不同液体输液对犬失血性休克时的血流动力学,氧转运及血管外…

以犬为实验对象研究不同液体输注对失血性休克时的血流动力学，氧转运及血管外肺水的影响。方法：选择成年健康犬１５只，静脉麻醉后通过动脉放血至平均动脉压４．６７ｋＰａ制作失血性休克模型，继分别以乳酸钠林格氏液，全血及多聚明胶等三种液体输注复苏，以ＰＡＷＰ值恢复至２．０ｋＰａ为输全液终点，观察血流动力学，氧转运和血管外肺水等各指标的变化。     

高渗晶-胶混合液、等渗晶体溶液和全血抗犬失血性休克效果的比较

目的 比较高渗晶-胶混合液、等渗晶体溶液和全血对失血性休克犬的血流动力学和全身氧供状态的影响。方法 18只犬麻醉后气管内插管,自主呼吸,经股动脉放血至平均动脉压6.7 kpa,维持1 h。然后分别以乳酸林格氏液(LR)、全血(WB)和7.5％氯化钠 10％羟乙基淀粉混合液(HHS)进行抗休克治疗,比较其效果。结果HHS使休克犬血流动力学参数和全身氧供恢复至休克前水平所需液体量和时间显著少于LR和WB,且作用维持时间长(P<0.05)。结论 失血性休克早期应用小容量HHS可改善血流动力学和全身氧供状态。     

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。     

缝隙连接在兔失血性休克复苏诱发肺损伤中的作用

目的 评价缝隙连接在兔失血性休克复苏诱发肺损伤中的作用.方法 健康家兔24只,体重1.5～2.2 kg,经股动脉放血制备失血性休克模型.随机分为2组(n=12),传统治疗组(A组)静脉输注乳酸钠林格氏液1.5 ml·kg-1·min-1 30 min(T3);辛醇组(B组)静脉输注乳酸钠林格氏液1.5 ml·kg-1·min-1 30 min(T3),同时腹腔注射99.5%辛醇5 mmol/kg.然后两组回输全部放血及等放血量的乳酸钠林格氏液后静脉输注乳酸钠林格氏液2.5 ml·kg-·h-1 150 min(T4).于放血前(T1)、模型制备成功即刻(T2)、T3、T4时记录左心室收缩压(LVSP)和HR,记录复苏期间兔的病死情况.于T时处死,测定肺组织Na+-K+-ATP酶和Ca2+-ATP酶的活性,计算肺通透性指数和肺湿重/干重(W/D)比,光镜下观察肺组织病理学结果.结果 与A组比较,B组T3时HR和LVSP降低,T4时LVSP升高,HR降低,Na+-K+-ATP酶和Ca2+-ATP酶活性升高,肺通透性指数降低,肺组织W/D比和病死率降低(P＜0.05或0.01).B组肺组织病理学损伤程度较A组明显减轻.结论 缝隙连接参与了兔失血性休克复苏诱发肺损伤.     

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.     

犬内毒素性休克时琥珀明胶和乳酸钠林格氏液的容量动力学

目的比较犬内毒素性休克时琥珀明胶和乳酸钠林格氏液的容量动力学。方法健康杂种犬20只,雌雄不拘,随机分为4组（n=10）,乳酸钠林格氏液组（CL组）经30min静脉输注乳酸钠林格氏液30ml/kg;琥珀明胶组（CG组）经30min静脉输注琥珀明胶10ml/kg;内毒素＋乳酸钠林格氏液组（LL组）静脉注射内毒素250μg/kg,再经30min静脉输注乳酸钠林格氏液30ml/kg;内毒素＋琥珀明胶组（LG组）静脉注射内毒素250μg/kg,再经30min静脉输注琥珀明胶10ml/kg。补液期间每隔5分钟测定血红蛋白浓度和红细胞压积;记录血液动力学指标和总尿量。应用物质守恒定律和容量动力学理论,计算血浆容量增加、外周容量增加、容量扩张效率、目标容积（V）和清除率（Kr）。结果与CL组比较,CG组V和Kr降低,LL组V升高（P〈0.05）;与CG组比较,LG组V和Kr升高（P〈0.05）;与LL组比较,LG组V和K降低（P〈0.05）。与CG组和LG组比较,CL组和LL组血浆容量增加和容量扩张效率降低,外周容量增加升高（P〈0.05）;与CL组和CG组比较,LL组和LG组血浆容量增加和容量扩张效率降低,外周容量增加升高（P〈0.05）。结论犬内毒素性休克时,乳酸钠林格氏液的扩容效率较琥珀明胶降低更为明显。     

术前晶体液和胶体液急性扩容稀释期间血流动力学变化的对比研究

目的：比较乳酸钠林格液与海脉素用于术前急性扩容稀释期间血流动力学的变化。方法：26例颅脑手术病人，随机等分为乳酸钠林格液组(LR组)和海脉素组(H组)。麻醉诱导后，分别用相应的液体以25ml／min的速度进行扩容稀释；用UNION CACH-2001无创阻抗法监测仪连续监测扩容期的血流动力变化。结果：LR组SVI、CI、TPR、MAP和HR无明显变化。H组MAP和HR无明显变化，SVI和CI逐渐增高，输入海脉素1000ml后，二者分别增加27．5％和17．3％，TPR下降22．3％。结论：麻醉诱导后用海脉素扩容稀释优于乳酸钠林格液。     

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。     

大量晶体液复苏不增加血管外肺水

为了确定晶体液(乳酸钠林格氏液)在失血性休克的复苏中是否增加血管外肺水(EVLW),作者用10只体重25～50kg的羊作了研究。麻醉后经颈内静脉插入肺动脉导管测定PCWP和CI。经颈动脉置管至远端主动脉测定动脉收缩压、平均动脉压(MAP)和EVLW。EVLW用Lewis和Elings介绍的温度—染料稀释技术测定。并直接测定氧饱和度和血气张力,静脉血掺杂(s/(?)t)及胶体渗透压(COP)。计算COP—PCWP差。测定上述基础值之后,每只动物均经肝素化的周围动脉插管放血至MAP50mmHg,并维持30分钟,在30分钟末再重复测定上述各值。然后开始输注乳酸钠林格氏液复苏,直到Cl、MAP、PCWP恢复至基础值水平。再以能维持基础值的速度继续输注1小时。     

犬烧伤休克延迟复苏的实验研究

目的探讨应用林格液进行烧伤休克延迟复苏的效果.方法12只犬随机分为对照组(S组,6只)和治疗组(LR组,6只).LR组采用35%TBSAⅢ度烧伤模型,伤后6h以乳酸林格液进行复苏,并以尿量为1.0ml@kg-1@h-1及心输出量为伤前值的70%～80%来调整输液速度及输入量,观察其在伤后第一个24h复苏中的容量负荷、平均动脉压(MAP)、左心室收缩压(LVSP)、左室内压最大上升/下降速率(±dp/dtmax)、心脏排血指数(CI)、氧供给(DO2)及氧消耗(VO2)等的变化.结果乳酸林格液在烧伤休克延迟复苏后第一个24h的复苏中,每1%烧伤面积的输液量为(887±1.02)ml/kg,比采用Parkland公式复苏多1.2倍,其中在复苏后4h内的输液量为(3.63±0.99)ml/kg,为总入量的41%;MAP、LVSP、±dp/dtmax、CI、DO2及VO2等指标在复苏后2h即达到或接近对照组水平.结论乳酸林格液在烧伤休克延迟复苏中,比早期复苏需要更多的液体量才能满足需求,而血流动力学、心肌功能及氧动力学等在复苏后2h即有明显改善.     

Effects of hypertonic saline versus lactated Ringer's solution on cerebral oxygen transport during resuscitation from hemorrhagic shock

Hypertonic saline successfully restores systemic hemodynamics in dogs and humans with severe hemorrhagic shock and, in contrast to lactated Ringer's solution, does not increase intracranial pressure (ICP). This study compares cerebral oxygen delivery in 12 dogs subjected to hemorrhagic shock by the rapid removal of blood (mean arterial pressure of 40 mm Hg maintained for 30 minutes), and then resuscitated with lactated Ringer's solution (six dogs) or 7.5% saline solution (six dogs) to restore systolic arterial pressure. Both solutions effectively restored systemic hemodynamic stability, increasing cardiac output and systolic blood pressure while decreasing mean and diastolic arterial pressure and systemic vascular resistance. The ICP was significantly lower after resuscitation in the hypertonic saline group (p less than 0.05), but cerebral blood flow, which had decreased during shock, was not restored by either fluid, and cerebral oxygen transport fell further secondary to a hemodilutional reduction of hemoglobin. Although hypertonic saline may improve systemic hemodynamics and maintain a low ICP during resuscitation, it fails, as does Ringer's solution, to restore cerebral oxygen transport to prehemorrhagic shock levels.     

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.     

Hemodynamic and pulmonary effects of fluid resuscitation from hemorrhagic shock in the presense of mild pulmonary edema

The hemodynamic and pulmonary effects of fluid resuscitation with crystalloid and colloid solutions in the presence of mild pulmonary edema were investigated. Anesthetized dogs received oleic acid to increase pulmonary capillary permeability, and one hour later bled to produce hemorrhagic shock. One hour after the shock, resuscitation was performed with Ringer's lactate, 6% hydroxyethyl starch (HES) solution, or dog's plasma. Resuscitation from hemorrhagic shock restored hemodynamics to pre-hemorrhagic levels with all of the above solutions. Ringer's lactate resuscitation resulted in increases in extravascular lung water volume (EVLWV) and oxygen consumption, and decreases in colloid osmotic pressure and oxygen delivery. Resuscitation with HES solution and plasma did not result in increases in EVLWV, but with HES solution resulted in decreases in colloid osmotic pressure to pre-hemorrhagic levels in two hours. This suggests that the resuscitation with HES solution can not maintain colloid osmotic pressure for more than two hours. The author concludes that the hemodynamic and pulmonary effects of HES solution and plasma are similar in mild lung injury cases.     

Cerebrovascular effects of small volume resuscitation from hemorrhagic shock: comparison of hypertonic saline and concentrated hydroxyethyl starch in dogs

To determine if hypertonic and hyperoncotic resuscitation solutions exerted comparable effects on cerebral hemodynamics following hemorrhagic shock, we compared randomly assigned, equal volumes (6.0 ml/kg) of hypertonic (7.2%) saline (HS) and hyperoncotic (20%) hydroxyethyl starch (HES) for resuscitation from acute experimental hemorrhage in 12 anesthetized dogs. Regional cerebral blood flow (radiolabeled microspheres), intracranial pressure (cisternal catheter), and systemic hemodynamics were recorded. Rapid hemorrhage reduced the mean arterial pressure to 45 mm Hg for 30 min. Resuscitation fluids were infused over 5 min. Both fluids restored mean arterial pressure and cardiac output equally. However, at 60 min following resuscitation, cardiac output decreased in the HS group in comparison to the HES group (1.7 +/- 0.1 vs. 3.1 +/- 0.2 L/min, p <0.05). Cardiac output rapidly declined, however, in the HS group in comparison to the HES group (p <0.05 60 min following resuscitation). Intracranial pressure and cerebral perfusion pressure were similar at all intervals. Regional cerebral blood flow was similar following both fluids. Neither fluid restored cerebral oxygen transport to baseline values. Based on these data, the authors conclude that, following severe hemorrhagic shock of brief duration, systemic and cerebral hemodynamic values are restored equally well by highly concentrated colloid or by hypertonic saline, although hypertonic saline only transiently improves cardiac output.     

Acute effects of massive transfusion of a bovine hemoglobin blood substitute in a canine model of hemorrhagic shock

The capability of stroma-free hemoglobin solutions to act as a plasma expander with oxygen and carbon dioxide transport properties has encouraged the idea of their possible use in settings of massive blood loss. Using a canine hemorrhagic shock model (systolic arterial pressure ≤50 torr for 60 min), we evaluated the efficacy of an ultra-pure stroma-free bovine hemoglobin solution (PBHg) as a resuscitation fluid in hypovolemic and acidotic animals, using homologous blood (PRBC) and 10% human serum albumin (HSA) as control solutions. Following volume replacement, dogs were studied for 2 h under anesthesia and for 4 h subsequently while awake. Resuscitation with PBHg (30 ± 3 ml/kg) was able to restore stable hemodynamics and correct acidosis to an extent comparable to that in animals treated with PRBC. Additionally, oxygen transport was maintained at a higher level than that in dogs treated with HSA. Administration of PBHg in this shock model revealed no significant cardiopulmonary toxicity or adverse effects. These short-term results suggest that PBHg may be useful for effective resuscitation after major blood loss.     

Effects of resuscitation from hemorrhagic shock on cerebral hemodynamics in the presence of an intracranial mass

This study compares intracranial pressure, cerebral blood flow, and cerebral oxygen transport during hemorrhagic shock and following fluid resuscitation with crystalloid or colloid solution in a canine model with an epidural mass lesion. After placement of an epidural balloon, intracranial pressure was increased to 30 mm Hg for 5 minutes and then permitted to vary without further manipulation. Hemorrhagic shock was produced by the rapid removal of blood to achieve a mean arterial pressure of 55 mm Hg for 30 minutes. Resuscitation then was performed with intravenous lactated Ringer's solution, 60 ml/kg, or with 6.0% hetastarch, 20 ml/kg. Following both solutions mean arterial pressure and cardiac output were increased and hemoglobin concentration was reduced. Intracranial pressure was significantly lower immediately after resuscitation in the hetastarch group; it then gradually increased so that the difference was much less 1 hour later. Cerebral blood flow decreased during shock and was not restored by either fluid; cerebral oxygen transport fell further with resuscitation in both groups due to hemodilutional reductions in hemoglobin. Although colloid resuscitation improved systemic hemodynamics and maintained lower intracranial pressure, it failed, as did crystalloid resuscitation, to restore cerebral oxygen transport to prehemorrhagic shock levels.     

Intrathoracic blood volume as an end point in resuscitation of the severely burned: an observational study of 24 patients

BACKGROUND: Treatment of burn shock according to empirical resuscitation formulas is still considered the gold standard, and the burn community does not advocate the use of invasive cardiorespiratory monitoring in general. As a consequence, data dealing with early postburn hemodynamics are sparse, and only few studies have paid attention to the topic of end-point burn shock resuscitation. However, recent studies have suggested that burn survival may be improved when invasive monitoring is used to guide fluid therapy during the shock phase. MATERIALS AND METHODS: In an observational study of 24 patients with severe burns, the transpulmonary double indicator dilution technique was used for semi-invasive hemodynamic monitoring. The clinical utility of the intrathoracic blood volume (ITBV) as an end-point variable for fluid resuscitation was evaluated, comparing correlation of filling pressure obtained by a pulmonary artery catheter and intrathoracic blood volume to cardiac index and oxygen delivery. In addition fluid volume predicted by the Parkland burn formula was compared with the actual fluid volume given when ITBV was used as end point for resuscitation. RESULTS: ITBV-guided resuscitation was associated with restoration of preload and peripheral delivery of oxygen within 24 hours in the majority of patients. Augmentation of ITBV was significantly correlated with changes in cardiac index and oxygen transport rate. No such correlation could be demonstrated for the conventional preload parameters such as central venous pressure and pulmonary capillary wedge pressure. Thus, ITBV seemed in burned, hypovolemic patients a better indicator of the preload component of the cardiac output than the conventional preload parameters obtained with the pulmonary artery catheter. Significantly larger volumes of crystalloids than predicted by the Parkland formula were administered when ITBV was used as end point for resuscitation. The extravascular lung water remained normal during this extraordinary high volume load. CONCLUSION: ITBV may be a reliable preload indicator to guide volume therapy in life-threatening burns, and end-point-fixed resuscitation to this parameter seems to be associated with significantly higher fluid administration than calculated compared with traditional burn formulas. The effects of burn resuscitation to fixed end points on survival and multiple organ failure should be evaluated in future randomly assigned trials.