Hypertonic saline solution resuscitation in hemorrhagic shock dogs

Objective: To find out the optimal concentration,infusion rate and dosage of saline for resuscitation. Methods: Forty-five dogs were used to establish hypovolemic shock models. The dogs were resuscitated with saline of different concentrations and different dosages under different infusion rates, and the resuscitation results were compared. Results: The best concentration was 7.5%, the best rate of infusion 20 ml/min ( a volume equivalent to 15 % of the shed blood ) and the best dosage 5.71 ml/kg. The method was effective for resuscitation, the mean arterial pressure (MAP) could be elevated to 89 % of the baseline,and this MAP could be kept for more than one hour. Conclusions： Using 7.5% sodium chloride solution equivalent to 15% of the shed blood at an infusion rate of 20 ml/min can achieve a best resuscitation result.     

Hypertonic saline resuscitation in a porcine model of severe hemorrhagic shock

The purpose of this study was to investigate the effect of 7.5% hypertonic saline solution (HTS) as the initial solution in resuscitation of a pig in shock. Twenty-two animals were bled 50% of their blood volume over 30 minutes and maintained in shock for 60 minutes. The 14 survivors were divided into two groups. The first group was given 20 mL/kg of lactated Ringer's solution (LR) over a ten-minute period, while the second group was given 10 mL/kg of HTS. Both groups were then given LR at 2 mL/kg/min until the mean arterial pressure reached 80 mm Hg. The HTS group achieved a more rapid rise in mean arterial pressure over the first ten minutes of resuscitation. During this period, the cardiac index increased significantly more in the HTS group when compared with the LR group. All animals in the HTS group developed an adequate urine output. Only two animals in the LR group developed an adequate urine output. Hypertonic saline solution markedly improved survival, and there were significant improvements in hemodynamics. This was accomplished with smaller volumes of resuscitation fluid and may prove useful under conditions where intravascular access is limited.     

Hypertonic saline resuscitation improves intestinal microcirculation in a rat model of hemorrhagic shock

BACKGROUND: Conventional resuscitation (CR) from hemorrhagic shock (HS) often restores and maintains hemodynamics but fails to restore intestinal perfusion. Post-CR intestinal ischemia has been implicated in the initiation of a gut-derived exaggerated systemic inflammatory response and in the progressive organ failure following HS. We propose that intestinal ischemia can be prevented with hypertonic saline resuscitation (HTSR). METHODS: Anesthetized male Sprague-Dawley rats (200 to 215 g) were hemorrhaged to 50% of mean arterial pressure (MAP) for 60 minutes and randomly assigned to 1 of the resuscitation groups (n = 7 each): Group I: sham operation and no HS; Group II: HS + CR with the return of the shed blood + 2 volumes of normal saline (NS); Group III: HS + return of the shed blood + hypertonic saline (HTS); (7.5 % NaCl, 4 ml/kg); Group IV: HS + HTS, then return of the shed blood after 60 minutes; Group V: HS + HTS, then 1 volume of NS after 60 minutes. Microvascular diameters of inflow (A1) and proximal and distal premucosal arterioles (A3) in terminal ileum and flow in A1 were measured using in vivo videomicroscopy and optical Doppler velocimetry. Hematocrit, plasma osmolarity, and electrolytes were measured in Groups II and III. RESULTS: HS caused a selective vasoconstriction in A1 arterioles that was not seen in the premucosal arterioles. CR restored and maintained MAP and caused generalized, progressive vasoconstriction at all intestinal arteriolar levels that is associated with hypoperfusion. HTSR failed to restore or maintain MAP or intestinal A1 arteriolar blood flow until the shed blood was returned. However, HTSR prevented the post-resuscitation, premucosal vasoconstriction and produced an insidious selective vasodilation in the A3 arterioles, which was most significant with early blood return (Group III). This selective arteriolar vasoactivity was associated with a significant improvement of endothelial cell function. Plasma hyperosmolality and hypernatremia persisted during the entire 2 hours post-resuscitation with HTS. CONCLUSIONS: Small-volume HTSR can be used as a resuscitation regimen at the trauma scene and for selective clinical conditions where hypotensive resuscitation is indicated. HTSR improves intestinal perfusion by selective vasodilation of the precapillary arterioles even at MAP close to shock levels.     

不同液体容量复苏对失血性休克犬血管外肺水的影响

目的 评价不同液体容量复苏对失血性休克犬血管外肺水的影响。方法 杂种犬32只,雌雄不拘,随机分为4组：NS组、HES组、HS组和HHS组,每组8只,股动脉放血建立失血性休克模型后,各组分别静脉输注容积相当于3倍失血量的生理盐水、失血量等容积的6%羟乙基淀粉130/0．4溶液、7．5%氯化钠溶液6 ml/kg及7．5%氯化钠-6%羟乙基淀粉130/0．4溶液6 ml/kg行容量复苏。经右颈内静脉持续监测中心静脉压、右股动脉置入PiCCO导管监测平均动脉压、心脏指数、每搏输出量、体循环阻力指数、血管外肺水指数及全心舒张末期容量指数,记录放血之前（基础值）、失血性休克模型成功即刻、容量复苏开始后5、30、60、120及180min的上述指标。结果 （1）各组在失血性休克的早期复苏中均可改善血液动力学,HES组、HHS组、HS组和NS组血液动力学改善持续时间依次缩短;（2）复苏早期HS组与HHS组血管外肺水无增加,NS组明显增加,而HES组下降。结论 （1） 7．5%氯化钠溶液与7．5%氯化钠-6%羟乙基淀粉130/0．4溶液小容量液体复苏可有效恢复犬失血性休克早期血液动力学的稳定,且不增加休克后血管外肺水,7．5%氯化钠-6%羟乙基淀粉130/0．4溶液效果较好;（2）6%羟乙基淀粉130/0．4溶液用于犬失血性休克早期复苏不仅可以改善血液动力学,而且能防止复苏后肺水肿。     

Hypertonic saline dextran attenuates leukocyte accumulation in the liver after hemorrhagic shock and resuscitation

BACKGROUND: Hemorrhagic shock and resuscitation triggers a global ischemia/reperfusion phenomenon, in which activated leukocytes are considered strong contributors to the ensuing tissue damage. METHODS: The aim of the study was to investigate the effects of hypertonic saline dextran (HSD) on the early leukocyte/endothelial interactions (intravital fluorescence microscopy) in a rat model of hemorrhagic shock (1 hour at mean arterial pressure of 40 mm Hg). The resuscitation was performed with lactated Ringer's solution (RL, four times shed blood/20 minutes, n = 6), 6% dextran 60 (DEX, 100% shed blood/5 minutes, n = 8), and 7.2% NaCl/10% dextran 60 (HSD, 10% shed blood/2 minutes, n = 8). RESULTS: After 1 hour of resuscitation, shock-induced stasis/adherence of leukocytes was further enhanced with RL (sinusoids 17.6+/-6.9%; venules 33.9+/-8.5%), whereas DEX and HSD attenuated leukocyte stagnation in sinusoids (DEX -7.4+/-6,1%; HSD -14.7+/-2.9%, p<0.01 vs. RL) and leukocyte adherence in postsinusoidal venules (DEX -12.2+/-8.6%, p<0.05 vs. RL; HSD -27+/-7.4%, p<0.01 vs. RL). CONCLUSION: HSD reduced significantly the number of leukocytes accumulated in the liver after resuscitation of hemorrhagic shock, probably due to a combination of mechanisms of both components.     

Hypertonic saline resuscitation of head injury: effects on cerebral water content

Ideal resuscitation would simultaneously replete intravascular volume and minimize cerebral edema. We assessed the effects of hypertonic saline (HS) shock resuscitation on cerebral edema after head injury. Rats were subjected to hemorrhagic shock (40 mm Hg for 1 hour) in the presence or absence of mechanical brain injury, followed by 1 hour of resuscitation with either hypertonic saline (6.5%) or lactated Ringer's (LR). After resuscitation, animals were sacrificed and brain water contents determined. Results: Less HS than LR was needed for resuscitation both in animals without brain injury (7 +/- 2 ml/kg vs. 97 +/- 16 ml/kg; p less than 0.0003) and with brain injury (10 +/- 1 ml/kg vs. 68 +/- 6 ml/kg; p less than 0.0001). Brain water content (ml H2O/gm dry wt) after HS resuscitation was decreased compared to LR resuscitation in animals without brain injury (3.36 +/- 0.12 vs. 3.74 +/- 0.08; p less than 0.025) and in the uninjured hemisphere of head-injured animals (3.29 +/- 0.11 vs. 3.78 +/- 0.09; p less than 0.025). Brain water content was increased in injured brain in both resuscitation groups, but the increase was the same (HS 4.10 +/- 0.13; LR 4.25 +/- 0.17; p greater than 0.05). Conclusions: HS resuscitation of hemorrhagic shock decreases brain water content in uninjured but not injured brain. HS may be useful in resuscitation of combined hemorrhagic shock and head injury.     

Hypertonic saline and pentoxifylline attenuates gut injury after hemorrhagic shock: the kinder, gentler resuscitation

BACKGROUND: We have previously demonstrated that postshock resuscitation with Hypertonic saline and Pentoxifylline (HSPTX) attenuates pulmonary and histologic gut injury when compared with Ringer's lactate (RL). In this study, we hypothesized that the decrease in gut injury observed with HSPTX is associated with the attenuation of inducible nitric oxide synthase (iNOS) activity and production of ileal proinflammatory mediators after hemorrhagic shock. METHODS: In a rat model of hemorrhagic shock, resuscitation was conducted with RL (32 mL/kg; n = 7) or HSPTX (4 mL/kg 7.5% NaCl + PTX 25 mg/kg; n = 7). Sham animals that did not undergo shock were also studied. Four hours after resuscitation, the terminal ileum was collected for evaluation of nitrite, tumor necrosis factor (TNF)-alpha, Interleukin (IL)-6, and cytokine-induced neutrophil chemoattractant (CINC) by enzyme immunoassay. Heme oxygenase-1 (HO-1), iNOS, cytoplasmic inhibitor of kappa B (Ikappa B) phosphorylation, and nuclear factor (NF)kappa B p65 nuclear translocation were determined by Western blot. RESULTS: HSPTX resuscitation resulted in a 49% decrease in iNOS when compared with RL (p < 0.05). Similar results were obtained when examining nitrite (882 +/- 59 vs. 1,435 +/- 177 micromol/L; p < 0.01), and HO-1 content (p < 0.05). RL resuscitation resulted in markedly higher levels of TNF-alpha (83 +/- 27 vs. 9 +/- 5 pg/mL; p < 0.01), IL-6 (329 +/- 58 vs. 118 +/- 43 pg/mL; p < 0.05), and CINC (0.43 +/- .06 vs. 0.19 +/- .08 ng/mL; p < 0.05) than HSPTX. The increase in cytokines observed with RL was also associated with an increase in I-kappaB phosphorylation (p < 0.01) and NF-kappaB p65 nuclear translocation (p < 0.001). CONCLUSION: The attenuation in gut injury after postshock resuscitation with HSPTX is associated with downregulation of iNOS activity and subsequent proinflammatory mediator synthesis. HSPTX has the potential to be a superior resuscitation fluid with significant immunomodulatory properties.     

高渗盐复合液用于颅脑外伤合并失血性休克的治疗

目的研究高渗盐溶液（7．5％氯化钠／6％右旋糖酐液,HSD）及高渗盐复合液（高渗氯化钠／羟乙基淀粉40注射液,霍姆）用于颅脑外伤合并失血性休克患者的治疗效果。方法将93名颅脑外伤合并失血性休克的患者随机分为2组,为霍姆组（HH组）和HSD组,分别使用霍姆和HSD进行液体复苏,于To（入院时）、15分钟（L）、30分钟（B）、60分钟（B）不同时间点监测记录平均动脉压（MAP）、心率（HR）、尿量（VOL）变化;监测人院时及输液60分钟后的血红蛋白（Hb）、红细胞压积（HCT）、GCS评分;记录早期复苏时间、术前总输液量、胶体液比例;记录入院后24小时死亡率、1周死亡率。结果输液后30分钟、60分钟,HH组的平均动脉压显著大于HsD组（P≮O．05）。输液60分钟,HH组的心率显著小于HSD组（P〈0．05）。在15分钟、30分钟、60分钟,HH组的尿量显著多于HSD组（P〈0．05）。HH组患者60分钟后测得HCT与Hb均较人院时有显著下降（P〈0．05）。HSD组60分钟后的HCT与入院时无显著性差异（P〉O．05）,而输液60分钟后的Hb显著低于入院前（P〈O．05）。GCS评分,HH组液体复苏前后有显著性差异（P〈O．05）,而HSD组前后却没有显著差异。液体复苏60分钟后的GCS值HH组显著大于HSD组（RO．05）。HH组手术前平均输液量显著少于HSD组fP〈0,05）。人院24小时内及1周内,HH纽死亡率均稍低于HSD组死亡率,但无显著差异（P〉O．05）。结论在颅脑外伤合并创伤失血性休克的情况下,补充高渗盐复合液不仅能更快的纠正组织低灌注,保护重要心、脑、肺等脏器,降低颅内压,还能减少输液量。     

Hypertonic saline resuscitation attenuates neutrophil lung sequestration and transmigration by diminishing leukocyte-endothelial interactions in a two-hit model of hemorrhagic shock and infection

BACKGROUND: Hypertonic saline (HTS) attenuates polymorphonuclear neutrophil (PMN)-mediated tissue injury after hemorrhagic shock. We hypothesized that HTS resuscitation reduces early in vivo endothelial cell (EC)-PMN interactions and late lung PMN sequestration in a two-hit model of hemorrhagic shock followed by mimicked infection. METHODS: Thirty-two mice were hemorrhaged (40 mm Hg) for 60 minutes and then given intratracheal lipopolysaccharide (10 microg) 1 hour after resuscitation with shed blood and either HTS (4 mL/kg 7.5% NaCl) or Ringer's lactate (RL) (twice shed blood volume). Eleven controls were not manipulated. Cremaster intravital microscopy quantified 5-hour EC-PMN adherence, myeloperoxidase assay assessed lung PMN content (2 1/2 and 24 hours), and lung histology determined 24-hour PMN transmigration. RESULTS: Compared with RL, HTS animals displayed 55% less 5-hour EC-PMN adherence (p = 0.01), 61% lower 24-hour lung myeloperoxidase ( p= 0.007), and 57% lower mean 24-hour lung histologic score ( p= 0.027). CONCLUSION: Compared with RL, HTS resuscitation attenuates early EC-PMN adhesion and late lung PMN accumulation in hemorrhagic shock followed by inflammation. HTS resuscitation may attenuate PMN-mediated organ damage.     

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。     

高渗/高胶液与休克复苏

临床中通常使用等渗晶体、胶体或成份血作为休克复苏液 ,但鉴于这些液体在复苏中的不力表现 ,寻找一种全新的复苏液成为当务之急。近年来高渗 /高胶液在临床应用中以取得满意效果并展现出良好前景。笔者就高渗 /高胶液复苏机制 ,对机体的影响及使用中的问题做一综述。     

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.     

Hypertonic saline solution-hetastarch for fluid resuscitation in experimental septic shock

Hypertonic colloid solutions have been found efficacious in the resuscitation from hemorrhagic/traumatic shock. The present study investigated the hemodynamic, gasometric, and metabolic effects of hypertonic colloids in endotoxic shock in the dog. Thirty minutes after administration of 3 mg/kg normal body weight of Escherichia coli endotoxin, dogs were randomly assigned to receive 10 mL/kg hydroxyethylstarch (HES) either in 0.9% NaCl (HES, 10 dogs) or in 7.5% NaCl (HT-HES, 10 dogs) in 30 min. Thereafter, 0.9% NaCl solution was administered in volumes adequate to maintain pulmonary artery balloon-occluded pressure at baseline levels. Total fluid administered averaged 64 +/- 30 mL/kg (mean +/- SD) in the HES group and 73 +/- 34 mL/kg in the HT-HES group. As these differences were not statistically significant, total sodium load was higher in the HT-HES group. The persistent volume effect was associated with persistently lower hematocrit and protein levels in the HT-HES group. Initial fluid resuscitation with HT-HES resulted in arterial pressure, cardiac filling pressures, cardiac output, stroke volume, and rates of oxygen delivery and oxygen consumption that were greater than those with HES. Vascular resistances were similar. Analysis of left ventricular function curves also indicated an improvement in cardiac performance. However, these effects almost completely vanished during the remainder of the study. In the HT-HES group, serum sodium and osmolality levels increased to 167 +/- 4 mEq/L and 344 +/- 4 mOsm/kg H2O, respectively.(ABSTRACT TRUNCATED AT 250 WORDS)     

Hypertonic saline resuscitation of hemorrhagic shock diminishes neutrophil rolling and adherence to endothelium and reduces in vivo vascular leakage

OBJECTIVE: To evaluate the in vivo effects of hypertonic saline (HTS) resuscitation on the interactions of endothelial cells (ECs) and polymorphonuclear neutrophils (PMNs) and vascular permeability after hemorrhagic shock. SUMMARY BACKGROUND DATA: The PMN has been implicated in the pathogenesis of EC damage and organ injury following hemorrhagic shock. Compared to Ringer's lactate (RL), HTS resuscitation diminishes PMN and EC adhesion molecule expression and organ sequestration of PMNs. METHODS: In a murine model of hemorrhagic shock (50 mmHg for 45 minutes followed by resuscitation) using intravital microscopy on cremaster muscle, the authors studied PMN-EC interactions and vascular leakage (epifluorescence after 50 mg/kg fluorescent albumin) in three resuscitation groups: HTS (shed blood + 4 cc/kg 7.5% HTS, n = 12), RL (shed blood + RL [2x shed blood volume], n = 12), and sham (no hemorrhage or resuscitation, n = 9). EC ICAM-1 expression was evaluated by immunohistochemistry. Data, presented as mean +/- SEM, were evaluated by analysis of variance with Bonferroni correction. RESULTS: There were no differences between groups in flow mechanics. Compared to RL, HTS animals (t = 90 minutes) displayed diminished PMN rolling and PMN adhesion to EC at time intervals beyond t = 0. There were no differences between the sham and HTS groups. Vascular leakage was 45% lower in HTS than in RL-resuscitated animals. Cremaster EC ICAM-1 expression was similar in the two groups. CONCLUSIONS: Using HTS instead of RL to resuscitate hemorrhagic shock diminishes vascular permeability in vivo by altering PMN-EC interactions. HTS could serve as a novel means of immunomodulation in hemorrhagic shock victims, potentially reducing PMN-mediated tissue injury.     

7.5%高渗氯化钠溶液复苏失血性休克对红细胞能量代谢的影响

目的：观察小剂量高渗氯化钠（ＨＳ）复苏失血性休克时红细胞（ＲＢＣ）能量代谢的变化。方法：２０只健康家兔被随机分为三组，（甲组）正常血容量输注ＨＳ组；（乙组）休克输注ＮＳ复苏组；（丙组）休克输注ＨＳ复苏组。以ＲＢＣ内ＡＴＰ和２，３－ＤＰＧ水平作为ＲＢＣ能量代谢的指标。结果：休克后ＲＢＣ内ＡＴＰ和２，３－ＤＰＧ水平显著下降，应用小剂量ＨＳ复苏后两项指标均有所回升，在输注后１２０分钟有显著增高。结论：应用小剂量ＨＳ可使失血性休克后的ＲＢＣ能量代谢状态发生明显改善，这可能是促进ＨＳ有效复苏休克的重要因素。     

Hypertonic/hyperoncotic fluid resuscitation after hemorrhagic shock in dogs.

We compared canine systemic and cerebral hemodynamics after resuscitation from hemorrhagic shock with 4 mL/kg (a volume approximating 12% of shed blood volume) of 7.2% saline (HS; 1233 mEq/L sodium), 20% hydroxyethyl starch (HES) in 0.8% saline, or a combination fluid consisting of 20% hydroxyethyl starch in 7.2% saline (HS/HES). Eighteen endotracheally intubated mongrel dogs (18-24 kg) were ventilated to maintain normocarbia with 0.5% halothane in nitrous oxide and oxygen (60:40). After a 30-min period of hemorrhagic shock (mean arterial blood pressure = 40 mm Hg), extending from time T0 to T30, animals received one of three randomly assigned intravenous resuscitation fluids: HS, HES, or HS/HES. Data were collected at baseline, at the beginning and end of the shock period (T0 and T30), immediately after fluid infusion (T35), and at 60-min intervals for 2 h (T95, T155). After resuscitation, mean arterial blood pressure and cardiac output increased similarly in all groups, but failed to return to baseline. Intracranial pressure decreased during shock and increased slightly, immediately after resuscitation in all groups. During shock, cerebral blood flow (cerebral venous outflow method) declined in all groups. After resuscitation, cerebral blood flow increased, exceeding baseline in the HS and HS/HES groups but remaining low in the HES group (P less than 0.05 HS vs HES at T35). We conclude that small-volume resuscitation (4 mL/kg) with HS, HS/HES, or HES does not effectively restore or sustain systemic hemodynamics in hemorrhaged dogs. In dogs without intracranial pathology, the effects on cerebral hemodynamics are also comparable, except for transiently greater cerebral blood flow in the HS group in comparison with the HES group.     

Hypertonic resuscitation modulates the inflammatory response in patients with traumatic hemorrhagic shock

OBJECTIVE: To determine the effect of resuscitation with hypertonic saline/dextran (HSD) on the innate immune response after injury. SUMMARY OF BACKGROUND DATA: Hypovolemic shock causes a whole body ischemia/reperfusion injury, leading to dysregulation of the inflammatory response and multiple organ dysfunction syndrome. Hypertonicity has been shown to modulate the innate immune response in vitro and in animal models of hemorrhagic shock, but the effect on the inflammatory response in humans is largely unknown. METHODS: Serial blood samples were drawn (12, 24, 72 hours and 7 days after injury) from patients enrolled in a prospective, randomized, double-blind trial of traumatic hypovolemic shock, HSD (250 mL) versus lactated Ringer's solution (LR) as the initial resuscitation fluid. Neutrophil (PMN) CD11b/CD18 expression was assessed via whole blood FACS analysis with and without stimulation (fMLP 5 micromol/L or PMA 5 micromol/L). PMN respiratory burst was assessed using the nitro-blue tetrazolium assay. Monocytes stimulated with 100 ng LPS for 18 hours were assessed for cytokine production (TNF-alpha, IL-1Beta, IL-6, IL-10, IL-12). RESULTS: Sixty-two patients (36 HSD, 26 LR) and 20 healthy volunteers were enrolled. CD11b expression, 12 hours after injury, was increased 1.5-fold in patients resuscitated with LR compared with controls. Those resuscitated with HSD had a significant reduction in CD11b expression 12 hours after injury, compared with LR. There was no difference in respiratory burst early after injury. Monocytes from injured patients expressed lower levels of all cytokines in comparison to normal controls. Patients give HSD showed a trend toward higher levels of IL-1beta and IL10 production in response to LPS, 12 hours after injury. CONCLUSION: HSD resuscitation results in transient inhibition of PMN CD11b expression and partial restoration of the normal monocyte phenotype early after injury.