卡巴胆碱对烧伤休克犬口服补液时胃排空和胃黏膜二氧化碳分压的影响

目的 研究卡巴胆碱对烧伤犬休克早期口服补液时胃排空和胃黏膜二氧化碳分压(PgCO2)的影响.方法 将24只成年雄性Beagle犬随机分为4组:35%总体表面积(TBSA)烧伤后口服葡萄糖一电解质液(GES)组及其卡巴胆碱干预组(35%TBSA GES组和35%TBSA GES/CAR组);50%TBSA烧伤后口服GES液组及其卡巴胆碱干预组(50%TBSA GES组和50%TBSA GES/CAR组),每组6只.采用凝固汽油燃烧法分别造成颈背部35%TBSA Ⅲ度烧伤和颈背部+胸腹部50%TBSA Ⅲ度烧伤.各组于烧伤后0.5 h开始按Parkland公式量和速率(4 ml·kg-1·1%TBSA-1,前8 h内补1/e量,后16 h内补另1/2量)口服补液;GES/CAR组于伤后0.5 h口服卡巴胆碱(20 μg/kg溶于GES中).烧伤后2、4、8和24 h测定胃排空率和PgCO2,并观察胃不耐受症状.结果 烧伤后各组犬胃排空率均显著低于伤前(P均＜0.05),伤后2 h 35%TBSA GES组降至51.5%.伤后4 h 50%TBSA GES组降至39.2%,之后逐渐恢复,但伤后24 h仍显著低于伤前(P均＜0.05).35%TBSA GES/CAR组伤后各时间点胃排空率均显著高于同烧伤面积GES组(P均＜0.05),平均提高15.0%,伤后8 h恢复至伤前水平;50%TBSA GES/CAR组于8 h起胃排空率显著高于同烧伤面积GES组,但伤后24 h仍低于伤前水平(P＜0.05).伤后各组犬PgCO2均较伤前显著升高(P均＜0.05),35%TBSA GES/CAR组伤后各时间点显著低于同烧伤面积GES组,50%TBSA GES/CAR组伤后4 h起显著低于同烧伤面积GES组(P均＜0.05).伤后各组犬出现呕吐等胃不耐受症状情况比较:50%TBSA GES组(83.3%,5/6)＞50%TBSA GES/CAR组(50.0%,3/6)＞35% TBSA GES组(16.7%,1/6)＞35%TBSA GES/CAR组(0,0/6).结论 卡巴胆碱能显著改善Beagle犬烧伤休克早期胃对GES的排空,降低PgCO2,提高口服液体复苏的效果.     

卡巴胆碱对犬50%总体表面积烧伤口服补液时肺血管通透性和肺组织含水量的影响

目的 研究卡巴胆碱(CAR)对犬50%总体表面积(TBsA)烧伤休克期口服补液时肺血管通透性和肺组织含水量的影响.方法 成年雄性Beagle犬12只,先行颈动、静脉置管,24 h后造成50%TBSAⅢ度烧伤.伤后24 h随机分为口服补液组和口服补液+CAR组,每组6只,从胃内分别输注葡萄糖一电解质溶液(GES)和含CAR的GES液(20 gg/kg CAR溶于GES),伤后24 h起实施静脉延迟补液,补液量和速率均根据Parkland公式确定.于伤前(0)及伤后2、4、8、24、48和72 h测定各组犬呼吸频率(RR)、动脉血氧分压(PaO2)、血管外肺水指数(ELWI)和肺血管通透性指数(PVPI);于伤后72 h处死动物,取肺组织测定髓过氧化物酶(MPO)活性、丙二醛(MDA)含量以及肺组织含水量.结果 烧伤后两组动物RR、ELWI和PVPI较伤前均显著增加,PaO2显著降低(P均<0.01);伤后72 h PaO2恢复至伤前水平.口服补液+CAR组伤后4、8和24 h RR、ELWI和PVPI显著低于口服补液组,伤后8、24、48 h PaO2显著高于口服补液组(P<0.05或P<0.01),但伤后72 h两组间上述指标差异均无统计学意义(P均>0.05).伤后72 h口服补液+CAR组肺组织MPO活性、MDA含量及肺组织含水量均显著低于口服补液组[(2.64±0.38)U/mg比(4.12±0.46)U/rag,P<0.01;(3.60±0.54)μtmol/mg比(5.14±0.62)μmol/mg,P<0.01;(77.40±0.56)%比(78.30±0.54)%,P<0.01].结论 50%TBSA烧伤口服补液时给予CAR能抑制肺组织炎症反应和过氧化损伤,减轻烧伤休克引起的肺血管通透性增加和肺水肿.     

卡巴胆碱对大鼠烫伤休克期肠内补液时肠道的影响

目的 研究拟胆碱药卡巴胆碱对大鼠烫伤休克期肠内补液时肠道局部炎症反应和肠组织损伤的影响,为烧伤休克胃肠道补液研究提供依据.方法 38只雄性Wistar大鼠,采用沸水法(100℃,10 s)造成背部35%TBSAⅢ度烫伤.随机分为不复苏组(单烫组,n=8)、葡萄糖-电解质溶液(glucose electrolyte solution)复苏组(GES组,n=10)、卡巴胆碱治疗组(CAR组,n=10)和GES+卡巴胆碱复苏组(GES/CAR组,n=10).两液体复苏组大鼠在烫伤后30 min将GES经十二指肠造口匀速泵入,按Parkland公式设定补液速率,即烫伤后第一个24 h补液总量4 ml·1%TBSA-1·kg-1,前8 h匀速补一半.CAR组和GES/CAR组大鼠在伤后30 min将CAR以60μg·kg-1溶于0.5 ml生理盐水中一次注入十二指肠.所有大鼠在烫伤后4 h处死,取空肠组织测定一氧化氮合酶(N0s)、一氧化氮(NO)、肿瘤坏死因子-α(TNF-α)含量和髓过氧化物酶(MPO)活性,同时测定血浆二胺氧化酶(DAO)活性,采用组间方差分析统计比较各组上述指标的差别.结果 GES组的肠组织NOS、NO、TNF-α、MPO和血浆DAO水平与单烫组差异无统计学意义;GES/CAR组各指标较GES组均明显降低[NOS(1.276±0.39I vs.(1.818±0.436),P＜0.01;NO(0.925±0.402)vs.(1.561±0.379),P＜0.01;TNF-α(0.87±0.13)vs.(1.94±0.47),P＜0.01;MPO(0.465±0.092)vs.(0.832±0.214),P＜0.01;DAO(0.732±0.192)vs.(1.381±0.564),P＜0.01],CAR组各指标也较单烫组和GES组明显降低(P＜0.05或P＜0.01).结论 卡巴胆碱能减轻烫伤休克大鼠肠内液体复苏时的肠道局部炎症反应和组织损伤,其作用机制可能与其兴奋胆碱能神经N受体,抑制促炎因子释放的作用有关.     

卡巴胆碱对烧伤犬肠内补液时肠黏膜血流量和吸收效率的影响

目的 研究卡巴胆碱对50%总体表面积(TBSA)Ⅲ度烧伤休克Beagle犬肠内补液时肠黏膜血流量和吸收效率的影响.方法 成年雄性Beagle犬18只,采用凝固汽油燃烧法造成约(51.2±2.6)%TBSAⅢ度烧伤,伤后0.5 h开始按Parkland公式量和速率补液.随机将动物均分为静脉输葡萄糖一电解质液(GES)组(VGES)、肠内输GES组(EGES)和肠内输GES/卡巴胆碱组(EGES/CAR,含0.25 μg/kg卡巴胆碱的GES).在动物清醒状态下观察两个肠内补液组伤后8 h内小肠黏膜血流量(IBF)、水和Na+的吸收速率,以及3组动物血浆Na+浓度、血浆容量(PV)和伤后8 h小肠组织Na+-K+-ATP酶活性的变化.结果 伤后两个肠内补液组水和Na+的吸收速率均较伤前显著降低(P均＜0.05),EGES/CAR组自伤后1.5 h和2.5 h起显著高于EGES组(P均＜0.05),但8 h两组均低于伤前和按Parkland公式补液速率(P＜0.05).EGES组对肠内补液不耐受(腹泻)发生率为83%,显著高于EGES/CAR组的50%.伤后8 h EGES/CAR和EGES组输入肠内的液体仅有47.1%和63.8%被吸收;EGES/CAR组吸收液体总量和吸收率显著多于EGES组.伤后各组IBF均较伤前显著降低;伤后8 h已恢复到伤前水平(P＞0.05);EGES/CAR组IBF伤后2 h起高于EGES组(P＜0.05),但两个肠内补液组伤后8 h仍显著低于伤前和VGES组水平(P均＜0.05).3组伤后8 h小肠黏膜Na+-K+-ATP酶活性比较:VGES组＞EGES/CAR组＞EGES组(P＜0.05).两个肠内补液组伤后8 h内的血浆Na+浓度和PV均显著低于VGES组(P均＜0.05),但伤后4 h起EGES/CAR组显著高于EGES组(P均＜0.05).结论 50%TBSAⅢ度烧伤早期IBF和Na+-K+-ATP酶活性显著降低,肠内补液的吸收效率显著低于按Parkland公式输入速率,不能维持静脉补液的血浆Na+浓度和PV;而卡巴胆碱能增加IBF和Na+-K+-ATP酶活性,提高肠内补液的吸收速率、PV和血浆Na+浓度,改善口服补液的疗效.     

卡巴胆碱对烧伤休克口服补液时肠屏障功能的影响

目的 研究拟胆碱药卡巴胆碱对犬烧伤休克口服补液时肠屏障功能的影响.方法成年雄性Beagle犬20只,采用凝固汽油燃烧法造成35% TBSA Ⅲ度烧伤,烧伤后随机分为延迟复苏(DR)组、口服葡萄糖-电解质溶液(GES)组、口服卡巴胆碱(CAL)组、口服葡萄糖-电解质溶液 卡巴胆碱(GES CAL)组.GES按Parkland公式(4 mL?kg-1?1% TBSA-1)经胃管输注,卡巴胆碱20 μg/kg溶于10 mL生理盐水中,分别于伤后30 min和4 h经胃管注入.烧伤24 h后各组均给予静脉输注5%葡萄糖生理盐水液进行延迟复苏.测定各组动物伤前及伤后2、4、8、24、48、72 h血浆二胺氧化酶(DAO)活性、D-乳酸(D-LA)含量和D-木糖(D-XY)含量.结果烧伤后DR组血浆DAO、D-LA和D-XY显著高于另外三组(P＜0.01,P＜0.05).各治疗组间比较,GES CAL组血浆DAO伤后2 h和4 h显著低于GES组和CAL组(P＜0.05),GES CAL组D-XY伤后8 h和24 h显著低于GES组和CAL组(P＜0.05).结论卡巴胆碱对犬烧伤休克口服补液时肠屏障功能有保护作用.     

卡巴胆碱对烧伤休克犬肠内补液时肠组织缺血／再灌注损伤的影响

目的 探讨卡巴胆碱(CAR)对烧伤休克期肠内补液时肠缺血/再灌注损伤的保护作用.方法 18只成年雄性Beagle犬被随机分为3组,每组6只.采用凝固汽油燃烧法造成50%总体表面积(TBSA)Ⅲ度烧伤模型.伤后无治疗(不补液组)或于伤后30 min开始从十二指肠造口分别输入葡萄糖-电解质溶液(GES组)或含CAR的GES(20 μg/kg CAR溶于GES,GES/CAR组),伤后8 h内输液量依据Parkland公式计算.检测伤前和伤后1、2、4、6、8 h小肠黏膜血流量(IMBF)及血浆肿瘤坏死因子-α(TNF-α)含量.伤后8 h处死动物,取空肠组织用干湿重法测定小肠组织含水量;并测定一氧化氮合酶 (NOS)、丙二醛(MDA)、髓过氧化物酶(MPO)、黄嘌呤氧化酶(XOD)水平.结果 各组伤后IMBF均显著降低,TNF-α显著升高;伤后4 h起GES组IMBF显著高于不补液组,6 h后显著低于GES/CAR组(P均<0.01);不补液组与GES组TNF-α含量差异无统计学意义,但伤后2 h和4 h均显著高于GES/CAR组(P均<0.01).伤后8 h GES组NOS、MDA、MPO和XOD均显著高于不补液组,而GES/CAR组分别比GES组低26.0%、17.1%、50.0%和19.2%,差异均有统计学意义(P<0.05或P<0.01).GES/CAR组肠组织含水量也显著低于GES组(P<0.01).结论 CAR能有效减轻烧伤犬肠内补液时肠组织缺血/再灌注损伤,机制可能与增加肠黏膜血流,抗炎和抑制XOD活性,减少炎症因子和氧自由基生成有关.     

卡巴胆碱对重症急性胰腺炎患者治疗价值的研究

目的:探讨卡巴胆碱在重症急性胰腺炎治疗中的临床价值.方法:选取2007年1月至2008年12月唐山市3家三级医院ICU重症胰腺炎患者108例.随机分为卡巴胆碱组(55例)和正常治疗组组(53例).正常治疗组包括液体复苏、氧疗、禁食、止痛、胃肠减压、器官功能维护等;卡巴胆碱组在常规治疗的基础上给予卡巴胆碱肌肉注射,每次0.2 mg/kg,每日2次.于治疗前(0 h),治疗后24、48、72、96 h或患者死亡前观察两组患者胃肠功能评分及血清CRP的变化.结果:卡巴胆碱可以减低胃肠功能评分、改善肠道功能,抑制炎症因子释放,降低炎症反应.结论:卡巴胆碱在重症急性胰腺炎治疗中具有一定的临床价值.     

卡巴胆碱对脓毒症小鼠脾脏树突状细胞变化的影响

目的从调节脾脏树突状细胞（DC）活性的角度探讨卡巴胆碱在防治脓毒症中的作用机制。方法将雄性C57BL／6小鼠30只按随机数字表法均分为正常对照组、脓毒症组和卡巴胆碱组。腹腔注射脂多糖（LPS）制备小鼠脓毒症模型，用流式细胞仪检测DC表面分子CD11c、CD86和主要组织相容性抗原复合物Ⅱ（MHC-Ⅱ）的表达；采用免疫组化标记技术检测白细胞介素-1β（IL-1β）与IL-12p70的阳性细胞率。结果注射LPS后，脾脏DC数量增加，但与正常对照组比较差异无显著性；DC表面分子MHC-Ⅱ和cD86表达以及IL-1β和IL-12p70阳性细胞率均较正常对照组增高，差异均有显著性（P均〈0．05）；与脓毒症组比较，卡巴胆碱组脾脏DC的数量没有明显变化，但表面分子MHC-Ⅱ和CD86表达及IL-1β和IL-12p70阳性细胞率均明显降低，差异具有显著性（P均〈0．05）。结论卡巴胆碱能降低DC活性，有助于减轻脓毒症早期过度的免疫反应和炎症反应。     

高渗氯化钠对失血性休克犬器官血流量的影响

高渗氯化钠对失血性休克犬器官血流量的影响文亮毕敏研究了７．５％氯化钠对失血性休克犬颈内动脉、肝动脉、门静脉及肾动脉血流量的影响，现报道如下。１材料与方法选健康杂种犬７只，雌雄不拘，体重１０～１２ｋｇ。肌注氯胺酮１０ｍｇ／ｋｇ后平卧于手术台上，行气管内...     

手术中严重失血性休克的快速补液处理

手术中发生大血管破裂严重出血后，快速补充血容量是治疗的关键措施。但由于输血可降低机体免疫功能，增加术后感染率等并发症，用血浆代用品及平衡液等液体实施快速输注治疗是一种抗休克的有效措施，现报告如下。     

阿魏酸钠对家兔创伤失血性休克复苏胃黏膜损伤的保护作用

目的 探讨阿魏酸钠对创伤失血性休克复苏胃黏膜损伤的保护作用及机制.方法 家兔100只,按随机数字表法分为4组:A组为正常对照组、B组为模型组、C组和D组分别为复苏前及复苏后应用阿魏酸钠组,每组25只.以股骨粉碎性骨折及放血法建立家兔创伤失血性休克复苏胃黏膜损伤模型,复苏前20 min C组及复苏30 min时D组缓慢静注阿魏酸钠30 mg/kg.复苏90 min取胃黏膜组织,光镜下观察胃黏膜病理学改变,测定胃黏膜组织一氧化氮(NO)、内皮素(ET)和丙二醛(MDA)含量及超氧化物歧化酶(SOD)活性.结果 与A组比较,余3组MDA、ET和NO含量升高及SOD活性降低(P<0.01),胃黏膜有不同程度损伤.与B组比较,C、D两组MDA、ET和NO含量降低,而SOD活性升高 (P<0.05或0.01),胃黏膜损伤程度减轻.与C组比较,D组MDA、ET和NO含量升高及SOD活性降低(P<0.05).结论 阿魏酸钠对家兔创伤失血性休克复苏胃黏膜损伤具有保护作用,且复苏前应用效果较佳.其机制与阿魏酸钠清除氧自由基、降低ET水平及抑制NO过量产生有关.     

Effects of fluid resuscitation on mesenteric microvascular blood flow and lymphatic activity after severe hemorrhagic shock in rats

We investigated the acute microcirculatory effects, including mesenteric lymphatic pumping, of volume replacement with different iso- or hypertonic/oncotic solutions after severe hemorrhage (mean arterial pressure [MAP] approximately 35 mmHg during 30 min) in halothane-anesthetized Wistar rats. Resuscitation was achieved 30 min after induction of shock with one of the following solutions: autologous blood (BL); 0.9% NaCl (IS), 7.5% NaCl (HS); 5% bovine serum albumin (BSA); 0.9% NaCl-6% hydroxyethyl starch (HES), or 7.5% NaCl-HES (HES 7.5). MAP was partially and transiently restored by infusion of IS or HS, whereas in the groups treated with BL, HES, HES 7.5, or BSA, there was a complete restoration of blood pressure in the 30-min period after infusion. Microvascular blood flow (MBF), measured by laser Doppler flowmetry, was reduced by 59% +/- 7% 10 min after bleeding. MBF was also transiently restored after infusion of IS, HS, BL, BSA, or HES. HES 7.5 was the only solution able to induce immediate and sustained (60 min) restoration of preshock levels of MBF. Volume replacement with IS or HES 7.5 resulted respectively in long-lasting or transient lymphatic pumping overload. On the other hand, resuscitation with all other solutions, except BSA, did not restore lymphatic activity to preshock levels. We also observed a significant reduction of the diameter of mesenteric terminal arterioles (15-30 microm) after bleeding, which was reversed temporarily in IS, BL, and HES groups, whereas resuscitation with HES 7.5 solution was able to maintain arterioles dilated until the end of the experimental period. Therefore, it is concluded that the association of hyperoncotic and hyperosmotic solutions, represented here by HES 7.5, induces positive effects with respect to the macro- and microhemodynamics accompanied by restoration and maintenance of the interstitial drainage system, being indicated for maintenance of postresuscitation cardiovascular and microvascular function.     

异丙酚对失血性休克复苏兔胃黏膜钙离子的影响

目的 观察异丙酚对失血性休克复苏兔胃黏膜损伤及Ca2+的影响.方法 将成年新西兰雄性大白兔100只随机分为对照组(S)、模型组(HR-GMI)及失血前(P1)、复苏前(P2)和复苏后(P3)应用异丙酚组,每组20只.建立失血性休克复苏胃黏膜损伤(HR-GMI)模型.P1、P2及P3组分别于失血前、复苏前10 min及复苏20 min时静注异丙酚5 mg/kg后,以20 mg/(kg·h)持续泵注,对照组和HR-GMI组给予等量生理盐水.观察胃黏膜组织学改变,计算其病理损伤积分,检测胃黏膜Ca2+浓度.结果 ①与对照组比较,模型组胃黏膜损伤严重,病理损伤积分和Ca2+浓度明显升高(P均＜0.01).②与模型组比较,应用异丙酚各组胃黏膜损伤明显减轻,病理损伤积分亦明显降低,且P1和P2组Ca2+浓度明显降低(P＜0.05或P＜0.01).③与P3组比较,P1和P2组胃黏膜损伤较轻,且P1组的胃黏膜病理损伤积分和Ca2+浓度明显降低(P均＜0.05).结论 异丙酚可降低失血性休克复苏兔胃黏膜组织内Ca2+浓度,减轻胃黏膜损伤,失血前应用效果更佳.     

Enalaprilat improves systemic and mesenteric blood flow during resuscitation from hemorrhagic shock in dogs

We investigated the systemic and mesenteric cardiovascular effects of administering enalaprilat during resuscitation from hemorrhage. Dogs were hemorrhaged (mean arterial pressure [MAP] 40-45 mmHg for 30 min, then 30-35 mmHg for 30 min) and were then resuscitated with intermittent lactated Ringer's solution (200 mL/kg/h during first 40 min, and 60 mL/kg/h during the following 130 min, MAP 75-80 mmHg). A constant-rate infusion of saline with or without enalaprilat (0.02 mg/kg/h) was initiated after 40 min of resuscitation. Blood flows declined with hemorrhage, increased with resuscitation, and then declined during the initial 40 min of resuscitation. Enalaprilat administration resulted in blood flow increases not seen in the controls (ending values for cardiac index: 2.8 +/- 0.4 L/min/m2 vs. 1.6 +/- 0.3 L/min/m2; celiac arterial flow 314 +/- 66 L/min/m2 vs. 139 +/- 13 mL/min/m2; and portal venous flow 596 +/- 172 L/min/m2 vs. 414 +/- 81 mL/min/m2 for enalaprilat versus controls, respectively). The greater flows with enalaprilat appeared to be due to prevention of the increases in afterload noted in the controls (ending arterial elastance values 3.73 +/- 0.97 mmHg/m2/mL vs. 7.74 +/- 1.80 mmHg/m2/mL for enalaprilat versus controls, respectively). We conclude that administration of a constant-rate infusion of enalaprilat during resuscitation can be used to improve systemic and mesenteric blood flow.     

不同时间输注红细胞悬液对大鼠失血性休克复苏的影响

目的探讨红细胞悬液延迟输注30 min对大鼠失血性休克复苏的影响。方法 24只Wistar大鼠随机分为假手术(SHAM)、RBC 1和RBC 2组(n=8),RBC 1和RBC 2组制备重度失血性休克大鼠模型,先后采用晶胶复合液和红细胞悬液复苏,RBC 2组红细胞悬液延迟输注30 min;监测生理、血气等指标。结果与RBC1组相比,RBC 2组平均动脉压(MAP)和体温恢复延迟,RBC 1组复苏结束后2组MAP分别为(116.99±11.06)和(73.72±14.34)mm Hg(P0.01);RBC 1组复苏结束后30 min,2组MAP分别为(103.07±9.59)和(120.61±10.73)mmHg(P0.01)。RBC 1组复苏结束后120 min RBC 1组体温(37.28±0.80)℃明显低于RBC 2组(38.83±0.58)℃(P0.01)。与SHAM组相比,RBC 1和RBC 2组休克后pH、PCO2、BE和ctHb明显降低,PO2明显升高;复苏后PCO23 h,RBC 1和RBC 2组碱剩余(BE)值明显低于SHAM组。结论在失血性休克液体复苏的基础上,红细胞悬液延迟输注30 min对失血性休克大鼠模型的生理、血气等指标无明显影响。提示紧急救治中输血准备工作耗时可能不影响失血性休克的复苏效果。     

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.