高张氯化钠右旋糖酐液在犬烧伤休克延迟复苏中的作用

目的从血流动力学、心肌力学及代谢等方面探讨高张氯化钠右旋糖酐液(7.5%氯化钠 6%右旋糖酐70,HSD)在烧伤休克延迟复苏中的作用。方法采用犬35%TBSAⅢ度烧伤模型,伤后6 h 分别用乳酸林格液及 HSD 进行复苏,并以每 h 尿量为1.0ml/kg 及心输出量为伤前值的70%～80%来调整输液速度及输液量,观察 HSD 在复苏中容量负荷、左心室等容收缩期最大压力变化速率及左心室舒张期压力下降最大变化速率(±dp/dt_(max))、心脏指数(CI)、氧供给(DO_2)及氧消耗(VO_2)等的变化。结果 HSD 在烧伤休克延迟复苏伤后第一个24 h 输液量比乳酸林格液复苏少30.56%,其中复苏后4 h 的输液量比乳酸林格液少59.50%,在复苏后0.5～2 h, dp/dt_(max)、CI、DO_2及 VO_2的增加幅度明显高于乳酸林格液复苏。结论 HSD 在烧伤休克延迟复苏中具有容量负荷小、改善心肌功能及促进组织代谢等作用。     

高张氯化钠右旋糖酐液在犬烧伤休克延迟复苏中的作用

目的从血流动力学、心肌力学及代谢等方面探讨高张氯化钠右旋糖酐液（７．５％氯化钠＋６％右旋糖酐７０，ＨＳＤ）在烧伤休克延迟复苏中的作用。方法采用犬３５％ＴＢＳＡⅢ度烧伤模型，伤后６ｈ分别用乳酸林格液及ＨＳＤ进行复苏，并以每ｈ尿量为１０ｍｌ／ｋｇ及心输出量为伤前值的７０％～８０％来调整输液速度及输液量，观察ＨＳＤ在复苏中容量负荷、左心室等容收缩期最大压力变化速率及左心室舒张期压力下降最大变化速率（±ｄｐ／ｄｔｍａｘ）、心脏指数（ＣＩ）、氧供给（ＤＯ２）及氧消耗（ＶＯ２）等的变化。结果ＨＳＤ在烧伤休克延迟复苏伤后第一个２４ｈ输液量比乳酸林格液复苏少３０５６％，其中复苏后４ｈ的输液量比乳酸林格液少５９５０％，在复苏后０５～２ｈ，＋ｄｐ／ｄｔｍａｘ、ＣＩ、ＤＯ２及ＶＯ２的增加幅度明显高于乳酸林格液复苏。结论ＨＳＤ在烧伤休克延迟复苏中具有容量负荷小、改善心肌功能及促进组织代谢等作用。     

高张盐溶液与中分子右旋糖酐复苏烧伤休克对犬心肌功能的影响

采用含 Na~ 250mmol/L 的乳酸钠高张盐溶液与6%中分子右旋糖酐(HLD)复苏烧伤休克,与乳酸钠林格氐液(LR)比较,综合评价其复苏效果并探讨其部分机制。结果表明 HLD 组心脏指数(CI) 在伤后4、8、12、24h 均明显高于 LR 组(P<0.05)。HLD 组心肌收缩功能(dp/dtmax),心肌舒张功能(—dp/dt max)在伤后12、24h 也高于 LR 组(P<0.05)。HLD 组在伤后24h 的心肌 MDA 含量(1.74±0.28×10~(-2)mol/g 组织)明显低于 LR 组(3.23±0.56×10~(-2)mol/g 组织,P<0.05)。而其心肌 SOD 活力(157.49±32·23u/mg 组织)明显高于 LR 组(46.88±16.28u/mg,P<0.01)。提示:与 LR 复苏相比,HLD 复苏烧伤休克能明显改善心肌功能,并可持续到伤后24h。HLD 可能通过提高心肌组织 SOD 活力从而降低心肌组织脂质过氧化物含量,减轻脂质过氧化物对细胞膜的损伤,进而起到保护心肌、改善心肌功能的作用。     

口服补液复苏对严重烧伤家兔心肌力学指标的改善作用

目的 了解口服补液复苏对严重烧伤家兔心脏功能的保护作用. 方法 150只家兔随机分为正常对照组(6只)、烧伤组(42只)、立即补液组(42只)、延迟补液组(30只)和延迟快速补液组(30只).正常对照组不致伤不补液.其余4组家兔均造成40%TBSAⅢ度烧伤,烧伤组不补液,余下3组伤后用灌胃的方式进行口服补液复苏.经家兔颈动脉左心室内置管,测量正常对照组及4组致伤家兔伤后2、6、8、12、24、36、48 h的平均动脉压(MAP)、左心室收缩压(LVSP)、左心室舒张末期压(LVEDP)以及左心室压力最大上升/下降速率(LV±dp/dt max),另检测休克期尿量. 结果烧伤组家兔LVSP、LV±dp/dt max较正常对照组显著下降.立即补液组和延迟快速补液组上述指标在伤后24 h内高于烧伤组,其中立即补液组LV+dp/dt max在伤后8 h达峰值[(892±116)kPa/s,1 kPa=7.5 mm Hg],LV-dp/dt max在伤后6 h达峰值[(724±149)kPa/s];伤后8 h,延迟快速补液组LV±dp/dt max均达峰值.延迟补液组伤后各时相点LVSP、LV±dp/dt max与烧伤组接近.各组家兔MAP、伤后第1个24 h尿量的比较情况大致与以上指标相似.烧伤组与其余4组比较,各时相点LVEDP差异无统计学意义(P>0.05). 结论严重烧伤家兔伤后24 h内给予有效的口服补液,可改善心肌力学指标;延迟复苏的家兔按照延迟复苏补液公式预估补液量,才能进行有效复苏.     

延迟复苏对烧伤休克犬氧代谢的影响

目的探讨在烧伤休克延迟复苏情况下,快速补液对烧伤犬氧代谢的影响。方法建立40%TBSAⅢ度烫伤犬模型,将24只伤犬随机分为对照组、延迟均匀复苏组和延迟快速复苏组,每组8只。观察犬伤前及伤后2、6、8、12、24、36、48h氧供(DO2)、氧耗(VO2)、氧摄取率(O2ext)及血液中碱缺失(BD)和乳酸(LA)含量的变化。结果烧伤后各组犬DO2均显著下降,明显低于伤前值(P<0.01),而O2ext均大幅增加,明显高于伤前值(P<0.01)。伤后8h延迟快速复苏组DO2为(7.35±0.21)L·min-1·m-2,明显高于延迟均匀复苏组(5.32±0.96)L·min-1·m-2(P<0.01);其VO2(2.02±0.58)L·min-1·m-2也明显高于延迟均匀复苏组(1.71±0.38)L·min-1·m-2(P<0.01);但O2ext有所下降,延迟快速复苏组为(27.7±5.9)%,明显低于延迟均匀复苏组(32.2±3.9)%(P<0.01)。烧伤后各组犬BD均大幅降低并明显低于伤前(P<0.01),但复苏后逐渐升高,伤后8h延迟快速复苏组为(-6.5±0.7)mmol/L,显著高于延迟均匀复苏组(-9.3±1.4)mmol/L(P<0.01)。伤后各组犬LA均大幅升高,明显高于伤前(P<0.01),复苏后逐渐降低,伤后8h延迟快速复苏组LA为(2.30±0.20)mmol/L,显著低于延迟均匀复苏组(2.67±0.30)mmol/L(P<0.01)。结论快速补液可以显著改善烧伤犬组织的氧代谢状况,有益于烧伤休克的延迟复苏。     

高张氯化钠右旋糖酐液在犬烧伤休克延迟复苏中的作用

目的 从血流动力学、心肌力学及代谢等方面探讨高张氯化钠右旋糖酐液（７．５％氯化钠＋６％右旋糖酐７０，ＨＳＤ）在烧伤休克延迟复苏中的作用。方法 采用犬３５％ＴＢＳＡⅢ度烧伤模型，伤后６ｈ分别用乳酸林格液及ＨＳＤ进行复苏，并以每ｈ尿量为１．０ｍｌ／ｋｇ及心输出量为伤前值的７０％￣８０％来调整输液速度瘃输液量，观察ＨＳＤ在复苏中容量负荷、左心室等容收缩期最大压力变化速度及左心室舒张期压力下降最大变化速度     

延迟快速复苏对烧伤休克循环影响的临床研究

目的探讨在烧伤延迟复苏情况下,如何迅速纠正休克.方法通过对20例烧伤面积大于40%TBSA、因延迟复苏导致休克的患者,进行延迟快速复苏.观察休克期液体出入量、动咏压(BP)、肺动脉压(PAP)、肺动脉楔状压(PAWP)、中心静脉压(CVP)、心输出量(CO)、肺血管阻力(PVR)、外周血管阻力(SVR)、氧供应(DO2)、氧消耗(VO2)、氧摄取率(O2ext)、乳酸(LA)及碱缺失(BD)等血流动力学和氧代谢指标的变化.结果快速补液后2h内输入液体占“第一个24h公式计算量”的(38.8±6.1)%,如果加上院外补液量则占“第一个24h公式计算量”的(48.3±5.0)%.第一个24h实际补入量占“第一个24h公式计算量”的(131.4±14.3)%;第二个24h实际补入量占“第二个24h公式计算量”的(103.2±7.2)%.快速补液后,尿量大幅增加,CO显著升高,DO2增强,SVR、LA、BD大幅下降,PVR虽大幅升高,但PAWP、PAP和CVP并未超过正常.结论在严密血流动力学监护下,烧伤后延迟复苏初期加快补液速度是可行且有益的,烧伤休克的延迟复苏需要显著增加补液量.指导休克延迟快速复苏应以监护心输出量及PAP、PAWP、CVP等血流动力学指标为主,辅以血中LA、BD水平及尿量变化等临床指标的监测.     

δ阿片受体激动剂对脓毒症大鼠血液动力学和氧代谢的影响

目的 探讨δ阿片受体激动剂(DADLE)对脓毒症大鼠血液动力学和氧代谢的影响.方法清洁级健康雄性SD大鼠80只,采用随机数字表法,将大鼠随机分为4组(n=20):假手术组(S组)仅穿线,不结扎穿孔;脓毒症组(SEP组)采用盲肠结扎穿孔法制备脓毒症模型;DADLE1组和DADLE2组分别于制模前0.5 h和制模后即刻经腹腔注射DADLE 10 mg/kg,浓度为0.5mg/ml.于制模后即刻、2 4 6 h(T1～4)时记录心排血量(CO)、MAP、左心室收缩压(LVSP)和心室压力最大变化速率(±dp/dtmax),计算心指数(CI).于T4时从左颈总动脉及右颈外静脉取血样,计算氧供给(DO2)、氧消耗(VO2)、氧摄取率(ER02).结果 与S组比较,SEP组MAP、LVSP T2时升高,T3,4时降低,±dp/dtmax升高,DADLE1组和DADLE2组MAP T2时升高,T3,4时降低,LVSP T2,3时升高,T4时降低,±dP/dtmax升高,SEP组、DADLE1组和DADLE2组CI、DO2和VO2降低,ERO2升高.与SEP组比较,DADLE1组和DADLE2组MAP、LVSP、±dp/dtmax T3,4时升高,CI、DO2和VO2升高,ERO2降低(P＜0.05).DADLE1组和DADLE2组间上述各指标差异无统计学意义(P＞0.05).结论 DADLE能改善脓毒症大鼠血液动力学和氧代谢.

Abstract：

Objective To investigate the effects of δ-opioid receptor agonist DADLE (D-Ala2-D-Leu5-enkephalin) on the hemodynamics and oxygen metabolism in rats with sepsis. Methods Eighty healthy male SD rats were randomly divided into 4 groups ( n = 20 each) : sham operation group (group S), sepsis group (group SEP) ,DADLE, group and DADLE2, group. Sepsis was induced by cecum ligation and puncture (CLP) in SEP, DADLE,and DADLE2 groups. In DADLE1 and DADLE2 groups, 0.5 mg/ml DADLE 10 mg/kg was injected intraperitoneally (IP) 0.5 h before CLP and immediately after CLP respectively. Mean arterial pressure (MAP), left ventricular systolic pressure (LVSP) and ± dp/dtmax were recorded at 0, 2, 4 and 6 h after CLP (T1-4). Blood samples from left common carotid artery and right external jugular vein were collected at T4 for blood gas analysis. The cardiac index (CI), O2 delivery (DO2), O2 consumption (VO2) and O2 extraction rate (ERO2) were calculated.Results Compared with group S, MAP and LVSP were significantly increased at T2, while decreased at T3,4, and ± dp/dtmax was significantly increased in group SEP, MAP was significantly increased at T2, while decreased at T3,4, LVSP was significantly increased at T2,3, while decreased at T4 , and ± dp/dtmax was significantly increased in DADLE, and DADLE2 groups, and CI, DO2 and VO2 were significantly decreased and ERO2 was increased in SEP, DADLE, and DADLE2 groups (P＜0.05). Compared with group SEP, MAP, LVSP and ± dp/dtmax at T3,4 and CI, DO2 and VO2 were significantly increased, while ERO2 was significantly decreased in DADLE1 and DADLE2 groups (P ＜ 0.05). There was no significant difference in the parameters mentioned above between DADLE1 and DADLE2 groups ( P ＞ 0.05). Conclusion δ-opioid receptor agonist DADLE can obviously improve the hemodynamics and oxygen metabolism in septic rats.     

麻醉、手术、液体复苏和内毒素对烧伤后细菌移位的影响

观察临床有关因素对烧伤后肠道细菌移位的影响。将6个月龄的48头母猪随机分成8组:①对照组(C),仅作全身麻醉;②手术组(O),行Swan-Ganz及动静脉导管插入术;③烧伤组(B),制成40％TBSAⅢ°火焰烧伤模型,伤后1小时起按乳酸林格液2ml/kg/h维持;④烧伤和手术组(BO),同O组和B组;⑤烧伤、手术和复苏组(BOR),在BO组基础上每天给予乳酸林格液2ml/kg/h维持,同时用乳酸林格液4ml/kg/％进行复苏;⑥烧伤、手术、复苏和内毒素组(BORE),在BOR组基础上于     

失血性休克时大鼠全身氧供给与氧消耗关系变化的研究

目的　研究失血性休克时大鼠全身氧供给 (DO2 )与氧消耗 (VO2 )关系变化。方法　按每次 4ml/kg ,每隔 0 5h分次从静脉放血 ,观察大鼠休克过程中DO2 ,VO2 ,氧摄取率 (ExtO2 )等变化。结果　失血 2 0h时平均动脉压开始明显下降 (P <0 0 1 )。在休克早期 ,DO2 呈进行性下降 ,ExtO2 出现代偿升高 ,VO2 维持相对不变 ,呈非氧供依赖关系 ;当DO2 降至2 7 64ml·min- 1 ·kg- 1 后 ,VO2 随DO2 线性降低 (P <0 0 1 ) ,即呈氧供依赖关系 ,并伴血乳酸浓度升高。结论　失血性休克时DO2 与VO2 间呈双相变化关系 ,氧供依赖关系的变化反映了全身组织缺氧的存在     

Fluid resuscitation with deferoxamine prevents systemic burn-induced oxidant injury.

We studied the effect of deferoxamine (DFO) infused after burns on hemodynamic stability as well as local and systemic inflammation and oxidant-induced lipid peroxidation. Eighteen anesthetized sheep were given a 40% of total body surface burn and fluid resuscitated to restore oxygen delivery (DO2) and filling pressures to baseline values. Animals were resuscitated with lactated Ringer's (LR) alone or LR plus 1,500 ml of a 5% hetastarch complexed with DFO (8 mg/ml). Animals were killed 6 hours postburn. The sheep resuscitated with LR and LR plus hetastarch demonstrated significant lung inflammation and significant increases in lung and liver malondialdehyde (MDA) from controls of 47 +/- 6 and 110 +/- 7 nMol/gm to 63 +/- 13 and 202 +/- 59 for LR and 67 +/- 4 and 211 +/- 9 for LR + hetastarch, respectively. The group resuscitated with hetastarch alone required 15% less fluid. VO2 returned to baseline values in both groups by 2 hours. Resuscitation with the 5% hetastarch-DFO decreased total fluids by 30% over LR and prevented the increase in lung and liver MDA. In addition, postburn VO2 increased by 25% above baseline values. Burn tissue edema, measured as protein-rich lymph flow, was significantly increased with the administration of DFO compared with the other groups. We conclude that DFO used for burn resuscitation prevents systemic lipid peroxidation and decreases the vascular leak in nonburn tissues while also increasing O2 utilization. Resuscitation with hetastarch-DFO may accentuate burn tissue edema, possibly by increased perfusion of burn tissue.     

Oxygen consumption early postburn becomes oxygen delivery dependent with the addition of smoke inhalation injury.

We determined the relationship between oxygen delivery, DO2, and oxygen consumption, VO2, in sheep after a moderate smoke inhalation injury and 15% TBSA third-degree burn compared with burn alone and controls. Comparison was made beginning three hours after injury when carboxyhemoglobin levels were back to baseline values. We decreased DO2 between three and eight hours by 25% by either removing blood (controls) or decreasing the resuscitation fluid infusion rate. Lung oxidant, measured as tissue malondialdehyde (MDA) levels, and histologic changes were also assessed. Animals were killed at 24 hours. We found that in controls and animals with a burn alone, a 25% decrease in DO2 was compensated for by an increase in O2 extraction, maintaining VO2 constant. Correlation of DO2 to VO2 was r2 = 0.3, indicating independence of VO2 from DO2. With the combined injury, VO2 decreased in proportion to DO2, since O2 extraction did not increase. The correlation of DO2 to VO2 was r2 = 0.9, indicating delivery-dependent consumption, a pathologic process most likely caused by increased inflammatory mediators from the combined injury. Lung lipid peroxidation was markedly increased in the combined injury, 148 +/- 18 nmol MDA/gram of tissue compared with burn alone, 64 +/- 5 nmol/g, or controls, 45 +/- 4 nmol/g. However, no decrease in arterial O2 tension or increase in lung water was noted, i.e., the sheep did not have ARDS, which is known to impair O2 extraction. We conclude that a pathologic O2 delivery-dependent consumption develops with the combination of burn and inhalation injury, increasing the potential for tissue hypoxemia. This change corresponds with increased lung tissue oxidant change.     

液体复苏加山莨菪碱对烧伤兔心肌功能的影响

目的 探讨山莨菪碱对烧伤兔心肌功能的影响。方法 采用新西兰兔２５％Ⅲ度烫伤模型，分别于伤前，伤后即刻１，３，５，７小时测定左心室内压峰值，左心室内压最大变化速率，并观察严重烧伤休克期液体复苏加山莨菪碱对上述指标的影响。结果 严重烧伤后早期即发生心肌的收缩功能和舒张功能障碍，并呈进行性减退。单纯给予山莨菪碱或单纯输液治疗对兔严重烧伤后的心功能在短期内有支持作用，但治疗效果欠佳，且单纯山莨菪碱治疗组心     

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.     

Cardiovascular effect of 7.5% sodium chloride-dextran infusion after thermal injury.

HYPOTHESIS: Clinical study can help determine the safety and cardiovascular and systemic effects of an early infusion of 7.5% sodium chloride in 6% dextran-70 (hypertonic saline-dextran-70 [HSD]) given as an adjuvant to a standard resuscitation with lactated Ringer (RL) solution following severe thermal injury. DESIGN: Prospective clinical study. SETTING: Intensive care unit of tertiary referral burn care center. PATIENTS: Eighteen patients with thermal injury over more than 35% of the total body surface area (TBSA) (range, 36%-71%) were studied. INTERVENTIONS: Eight patients (mean +/- SEM, 48.2% +/- 2% TBSA) received a 4-mL/kg HSD infusion approximately 3.5 hours (range, 1.5-5.0 hours) after thermal injury in addition to routine RL resuscitation. Ten patients (46.0% +/- 6% TBSA) received RL resuscitation alone. MAIN OUTCOME MEASURES: Pulmonary artery catheters were employed to monitor cardiac function, while hemodynamic, metabolic, and biochemical measurements were taken for 24 hours. RESULTS: Serum troponin I levels, while detectable in all patients, were significantly lower after HSD compared with RL alone (mean +/- SEM, 0.45 +/- 0.32 vs 1.35 +/- 0.35 microg/L at 8 hours, 0.88 +/- 0.55 vs 2.21 +/- 0.35 microg/L at 12 hours). While cardiac output increased proportionately between 4 and 24 hours in both groups (from 5.79 +/- 0.8 to 9.45 +/- 1.1 L/min [mean +/- SEM] for HSD vs from 5.4 +/- 0.4 to 9.46 +/- 1.22 L/min for RL), filling pressure (central venous pressure and pulmonary capillary wedge pressure) remained low for 12 hours after HSD infusion (P = .048). Total fluid requirements at 8 hours (2.76 +/- 0.7 mL/kg per each 1% TBSA burned [mean +/- SEM] for HSD vs 2.67 +/- 0.24 mL/kg per each 1% TBSA burned for RL) and 24 hours (6.11 +/- 4.4 vs 6.76 +/- 0.75 mL/kg per each 1% TBSA burned) were similar. Blood pressure remained unchanged, and serum sodium levels did not exceed 150 +/- 2 mmol/L (mean +/- SD) in either group. CONCLUSIONS: The absence of deleterious hemodynamic or metabolic side effects following HSD infusion in patients with major thermal injury confirms the safety of this resuscitation strategy. Postburn cardiac dysfunction was demonstrated in all burn patients through the use of cardiospecific serum markers and pulmonary artery catheter monitoring. Early administration of HSD after a severe thermal injury may reduce burn-related cardiac dysfunction, but it had no effect on the volume of resuscitation or serum biochemistry values.