血管加压素对内毒素休克抗休克作用的探讨

【摘 要】 目的 探讨血管加压素（Vasopressin，VP）在内毒素休克中的抗休克作用，及对肾脏功能的影响。 方法 将24只兔随机分为两组，每组12只，用注射大肠杆菌类毒素（LPS）的方法制作内毒素休克兔模型。对照组（A组）不采取复苏措施；血管加压素组（B组）以血管加压素复苏。分时段监测血压，测定血NO、BUN、Cr等。并取肾脏标本行病理检查。 结果 血管加压素除了收缩血管，升高血压的作用外，能抑制一氧化氮的生成，起到抗休克的作用，对肾功能影响较小。 结论 血管加压素在感染性休克的治疗中具有较好的抗休克作用。     

溶液温度对失血性休克兔循环功能的影响

目的探讨不同温度液体复苏对失血性休克兔循环功能的影响,以筛选较为适宜的抗休克补液温度.方法将实验兔(n=30)以随机的方法分为假手术组(n=7)、温热组(n=8)、常温组(n=7)、低温组(n=8).选择休克前(t1)、休克模型形成后30min(t2)、液体复苏后1h(t3)、2h(t4)、4h(t5),观察心率、平均动脉压、中心静脉压和休克指数的变化.结果温热组失血性休克兔在液体复苏后心率稳定,而常温及低温组心率明显下降.液体复苏后4 h,温热组与常温组、低温组之间比较有统计学差异.温热组平均动脉压升高平稳,常温及低温组曲线有一定波动.液体复苏后4h,低温组平均动脉压较低,与其他3组比较有统计学差异.中心静脉压、休克指数组间比较无统计学差异.结论温热液体复苏使休克兔心率、平均动脉压、中心静脉压较为平稳,有助于改善休克兔循环功能.     

限制性液体复苏对失血性休克孕兔肾功能的影响

【目的】探讨不同液体复苏方案对失血性休克孕兔肾功能的影响。【方法】20只孕兔制成未控制性重度失血性休克模型,随机分为假休克组（P组）、休克未处理组（P0组）、限制性液体复苏组（PLH组）、传统液体复苏组（PNL组）,对比研究各组各时间点血清肌酐（Cr）的变化情况,并观察孕兔处死后肾脏病理检查结果。【结果】孕兔失血性休克可导致肾小球滤过功能损害,休克时各组的Cr均增高,模型第90 min、180min4、h PLH组血清Cr明显低于PNL组（P〈0.05）。P0组肾脏的病理损害最严重,PLH组肾脏病理损害较PNL组明显减轻。但较P组严重。【结论】限制性液体复苏能显著提高肾血液灌注和肾小球滤过率,降低血清Cr含量,改善肾功能,是抢救产科失血性休克的理想复苏方法。     

不同液体复苏对失血性休克大鼠微循环的影响

目的 探讨不同复苏液体种类对大鼠急性失血性休克微循环的影响.方法 对40只纯种Wistar大鼠参照Sandro B.Rizoli所建模型改良复制失血性休克动物模型,根据对急性失血性休克大鼠进行液体复苏时所选液体种类不同,随机分为无液体复苏组(A组)、低分子右旋糖苷-40组(B组)、7.5%高渗盐水组(C组)和高渗盐水+低分子右旋糖苷-40(D组),每组10只,于休克后24 h将动物处死,采集左侧肾皮质相应部位标本用于电镜检查.结果 休克无液体复苏组(A组)动物肾脏微循环破坏严重,单独应用低分子右旋糖苷组(B组)或单独应用高渗盐水组(C组)均有不同程度损伤,而联合应用高渗盐水+低右复苏组(D组)肾脏微循环基本完好.结论 不同复苏液体种类对休克机体微循环影响不同,联合应用高渗盐水+低右对保护肾脏微循环具有良好效果.     

溶液温度对失血性休克兔呼吸功能和酸碱平衡的影响

目的　探讨溶液温度对失血性休克兔呼吸功能和酸碱平衡的影响 ,筛选较为适宜的抗休克补液温度。方法　将实验兔随机分为 4组。假手术组不制作休克模型及液体复苏。温热、常温、低温组复制兔失血性休克模型后 ,给予 3倍失血量的平衡液及自体血复苏 ,液体温度分别控制在 (39.5± 1.3)℃、(2 0 .6± 1.3)℃、(10 .7± 1.6 )℃。选择休克前、休克模型形成后 30min、液体复苏后 1、2和 4h观察呼吸频率、动脉血气指标、血乳酸的变化。结果　液体复苏后 1h ,温热组PaO2 高于常温组及低温组 ,有统计学差异。液体复苏后 4h ,低温组及常温组PaCO2 低于温热组 ,有统计学差异。液体复苏后温热组呼吸较为平稳 ,动脉血 pH、SO2 上升时相较早 ,乳酸下降幅度较大。结论　温热溶液复苏对机体内环境的稳定 ,纠正酸碱失衡有一定意义。选用温热溶液复苏失血性休克更为有利     

高强度间歇运动对自发性高血压大鼠肾脏肾素-血管紧张素系统的影响

目的观察高强度间歇运动对自发性高血压大鼠(SHR)血压水平及肾功能的影响, 并探讨肾脏肾素-血管紧张素系统(RAS)在其间的作用机制。方法采用随机数字表法将20只雄性SHR大鼠分为高血压安静组及高血压运动组, 同时选取10只Wistar-Kyoto大鼠纳入正常血压组。正常血压组及高血压安静组大鼠均置于鼠笼内安静饲养, 高血压运动组大鼠则给予8周高强度间歇运动干预。于末次运动结束后检测各组大鼠血压水平、肾功能、肾脏一氧化氮(NO)和白细胞介素-6(IL-6)含量以及肾脏血管紧张素转换酶(ACE)、ACE2、血管紧张素1型受体(AT1R)、AT2R和Mas受体(MasR)蛋白表达量。结果与正常血压组比较, 高血压安静组大鼠血压升高(P<0.05), 肾功能减退(P<0.05), 肾脏NO含量减少(P<0.05), IL-6含量升高(P<0.05), ACE和AT1R蛋白表达以及AT1R/AT2R比值升高(P<0.05), ACE2、AT2R及MasR蛋白表达下降(P<0.05);与高血压安静组比较, 高血压运动组大鼠血压明显下降(P<0.05), ...     

失血性休克复苏延迟兔模型的构建

目的探讨失血性休克复苏延迟兔模型的构建方法。方法选择30只雄性新西兰大白兔,通过血压控制放血法构建失血性休克复苏延迟兔模型,随机将其分为3组,每组各10只,依据休克期控制平均动脉压(MAP)分组,MAP分别为40~50 mm Hg(轻度失血性休克组)、30~40 mm Hg(中度失血性休克组)、20~30 mm Hg(重度失血性休克组)。观察3组能否维持180 min休克状态,并观察比较放血开始时间点(T1)、失血性休克维持期结束时间点(T2)和观察结束时间点(T3)的MAP和肿瘤坏死因子(TNF-α)水平。结果失血性休克复苏延迟兔模型均成功建立。重度失血性休克组在休克维持中后期全部死亡,未能实现复苏延迟;轻、中度失血性休克组在成功维持休克状态180 min后均进行了液体复苏。T1时3组MAP比较差异无统计学意义(P0.05);T2、T3时MAP轻度失血性休克组均高于中度失血性休克组,差异均有统计学意义(P0.05)。在T1时,轻、中度失血性休克组血清TNF-α水平比较差异无统计学意义(P0.05);在T2和T3时均显著升高,组间每一时段两两比较差异均有统计学意义(P0.05);轻度失血性休克组血清TNF-α水平明显低于中度失血性休克组(P0.01)。结论失血性休克期MAP控制在30 mm Hg以上可以成功构建发生严重全身系统性炎症反应的失血性休克复苏延迟(180 min)兔模型。     

氨基胍对失血性休克兔血流动力学和一氧化氮的影响

目的 观察氨基胍(AG)在失血性休克复苏中的作用机制.方法 采用股动脉放血法复制家兔失血性休克模型,将20只家兔随机均分为生理盐水复苏对照组和AG复苏组;用Pclab生物信号采集系统分别记录休克前、休克30 min、休克150 min、复苏30 min、复苏180 min的血流动力学参数,并用硝酸还原酶法测定相应时间点的血清一氧化氮(NO)水平.结果 两组复苏前动脉收缩压(SAP)、心率(HR)、平均动脉压(MAP)、左心室收缩压(LVSP)、心室内压最大上升和下降速率(±dp/dt max)等血流动力学参数与血清NO含量比较差异均无统计学意义.与休克前比较,两组休克30 mid和150 min血流动力学参数显著下降,NO含量显著升高(P＜0.05或P＜0.01).复苏后,两组均能改善失血性休克家兔血流动力学参数,同时AG复苏能显著降低失血性休克家兔血清NO含量,而生理盐水复苏不能阻断血清NO升高;两组比较,AG具有更持久、更有效的抗失血性休克作用(P＜0.05或P＜0.01).结论 氨基胍能改善失血性休克家兔血流动力学参数,降低血清NO水平,从而起到抗失血性休克作用.     

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.     

溶液温度对失血性休克兔中心温度的影响

[目的 ]探讨采用不同温度液体复苏时对失血性休克兔中心温度的影响 ,筛选较为适宜的抗休克补液温度。 [方法 ]将实验兔 (n =3 0 )随机分为假手术组 (n =7)、温热组 (n =8)、常温组(n =7)、低温组 (n =8)。温热组、常温组、低温组复制兔失血性休克模型后 ,给予 3倍失血量的平衡液及自体血复苏 ,液体温度分别控制在3 9 .5℃± 1.3℃、2 0 .6℃±1.3℃、10 .7℃± 1.6℃。选择休克前 (T1)、休克模型形成后 3 0min (T2 )及液体复苏后 1h(T3 )、2h(T4)、4h(T5)时间点观察中心温度的变化。 [结果 ]液体复苏后1h、2h、4h温热组中心温度保持相对稳定 ,而常温组、低温组下降 ,差异有统计学意义 ;常温组与低温组间差异无统计学意义。 [结论 ]温热溶液可保持失血性休克兔中心温度相对恒定     

Vasopressin may be useful in the treatment of systemic anaphylaxis in rabbits

Recent studies demonstrate that vasopressin is useful when treating hemorrhagic and septic shock. The effect of vasopressin on systemic anaphylaxis has not been investigated except in clinical case reports. Vasopressin increases blood pressure because of vasoconstriction through the V1 receptor. Thus, we evaluated the effect of vasopressin on circulatory depression and bronchoconstriction provoked by systemic anaphylaxis and survival rates in rabbits. In the first set of experiments, 15 nonsensitized rabbits received normal saline (control) and vasopressin at 0.8 or 0.08 U/kg. In the second set, 40 sensitized rabbits received horse serum to induce anaphylaxis, and then received the same drugs as in the first set. In the first set, mean arterial pressure (MAP) in vasopressin groups increased by 18% to 24% compared with the control. Vasopressin at 0.8 U/kg decreased MAP insignificantly before the increases of MAP occurred. In the second set, vasopressin at 0.08 U/kg improved the survival rate. At 45 min after antigen challenge, 69% of the rabbits that received vasopressin at 0.08 U/kg were alive, whereas 29% of the control rabbits and 23% of the rabbits that received vasopressin at 0.8 U/kg were alive. Vasopressin increased MAP by 36% to 109% compared with the control within 5 min, however, at 2 min, vasopressin at 0.8 U/kg had no effect on MAP. Pulmonary dynamics were similar. In conclusion, vasopressin at 0.08 U/kg improved survival rates and severe hypotension provoked by systemic anaphylaxis, suggesting that this agent may be useful in the treatment of systemic anaphylaxis.     

Systemic and renal macro- and microcirculatory responses to arginine vasopressin in endotoxic rabbits

OBJECTIVE: Arginine vasopressin is being used increasingly to treat vasodilatory hypotension, although little is known of its effects on regional perfusion. Arginine vasopressin hemodynamic effects in physiology are mainly mediated through the V1a receptor on blood vessels. To investigate this further, we studied the effect of arginine vasopressin on systemic and renal blood flow in anesthetized, ventilated rabbits given either intravenous saline or endotoxin, and the impact of blocking V1a receptors. DESIGN: Prospective, randomized, controlled study. SETTING: Animal research laboratory. SUBJECTS: Male White New Zealand rabbits. INTERVENTIONS: Measurement was made of mean arterial blood pressure, aortic and renal blood flow velocities (pulsed Doppler), and renal cortical and medullary flow (laser Doppler). MEASUREMENTS AND MAIN RESULTS: In a first series of animals, incremental intravenous boluses of arginine vasopressin ranging from 1 to 1000 ng were administered 90 mins postendotoxin or saline. In control rabbits (n = 9), increasing doses of arginine vasopressin elevated mean arterial blood pressure but reduced both aortic and renal blood flow velocity and renal cortical flow (p <.05). In endotoxic animals (n = 6), arginine vasopressin produced a similar increase in mean arterial blood pressure although aortic flow was maintained while renal blood flow velocity increased, mostly in its diastolic component (p <.05). Pretreatment with the V1a receptor antagonist in a second series of animals blunted all the effects observed in both control (n = 5) and endotoxic (n = 6) animals, suggesting that arginine vasopressin acted mainly through V1a subtype in this early phase of sepsis. CONCLUSIONS: Preservation of renal blood flow with arginine vasopressin during endotoxemia, in particular to the cortex, suggests it could be a promising agent for hemodynamic support during septic shock.     

Endogenous and exogenous vasopressin in shock

PURPOSE OF REVIEW: Vasopressin is critical for blood pressure regulation when cardiovascular homeostasis is threatened and some patients with shock have inappropriately low levels of hormone in plasma. The present review focuses on recent work that addresses the role of endogenous vasopressin in the pathogenesis of shock and the potential therapeutic indications and secondary effects of exogenous hormone in patients with shock. RECENT FINDINGS: Examples of types of shock resistant to catecholamine pressors in which exogenous vasopressin was effective in restoring arterial pressure continued to accumulate. Widespread determinations of plasma vasopressin in patients with shock suggest that endogenous vasopressin deficiency may be more frequent than previously thought. The generation of mice with deletion of vasopressin's V1a receptor highlighted the important role of the hormone on cardiovascular homeostasis. SUMMARY: Vasopressin administration is very effective in restoring arterial pressure in many forms of shock and this appears to be due, at least in part, to deficiency of endogenous hormone. Generation of mice lacking vasopressin V1a receptor open new and exciting avenues of inquiry to clarify the role of the hormone in cardiovascular homeostasis.     

创伤失血性休克兔肾动脉血流改变的多普勒监测

目的　检测创伤失血性休克 3 0、60及 12 0min时 ,兔肾动脉血流多普勒频谱的改变特征。方法　实验动物分为复苏组与对照组 ,应用Acuson12 8XP 10型彩超仪 ,测定兔肾动脉在休克后不同时间段的血流参数。结果　失血性休克后肾动脉收缩期血流峰值速度 (Vmax)、舒张期血流速度 (Vmin)和平均血流速度 (Vmean)显著减低 ,随时间呈递减趋势 ,与复苏组比较差异显著 (P <0 .0 1) ,但休克后复苏组上述诸值与休克前相比变化不明显。结论　失血性休克后肾血供随时间递减 ,采用静脉输注高渗氯化钠 右旋糖酐 (HSD)可以对抗上述病理过程     

Systemic and hepatosplanchnic macro- and microcirculatory dose response to arginine vasopressin in endotoxic rabbits

OBJECTIVE: Arginine vasopressin (AVP) is being used increasingly to treat vasodilatory hypotension, although its effects on hepatosplanchnic perfusion have been debated. DESIGN: Prospective study in a university-based experimental research laboratory. SUBJECTS AND INTERVENTIONS: We compared the effect of AVP on systemic, gut, and liver blood flow in anesthetized and ventilated rabbits given either saline or endotoxin. Incremental i.v. boluses of AVP ranging from 1 to 1,000[Symbol: see text]ng were administered 90[Symbol: see text]min post-endotoxin or saline. MEASUREMENTS AND RESULTS: Endotoxin induced a shock state with a transient decrease of mesenteric artery blood flow velocity (pulsed Doppler, in centimeters per second, V(mes)) but had no effect on liver surface microcirculation (laser Doppler in TPU, MicroFl(liver)). Gut microcirculatory (MicroFl(gut)) changes became independent of mean arterial pressure (MAP) after endotoxin. In control rabbits (n = 5), increasing doses of AVP elevated MAP but reduced aortic blood flow (pulsed Doppler, VAo), V(mes), and MicroFl(gut) (p < 0.05). In endotoxic animals (n = 6), AVP produced a similar rise in MAP (p < 0.05), while V(mes) and MicroFl(gut) only decreased for AVP doses above 100[Symbol: see text]ng (p < 0.05). Liver microcirculation was only minimally affected by AVP, although significantly, both in control and endotoxin animals. CONCLUSION: Preservation of mesenteric blood flow as well as gut and liver microcirculation, with therapeutic doses of AVP during endotoxemia, supports its use as a hemodynamic agent during septic shock.     

Clinical impact of vasopressin infusion on hemodynamics,liver and renal function in pediatric patients

OBJECTIVE: To study effects of vasopressin on hemodynamic, clinical, and laboratory variables in children with advanced vasodilatory shock. DESIGN AND SETTING: Retrospective study in a multidisciplinary tertiary pediatric critical care unit. PATIENTS AND PARTICIPANTS: Patients (n = 117; 32 noncardiac, 85 postcardiac surgery) requiring intravenous vasopressin infusion longer than 60 min for advanced shock (January 2004 to December 2005). INTERVENTIONS: Vasopressin infusion (n =157). MEASUREMENTS AND RESULTS: Both cardiac and noncardiac patients showed a significant decrease in inotrope requirement without change in central venous saturation or lactate during infusion. Both groups had increased urea and creatinine and decreased urine output with longer duration/higher cumulative dose of vasopressin. There was a significant increase in conjugated bilirubin level in the noncardiac group during vasopressin infusion; noncardiac patients showed higher AST levels with higher cumulative dose or longer duration of infusion. Postcardiac surgical patients showed a trend towards normal INR values which persisted after vasopressin infusion. Platelet counts were significantly lower during infusion in both groups. CONCLUSIONS: Vasopressin infusion improved the hemodynamic state in advanced shock without compromising cardiac function. Urine output and creatinine levels were adversely affected but were reversible. This effect was more pronounced with higher dose or duration of infusion. There was no major effect on liver function but a significant reduction in platelet counts. These data suggest that vasopressin is useful in states of vasodilatory shock with limitations regarding to its adverse renal effects and on platelet counts.     

Circulating vasopressin levels in septic shock

OBJECTIVE: To assess the frequency of vasopressin deficiency in septic shock. DESIGN: Prospective cohort study. SETTING: Intensive care unit at Raymond Poincaré University Hospital. PATIENTS: A cohort of 44 patients who met the usual criteria for septic shock for < 7 days. A second cohort of 18 septic shock patients were enrolled within the first 8 hrs of disease onset. INTERVENTIONS: None. MEASUREMENTS AND MAIN RESULTS: General demographics, severity scores, vital signs, standard biochemical data, and circulating vasopressin levels were systematically obtained at baseline in the two cohorts. Vasopressin deficiency was defined by a normal plasma vasopressin level in the presence of a systolic blood pressure of <100 mm Hg or in the presence of hypernatremia. Baroreflex sensitivity was systematically evaluated in patients of the first cohort when vasopressin deficiency was noted. In the second cohort of patients, plasma levels of vasopressin were obtained at baseline, 6, 24, 48, and 96 hrs after shock onset. In the first population, plasma vasopressin levels were inversely correlated to the delay from shock onset. Fourteen patients had relative vasopressin deficiency: 12 patients had systolic blood pressure <100 mm Hg, with impaired baroreflex sensitivity in four, and three patients had hypernatremia. In the second population, only two patients had relative vasopressin deficiency. The plasma levels of vasopressin significantly decreased over time (p < 10-3). CONCLUSIONS: Plasma vasopressin levels are almost always increased at the initial phase of septic shock and decrease afterward. Relative vasopressin deficiency is seen in approximately one-third of late septic shock patients.     

Arginine vasopressin,but not epinephrine,improves survival in uncontrolled hemorrhagic shock after liver trauma in pigs

OBJECTIVE: Epinephrine is widely used for treatment of life-threatening hypotension, although new vasopressor drugs may merit evaluation. The purpose of this study was to determine the effects of vasopressin vs. epinephrine vs. saline placebo on hemodynamic variables, regional blood flow, and short-term survival in an animal model of uncontrolled hemorrhagic shock and delayed fluid resuscitation. DESIGN: Prospective, randomized, laboratory investigation that used a porcine model for measurement of hemodynamic variables and regional abdominal organ blood flow. SETTING: University hospital laboratory. SUBJECTS: A total of 21 pigs weighing 32 +/- 3 kg. INTERVENTIONS: The anesthetized pigs were subjected to a penetrating liver injury, which resulted in a mean +/- sem loss of 40% +/- 5% of estimated whole blood volume within 30 mins and mean arterial pressures of <20 mm Hg. When heart rate declined progressively, pigs randomly received a bolus dose and continuous infusion of either vasopressin (0.4 units/kg and 0.04 units.kg-1.min-1, n = 7), or epinephrine (45 microg/kg and 5 microg.kg(-1).min(-1), n = 7), or an equal volume of saline placebo (n = 7), respectively. At 30 mins after drug administration, all surviving animals were fluid resuscitated while bleeding was surgically controlled. MEASUREMENTS AND MAIN RESULTS: Mean +/- sem arterial blood pressure at 2.5 and 10 mins was significantly (p <.001) higher after vasopressin vs. epinephrine vs. saline placebo (82 +/- 14 vs. 23 +/- 4 vs. 11 +/- 3 mm Hg, and 42 +/- 4 vs. 10 +/- 5 vs. 6 +/- 3 mm Hg, respectively). Although portal vein blood flow was temporarily impaired by vasopressin, it was subsequently restored and significantly (p <.01) higher when compared with epinephrine or saline placebo (9 +/- 5 vs. 121 +/- 3 vs. 54 +/- 22 mL/min and 150 +/- 20 vs. 31 +/- 17 vs. 0 +/- 0 mL/min, respectively). Hepatic and renal artery blood flow was significantly higher throughout the study in the vasopressin group; however, no further bleeding was observed. Despite a second bolus dose, all epinephrine- and saline placebo-treated animals died within 15 mins after drug administration. By contrast, seven of seven vasopressin-treated animals survived until fluid replacement, and 60 mins thereafter, without further vasopressor therapy (p <.01). Moreover, blood flow to liver, gut, and kidney returned to normal values in the postshock phase. CONCLUSIONS: Vasopressin, but not epinephrine or saline placebo, improved short-term survival in a porcine model of uncontrolled hemorrhagic shock after liver injury when surgical intervention and fluid replacement was delayed.     

不同液体复苏对颅脑外伤并发急性失血性休克大鼠脑保护作用比较

目的比较不同种类液体复苏对大鼠颅脑外伤并发急性失血性休克模型的局部脑血流（rCBF）、脑水肿和血脑屏障（BBB）的影响.方法SD大鼠60只随机分为5组：①假手术组（Ⅰ组）;②脑外伤＋休克组（Ⅱ组）;③生理盐水组（Ⅲ组）;④10%羟乙基淀粉（HES）组（Ⅳ组）;⑤小容量高晶体-高胶体渗透压混合液（HHS,7.5%NaCl与10%HES按1：1混合）（Ⅴ组）.记录外伤、休克和复苏前后平均动脉压（MAP）和rCBF的变化,测定复苏后3 h脑组织含水量以及脑组织伊文思蓝（EB）含量.结果在复苏后即刻,Ⅲ、Ⅳ、Ⅴ组MAP和rCBF均恢复正常,分别在15 min、30 min和45 min后开始下降,至120 min时,Ⅴ组显著高于Ⅲ、Ⅳ组（P＜0.05）.复苏后3 h,Ⅴ组脑组织含水量双侧正常,Ⅲ组双侧均显著高于Ⅰ、Ⅴ组（P＜0.05）;Ⅱ、Ⅲ组损伤侧脑组织EB含量显著高于Ⅳ、Ⅴ组（P＜0.05）.结论小容量HHS复苏能够有效、持久地恢复颅脑外伤并发失血性休克大鼠的MAP和rCBF,减轻脑水肿,改善BBB.NS恢复MAP和rCBF的时间较短,加重脑水肿和BBB破坏.10%HES的作用介于小容量HHS和NS之间.