息法致心脏停搏 ,夹管后 8min行标准心肺复苏 5min ,观察窒息和复苏期间的MAP与心电图变化。结果　气管夹闭前MAP为 (111± 7)mmHg(1mmHg =0 .13 3kPa) ,夹闭后MAP明显下降时间为 (172± 2 0 )s ,降至 5 0mmHg时间为 (2 2 8± 3 3 )s ,5min时为 (2 7± 12 )mmHg ,7min时为 (8± 4)mmHg ,MAP变化与心电图变化一致 ;自主循环恢复 16例 ,未恢复 2例 ,心肺复苏成功率为 89%。结论　该模型具有稳定、简单、重复性好的特点 ,能够满足心肺复苏实验研究需要。     

心肺转流术在犬心肺脑复苏中的应用

目的：观察犬在高钾停搏10分钟后行心肺转流术（CPB）复苏,并与常规心肺复苏（CPR）比较其自主循环恢复和脑复苏的效果。方法：将杂种家犬12只,以10％KCl静脉给药致心脏停搏（CA）10分钟后随机分为两组,每组6只。组1;用常规CPR法复苏;组2：用自行研制的心肺转流装置复苏。两组于CA前、CA10分钟,复苏后5分钟、10分钟和30分钟监测平均动脉压（MAP）、心率（HR)、心脏复跳时间、瞳孔大小、72小时存活率和动静脉血气并计算脑氧摄取率（CEO2)脑氧耗量（Ca-jvO2)。结果：组1中6只犬仅2只在CPR后10分钟、15分钟恢复自主心跳,但不稳定,并在60分钟内死亡;组2均于CPB后6－10分钟恢复自主心跳,CPB10分钟后MAP＞80mmHg,明显高于组1（P＜0．05）,其自主循环恢复率为100％,明显大于组1（P＜0．05）。两组CEO2和Ca-jvO2在CA10分钟、复苏后5分钟和10分钟均明显升高（P＜0．05）,且复苏后5分钟、10分钟和30分钟时组1明显高于组2（P＜0．05）。组2犬的瞳孔于复苏后第9－19分钟开始缩小,30分钟后恢复至正常,全组均存活72小时以上,72小时存活率为100％,明显高于组1（P＜0．05）。结论：CA10分钟后,用CPB复苏其自主循环恢复明显优于常规CPR,并有益于脑复苏。     

胸腹部联合损伤患者树突状细胞数量与表面标志的变化

目的　讨胸腹联合损伤后患者外周血树突状细胞 (DC)的变化。方法　胸腹联合损伤患者 ( 2 6例 ,胸腹联合损伤组 ) 2 4h内和健康人 ( 10例 ,对照组 )外周血分离出DC ,通过流式细胞仪检测各组的DC数量 (CMRF -4 4标记法 )及DC表面HLA -DR、CD80 、CD86表达水平以及DC诱导的T细胞反应性增殖。结果　胸腹联合损伤组DC细胞数为 ( 7.5± 3 .3 )× 10 6/L ,明显低于对照组的 ( 14 .9± 5 .1)× 10 6/L(P <0 .0 1)。胸腹联合损伤组DC表面HLA -DR及CD80 、CD86的表达水平与对照组相比明显下降 (P <0 .0 1)。DC诱导的T细胞增殖能力胸腹联合损伤组明显低于对照组 (P <0 .0 1)。结论　胸腹联合损伤患者早期外周血DC数量少 ,功能低下 ,与创伤早期免疫功能低下有关。     

限制性液体复苏在肝破裂失血性休克的应用体会

目的研究限制性液体复苏对肝破裂失血性休克的治疗效果。方法将两院2008年1月至2012年1月,共收治的肝破裂失血性休克58例患者随机分成两组常规组（A组）和限制组（B组）。比较两组复苏后的血压、心率、尿量和乳酸、碱缺失变化来了解患者的内环境状态,判断复苏效果。结果限制组平均输液量明显降低,血压、心率、尿量和乳酸、碱缺失（BE）显著改善。B组和A组比较HR、SBP、MAP、CVP、血乳酸,、尿量、碱缺失（BE）均P〈0．05有显著意义。结论在肝破裂失血性休克患者出血未控制情况下,限制性液体复苏不仅可维持重要脏器的血流灌注,而且降低了出血,改善了预后,取得了满意的疗效。     

蛋白酶抑制剂对大鼠呼吸心跳骤停后早期复苏脑内能量代谢的初步研究

目的探讨蛋白酶抑制剂乌司他丁（ulinastain,UTI）对大鼠呼吸心跳骤停后早期心肺复苏（cardiopulmonary resuscitation,CPR）脑内能量代谢的影响和脑保护作用。方法成年雄性SD大鼠30只,按照随机数字表法分为对照组（C组）、生理盐水复苏组（NS组）和UTI复苏组（UTI组）,每组10只。各组均行麻醉,气管插管及颈动脉插管。C组不做模型,UTI组及NS组采用窒息法制作大鼠心跳骤停（cardiac arrest,CA）CPR模型。UTI组于自主循环恢复（restoration of spontaneous circulation,ROSC）后2min内经颈动脉推注注射用UTI（105U／kg）,NS组推注等量的生理盐水。记录各组窒息至CA时间和复苏开始至ROSC时间,监测各组ROSC后1h内的平均动脉压（mean arterial pressure,MAP）。C组仅行气管插管及颈动脉插管,不进行窒息CA及CPR操作。C组于气管切开置管、颈动脉置管后1h,NS组和UTI组于ROSC后1h,经颈动脉取血和快速断头取脑组织。脑组织进行脑组织三磷酸腺苷（adenosine triphosphate,ATP）和乳酸（1actate,LA）含量测定,光镜和电镜下观察海马组织的病理改变。结果①组间MAP基线值差异无统计学意义（P〉0.05）。NS组和UTI组ROSC后2、5、30minMAP差异无统计学意义（P〉0.05）。NS组和UTI组MAP在ROSC后2min较基线值都有显著升高[NS组,（166±11）mmHg vs （143±12）mmHg,P〈0.01;UTI组,（170±11）mmHg vs （141±16）mmHg;1mmHg=0.133kPa;P〈O.01];ROSC后5min MAP[NS组,（91±9）mmHg;UTI组,（96±10）mmHg]呈下降趋势,低于基线值（P＜0.01）;ROSC后30min MAP[NS组,（125±12）mmHg;UTI组,（122±13）mmHg]可恢复并趋于稳定,但仍低于基线值（P〈0.05）。②与C组比较,NS组和UTI组大鼠脑组织LA值在ROSC后1h均明显升高[C组：NS组：UTI组,（0.29±0.13）mmol／g prot vs （0.69±0.14）mmol／g prot vs （0.53±0.08）mmol／g prot,P〈0.01）];与NS组比较,UTI     

高渗氯化钠羟乙基淀粉复合液对失血性休克肺的保护作用

目的观察用高渗氯化钠羟乙基淀粉复合液(7.5%氯化钠 6%羟乙基淀粉200/0.5,HHS)小容量复苏对失血性休克后肺损伤的影响。方法雄性SD大鼠随机分为五组:正常对照组(CON组,n=6):不放血不补液;其他大鼠通过放血使MAP降至45mmHg并维持120min,然后分为:休克组(SH组,n=6),不补液复苏;HHS组(n=8),用HHS5ml/kg静脉滴注;7.5%氯化钠高渗溶液组(HTS组,n=6),用7.5%NaCl5ml/kg静脉滴注;复方乳酸钠组(LR组,n=7),用3倍失血量的复方乳酸钠静脉滴注。观察休克2h末、补液结束即刻、15、30、60、120、180min时MAP、CVP的变化,测定补液结束2、24h存活动物的氧合指数和肺水含量、肺髓过氧化物酶(MPO)水平、肺损伤评分。结果在补液结束120、180min,HTS组MAP、CVP低于HHS和LR组(P<0.05);在补液结束24h,HHS组氧合指数、肺水含量、肺MPO水平、肺损伤评分优于HTS和LR组(P<0.05)。结论用HHS小容量复苏失血性休克,维持血流动力学稳定时间更长;对肺组织的保护作用优于7.5%氯化钠高渗溶液或复方乳酸钠。     

Target blood pressure for hypotensive resuscitation

Background

Good outcomes have resulted from hypotensive resuscitation of hemorrhagic shock patients. We hypothesized that mean arterial pressure (MAP) 60 mmHg is the target blood pressure for hypotensive resuscitation during uncontrolled hemorrhagic shock in trauma.

Methods

To determine the effective target MAP for hypotensive resuscitation during uncontrolled hemorrhagic shock, we randomly assigned 80 rats to one of 8 treatment groups (n = 10 for each group). We then observed the effects of different target MAPs (control, 40, 50, 60, 70, 80, 90 mmHg, and sham) on fluid resuscitation of uncontrolled hemorrhagic shock. Blood pressure, serum lactate, hematocrit, fluid therapy, blood loss, and plasma cytokine levels were measured at 0, 30, 90, 120, 180, 240, 300 min after the start of the surgical procedure.

Results

A target MAP of 90, 80 and 70 mmHg had increased blood loss and decreased hematocrit and IL-6 and TNF-α production. A target MAP of 60, 50 and 40 mmHg had lower blood loss, good hematocrit, higher IL-6 and TNF-α production, and decreased animal survival. Only target MAPs of 40 and 50 had and decreased animal survival. The differences in blood loss, hematocrit, lactate, post-resuscitation MAP, survival, IL-6, IL-10, and TNF-α production between rats with a target MAP of 60 mmHg and those with a target MAP of 70 mmHg were not significant. The amount of fluid therapy in the BP 60 groups was less than in the BP 70 groups (P < 0.001).

Conclusion

A MAP of 60 mmHg should be considered for evaluation in human studies as a target for hypotensive resuscitation.     

Improved survival after resuscitation with norepinephrine in a murine model of uncontrolled hemorrhagic shock

BACKGROUND: Recent studies have challenged current guidelines on fluid resuscitation. However, studies on resuscitation using norepinephrine in uncontrolled hemorrhagic shock are lacking. The authors examined the effects of norepinephrine in combination with saline infusion in uncontrolled hemorrhage in rats. METHODS: Rats subjected to a 15-min controlled hemorrhage (withdrawal of 3 ml blood/100 g body mass) followed by a 60-min uncontrolled hemorrhage (75% tail amputation) were randomly assigned to one of several treatment groups (10 rats/group) receiving different doses of norepinephrine (0 [NE0], 5 [NE5], 50 [NE50], or 500 [NE500] microg.100 g(-1).h(-1)). In the four hypotensive resuscitation groups (n = 40), mean arterial pressure was not allowed to fall below 40 mmHg by titrated infusion of normal saline. In the four normotensive resuscitation groups (n = 40), it was not allowed to fall below 80 mmHg. The endpoint was survival at 210 min. RESULTS: There was a significant difference (P < 0.05) in survival rate among groups. Among the hypotensive rats, 6 (60%) survived in the NE0 and NE5 dose groups, 9 (90%) survived in the NE50 dose group, and none survived in the NE500 dose group. Among the normotensive rats, none survived in the NE0 group, 4 (40%) survived in the NE5 dose group, all 10 (100%) survived in the NE50 group, and none survived in the NE500 group. CONCLUSIONS: The early use of norepinephrine in uncontrolled hemorrhagic shock in rats significantly improved survival when infused at a rate of 50 microg.100 g(-1).h(-1) in normotensive and hypotensive resuscitation strategies.     

Lactated Ringer's is superior to normal saline in the resuscitation of uncontrolled hemorrhagic shock

BACKGROUND: Normal saline (NS) and lactated Ringer's solution (LR) continue to be used interchangeably for the resuscitation of hemorrhagic shock in some institutions. We hypothesized that, aside from hyperchloremic acidosis, NS resuscitation would be similar to that of LR in a swine model of uncontrolled hemorrhage. METHODS: Twenty swine weighing a mean of 37 kg underwent invasive line placement, midline celiotomy, and splenectomy. After a 15-minute stabilization period, we recorded a baseline mean arterial pressure (MAP) and created a grade V liver injury. The animals bled freely for 30 minutes after which we measured blood loss. We blindly randomized the swine to receive NS (10 animals) versus LR (10 animals) to achieve and maintain the baseline MAP for 90 minutes postinjury. Laboratory values were obtained at baseline and upon completion of the 2-hour study period. RESULTS: Initial blood loss was 25 mL/kg in the NS group and 22 mL/kg in the LR group (p = 0.54). Animals required 256.3 +/- 145.4 mL/kg of fluid in the NS group as compared with 125.7 +/- 67.3 mL/kg in the LR group (p = 0.04). The urine output was higher in the NS group (46.6 +/- 39.5 mL/kg versus 18.9 +/- 12.9 mL/kg, p = 0.04). Upon study completion, the NS group had a significant hyperchloremia (119 +/- 1.9 mEq/L versus 105 +/- 2.9 mEq/L, p < 0.01) with acidosis (7.28 +/- 0.12 versus 7.45 +/- 0.06, p < 0.01) in comparison to the LR group. In addition, resuscitation with NS resulted in significantly lower fibrinogen levels (99 +/- 21 mg/dL versus 123 +/- 20 mg/dL, p = 0.02). The serum lactate was 4.7 +/- 2.2 in the LR group and 1.7 +/- 1.7 in the NS swine (p < 0.01) at the end of the study. CONCLUSIONS: Resuscitation of uncontrolled hemorrhagic shock with NS requires significantly greater volume and is associated with greater urine output, hyperchloremic acidosis, and dilutional coagulopathy as compared with LR. Resuscitation with LR results in an elevation of the lactate level that is not associated with acidosis. Lactated Ringer's solution is superior to NS for the resuscitation of uncontrolled hemorrhagic shock in swine.     

Resuscitation with normal saline (NS) vs. lactated ringers (LR) modulates hypercoagulability and leads to increased blood loss in an uncontrolled hemorrhagic shock swine model

BACKGROUND: Lactated ringers (LR) and normal saline (NS) are used interchangeably in many trauma centers. The purpose of this study was to compare the effects of LR and NS on coagulation in an uncontrolled hemorrhagic swine model. We hypothesized resuscitation with LR would produce hypercoagulability. METHODS: There were 20 anesthetized swine (35 +/- 3 kg) that underwent central venous and arterial catheterization, celiotomy, and splenectomy. After splenectomy blinded study fluid equal to 3 mL per gram of splenic weight was administered. A grade V liver injury was made and animals bled without resuscitation for 30 minutes. Animals were resuscitated with the respective study fluid to, and maintained, at the preinjury MAP until study end. Prothrombin Time (PT), Partial Thromboplastin Time (PTT), and fibrinogen were collected at baseline (0') and study end (120'). Thrombelastography was performed at 0'and postinjury at 30', 60', 90', and 120'. RESULTS: There were no significant baseline group differences in R value, PT, PTT, and fibrinogen. There was no significant difference between baseline and 30 minutes R value with NS (p = 0.17). There was a significant R value reduction from baseline to 30 minutes with LR (p = 0.02). At 60 minutes, R value (p = 0.002) was shorter while alpha angle, maximum amplitude, and clotting index were higher (p < 0.05) in the LR versus the NS group. R value, PT, and PTT were significantly decreased at study end in the LR group compared with the NS group (p < 0.05). Overall blood loss was significantly higher in the NS versus LR group (p = 0.009). CONCLUSIONS: This data indicates that resuscitation with LR leads to greater hypercoagulability and less blood loss than resuscitation with NS in uncontrolled hemorrhagic shock.     

Effect of methylprednisolone on reperfusion injury in severe uncontrolled hemorrhagic shock

Ucontrolledhemorrhagicshockisoneoftheseverediseasesinclinic .Severeuncontrolledhemorrhagicshockandhypotensiveresusicitationhavebecomeafocusintraumotologyandtherelatedfield .Researchessuggestthatoxygenfreeradicalinjuryispresentduringischemiaandreperfusionandthatoxygenfreeradical mediatedreperfusioninjurymightinvolveinoneofthemechanismsleadingtoirreversiblehemorrhagicshock .ThisstudyaimstoexplorethetreatmenteffectofMPonreperfusioninjuryfollowingsevereuncontrolledhemorrhagicshockindogsbyobservin…     

Resuscitation from hemorrhagic shock. Alterations of the intracranial pressure after normal saline, 3% saline and dextran-40.

Resuscitation from hemorrhagic shock by infusion of isotonic (normal) saline (NS) is accompanied by a transient elevation in intracranial pressure (ICP), although cerebral edema, as measured by brain weights at 24 hours, is prevented by adequate volume resuscitation. The transient increase in ICP is not observed during hypertonic saline (HS) resuscitation. The effect of colloid resuscitation on ICP is unknown. Beagles were anesthetized, intubated, and ventilated, maintaining pCO2 between 30-45 torr. Femoral artery, pulmonary artery, and urethral catheters were positioned. ICP was measured with a subarachnoid bolt. Forty per cent of the dog's blood volume was shed and the shock state maintained for 1 hour. Resuscitation was done with shed blood and a volume of either NS (n = 5), 3% HS (n = 5), or 10% dextran-40 (D-40, n = 5) equal to the amount of shed blood. Intravascular volume was then maintained with NS. ICP fell from baseline values (4.7 +/- 3.13 mmHg) during the shock state and increased greatly during initial fluid resuscitation in NS and D-40 groups, to 16.0 +/- 5.83 mmHg and 16.2 +/- 2.68 mmHg, respectively. ICP returned to baseline values of 3.0 +/- 1.73 mmHg in the HS group with initial resuscitation and remained at baseline values throughout resuscitation. NS and D-40 ICP were greater than HS ICP at 1 hour (p less than .001) and 2 hours (p less than .05) after resuscitation. These results demonstrate that NS or colloid resuscitation from hemorrhagic shock elevates ICP and that HS prevents elevated ICP.     

Improved Survival after Resuscitation with Norepinephrine in a Murine Model of Uncontrolled Hemorrhagic Shock

Background: Recent studies have challenged current guidelines on fluid resuscitation. However, studies on resuscitation using norepinephrine in uncontrolled hemorrhagic shock are lacking. The authors examined the effects of norepinephrine in combination with saline infusion in uncontrolled hemorrhage in rats.

Methods: Rats subjected to a 15-min controlled hemorrhage (withdrawal of 3 ml blood/100 g body mass) followed by a 60-min uncontrolled hemorrhage (75% tail amputation) were randomly assigned to one of several treatment groups (10 rats/group) receiving different doses of norepinephrine (0 [NE0], 5 [NE5], 50 [NE50], or 500 [NE500] [mu]g [middle dot] 100 g-1 [middle dot] h-1). In the four hypotensive resuscitation groups (n = 40), mean arterial pressure was not allowed to fall below 40 mmHg by titrated infusion of normal saline. In the four normotensive resuscitation groups (n = 40), it was not allowed to fall below 80 mmHg. The endpoint was survival at 210 min.

Results: There was a significant difference (P < 0.05) in survival rate among groups. Among the hypotensive rats, 6 (60%) survived in the NE0 and NE5 dose groups, 9 (90%) survived in the NE50 dose group, and none survived in the NE500 dose group. Among the normotensive rats, none survived in the NE0 group, 4 (40%) survived in the NE5 dose group, all 10 (100%) survived in the NE50 group, and none survived in the NE500 group.     

A comparison of lactated ringer's solution to hydroxyethyl starch 6% in a model of severe hemorrhagic shock and continuous bleeding in dogs

In this randomized, controlled study in dogs, we examined the short-term effects of blood pressure targeted fluid resuscitation with colloids or crystalloids solutions on systemic oxygen delivery, and lactate blood concentration. Fluid resuscitation using hydroxyethyl starch (HES) 6% to a mean arterial blood pressure (MAP) of 60 mm Hg was compared with lactated Ringer's solution (LR) to a MAP of 60 or 80 mm Hg (LR60 and LR80, respectively). The model was one of withdrawal of blood to a MAP of 40 mm Hg through an arterial catheter that was then connected to a system allowing bleeding to occur throughout the study whenever MAP exceeded 40 mm Hg. Target MAP was maintained for 60 min with a continuous infusion of the designated fluid replacement. All 15 dogs (5 in each group) survived until the last measurement. Blood loss in the LR80 group (2980 +/- 503 mL) (all values mean +/- SD) was larger than in the LR60 and HES60 groups (1800 +/- 389 mL, and 1820 +/- 219 mL, respectively) (P < 0.001). Whereas 840 +/- 219 mL of HES60 was needed to maintain target MAP, 1880 +/- 425 mL of LR was needed in the LR60 group, and 4590 +/- 930 mL in the LR80 group (P < 0.001). Lactate blood concentrations were smaller and delivered O(2) higher in the HES60 group (35 +/- 17 mg/dL and 239 +/- 61 mL/min, respectively) in comparison to the LR60 group (89 +/- 18 mg/dL and 140 +/- 48 mL/min, respectively) and the LR80 group (75 +/- 23 mg/dL and 153 +/- 17 mL/min, respectively) (P = 0.02 and P = 0.026). In conclusion, fluid resuscitation during uncontrolled bleeding, to a target MAP of 60 mm Hg, using HES60 resulted in larger oxygen delivery and smaller systemic lactate A resuscitation to a target MAP of 60 or 80 mm Hg using LR. IMPLICATIONS: Fluid resuscitation to a target mean arterial blood pressure of 60 mm Hg during uncontrolled bleeding resulted in larger oxygen delivery and smaller systemic lactate concentrations when hydroxyethyl starch 6% was used, in comparison to lactated Ringer's solution resuscitation to a target mean arterial blood pressure of 60 or 80 mm Hg.     

Early colloid replacement therapy in a near-fatal model of hemorrhagic shock

Several controlled, experimental, hypotensive models of hemorrhagic shock have evaluated the effects of timing, rate, and types of fluid replacement. In a near-fatal experimental model we evaluated the hemodynamic and metabolic effects of two types of solutions for fluid resuscitation. In this study, 30 young Large-White pigs were randomly assigned to three groups: Group I (control, n= 10), not bled; Group II (hydroxyethyl starch, HES, n = 10), submitted to controlled hemorrhage to a mean arterial blood pressure (MAP) of 30 mmHg and blood lactate >10 mM/L, at which time resuscitation was initiated with 7 mL/kg of HES 130/0.4 6% followed by 33 mL/kg of lactated Ringer's solution (LR) and retransfusion; Group III (LR, n = 10), submitted to controlled hemorrhage to a MAP of 30 mmHg and blood lactate >10 mM/L, at which time resuscitation was initiated with 40 mL/kg of LR followed by retransfusion. The resuscitation with HES 130/0.4 proved to be superior to LR, expressed by hemodynamic and perfusion variables. Despite improvement in tissue perfusion, MAP did not totally return to baseline values. In conclusion, early colloid infusion resulted in prompt recovery of tissue perfusion when compared with infusion with an equal volume of crystalloid.