Haemodynamic effects of volume resuscitation by hypertonic saline-dextran (HSD) in porcine acute cardiac tamponade

BACKGROUND: Hypertonic saline-dextran (HSD) has been utilized for small-volume resuscitation in acute circulatory shock. However, HSD has also been reported to induce myocardial depression. The aim of this study was to examine the effects of HSD on cardiac performance and splanchnic perfusion in a low cardiac output model based on experimental cardiac tamponade. METHODS: Seven anaesthetized, mechanically ventilated pigs of both sexes (weight 24 +/- 2 kg, mean +/- SEM) completed a randomized, cross-over protocol. A low cardiac output state was established by intrapericardial infusion of dextran. Animals were resuscitated by bolus infusions (4 ml kg(-1) in 2 min) of either 7.5% hypertonic saline-dextran or Ringer's acetated solution (RAc) and then observed during tamponade (20 min) and following its release (40 min). Central haemodynamics, portal venous (QPV) and renal arterial (QRA) flows were measured together with gastric, jejunal, hepatic and renal laser-Doppler flowmetry. RESULTS: Resuscitation using HSD in a low cardiac output state completely restored QPV and improved gastric, jejunal, hepatic and renal microcirculation as assessed by laser-Doppler flowmetry while no significant effect was observed in QRA. No such beneficial effects could be observed when animals were resuscitated using RAc. The improved haemodynamic state by HSD was maintained following release of cardiac tamponade while perfusion in RAc resuscitated animals returned to baseline or even remained depressed (hepatic and renal microcirculation). No signs of cardiodepression by HSD were observed. CONCLUSION: Resuscitation using HSD in a low cardiac output state restored splanchnic perfusion and microcirculation without any signs of cardiodepression.     

Evaluation of an intraosseous infusion device for the resuscitation of hypovolemic shock.

An intraosseous infusion device designed for the prehospital administration of hypertonic saline-dextran solutions was evaluated by resuscitating hemorrhaged conscious sheep. Eight animals underwent 2 hours of hemorrhagic hypotension (50 mm Hg, bled volume = 43 +/- 7 ml/kg). This was followed by the intraosseous infusion of 200 ml (4-5 ml/kg) of 7.5% NaCl-6% dextran 70 into the bone marrow of the sternum. Results were compared to seven control animals (bled volume = 31 +/- 6 ml/kg) resuscitated through a central venous catheter. Despite the small volumes infused, mean arterial blood pressure and cardiac output were rapidly normalized in both groups by 10 minutes post resuscitation (p less than 0.01). Plasma sodium concentration increased an average of 12 mEq/L and plasma volume was rapidly expanded regardless of route. The metabolic acidosis of hemorrhagic shock was rapidly corrected, pulmonary pressures remained normal, and hypoxemia did not occur after intraosseous resuscitation. The device provided safe and rapid vascular access via the sternal bone marrow space. The use of intraosseous infusion of hypertonic saline dextran solutions via the sternal bone marrow may allow prehospital rescuers to consistently incorporate fluid replacement therapy into 'scoop and run' policies by avoiding the time delays associated with failures in IV access.     

Resuscitation of severe thermal injury with hypertonic saline dextran: effects on peripheral and visceral edema in sheep

BACKGROUND: Edema of tissue not directly injured by heat is a common complication after resuscitation of burn shock. Hypertonic 7.5% NaCl 6% dextran (HSD) infusion reduces early fluid requirements in burn shock, but the effects of HSD on peripheral and visceral tissue edema are not well-defined. METHODS: We measured the microcirculatory absorptive pressures of burned and nonburned skin and tissue water content of skin and other tissues in anesthetized sheep after 70% to 85% total body surface area scald and resuscitation. Fluid infusion was initiated 30 minutes after injury using 10 mL/kg HSD (n = 11) or lactated Ringer's (LR) (n = 12), with infusion rates titrated to restore and maintain preburn oxygen delivery (DO2). Thereafter, both groups received LR infusions as needed to maintain DO2 until the study's end at 8 hours. Colloid osmotic pressure was measured in plasma, and combined interstitial colloid osmotic and hydrostatic pressures were measured in skin. RESULTS: Both treatments successfully restored DO2, but fluid requirements were less with the HSD group than with the LR group (43+/-19 mL/kg vs. 194+/-38 mL/kg, respectively, p < 0.05). The peripheral and visceral tissue water contents at 8 hours postinjury until the end of the study in both burn groups were significantly higher than in nonburn controls. However, HSD-treated sheep had significantly less water content in the colon (less 28%), liver (less 9%), pancreas (less 55%), skeletal muscle (less 21%), and nonburned skin (less 12%) compared with LR-treated sheep (p < 0.05 for each). HSD-treated sheep maintained significantly higher (3 to 5 mm Hg) plasma colloid osmotic pressure than LR-treated sheep. CONCLUSION: There were no observed differences in edema in burn skin between the two treatment groups. The early volume-sparing effect of HSD and reduction in tissue edema are likely attributed to an increased extracellular osmolarity and a better maintenance of the plasma oncotic pressure.     

Effects of hypertonic saline and dextran 70 on cardiac diastolic function after hemorrhagic shock

BACKGROUND: A bolus of 7.5% NaCl-6% Dextran 70 (HSD) is effective in resuscitating hypovolemic shock. Common hemodynamic findings with HSD are restoration of cardiac output, increased blood pressure, and improvement of peripheral circulation. However, the effect of HSD upon cardiac function is still controversial. In our previous study, when HSD did not improve cardiac contractility, it was speculated that it might affect cardiac diastolic function without a change in contractility. Therefore, we studied the effects of HSD on cardiac diastolic function. METHODS: Hemorrhagic shock was created by exsanguination of 31.4 +/- 0.9 ml/kg (NS group) or 29.0 +/- 3.6 ml/kg (HSD group). Then mean BP was maintained at 50 mm Hg for 30 min in both groups. The HSD group (n = 6) received HSD (4 ml/kg) and the NS (control) group (n = 5) received normal saline (40 ml/kg) after the shock. Cardiac diastolic functions were measured in both groups using the peak negative dP/dt and the left ventricular end-diastolic pressure-volume relationship (EDPVR) during the experimental period: before shock, immediately, and 2 h after resuscitation. RESULTS: Hemodynamic parameters in both groups demonstrated similar changes throughout the experimental period. The peak negative dP/dt, stiffness constant, and elasticity obtained by EDPVR did not differ significantly between the two groups. CONCLUSION: HSD seems to be an effective resuscitation fluid after hemorrhagic shock because the volume of HSD required to maintain circulation is significantly smaller than that of normal saline. However, our data revealed that HSD does not change cardiac diastolic function after hemorrhagic shock.     

Hypertonic saline-dextran resuscitation of acute canine bile-induced pancreatitis

In this study, we examined the effects of hypertonic saline-dextran resuscitation (2,400 mOsm of sodium chloride, 6 percent dextran 70) on cardiopulmonary function and extravascular lung water in acute canine pancreatitis. Acute pancreatitis was induced in 21 dogs by injecting 0.5 ml/kg of autologous bile into the pancreatic duct. In 10 dogs, resuscitation was begun with a 4 ml/kg bolus of hypertonic saline-dextran solution; 11 dogs received no bolus. Lactated Ringer's solution was infused in all dogs to maintain mean arterial pressure and cardiac output at baseline values. Pulmonary hypertension accompanied by a significant increase in pulmonary vascular resistance and a decrease in lung blood flow occurred in those dogs resuscitated with lactated Ringer's solution alone. By contrast, dogs in the hypertonic saline-dextran group maintained pulmonary artery pressure and pulmonary vascular resistance at baseline values while nutritive blood flow to the lung decreased progressively. Our data suggest that hypertonic saline-dextran resuscitation effectively restores cardiac function while it significantly reduces fluid requirements, as well as the pulmonary hypertension and pulmonary edema that frequently accompany lactated Ringer's resuscitation of acute pancreatitis.     

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.     

Small-volume hypertonic saline dextran resuscitation from canine endotoxin shock.

This study evaluated resuscitation of endotoxin shock with 7.5% hypertonic saline dextran (HSD 2400 mOsm) by measuring hemodynamic and regional blood flow responses. Endotoxin challenge (1 mg/kg) in adult dogs caused a significant decrease in mean arterial blood pressure (MABP), cardiac output (CO), left ventricular +/- dP/dt max, and regional blood flow (radioactive microspheres). Cardiocirculatory dysfunction and acid-base derangements persisted throughout the experimental period in untreated endotoxin shock (group 1, n = 10). In contrast both regimens of fluid resuscitation (group 2, n = 11: bolus of 4 mL/kg HSD followed by a constant infusion of lactated Ringer's [LR] to maintain MABP and CO at baseline values; group 3, n = 10; LR alone given as described for group 2) improved regional perfusion and corrected acid-base disturbances similarly in all dogs. Hypertonic saline dextran enhanced all indices of cardiac contraction and relaxation more than LR alone. The total volume of LR required to maintain MABP and CO at baseline values was less in the HSD group (59.2 +/- 6.8 mL/kg) than in the LR alone group (158 +/- 16 mL/kg, p = 0.01). The net fluid gain (infused volume minus urine output and normalized for kilogram body weight) was five times greater in the LR (24.8 +/- 6.2 mL/kg) than in the HSD group (4.6 +/- 1.2 mL/kg, p = 0.01). Lung water was similar in all dogs, regardless of the regimen of fluid resuscitation. Hypertonic saline dextran effectively resuscitates endotoxin shock in this canine model.     

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     

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。     

A pilot study on early versus delayed hypertonic saline dextran resuscitation in a porcine model of near-lethal liver injury: early hemodynamic response and short-term survival

BACKGROUND: We studied the effects of early versus delayed fluid resuscitation on hemodynamic response and short-term survival in a porcine model of severe hepatic injury associated with hemorrhagic shock. MATERIALS AND METHODS: Eighteen anesthetized swine were randomized after standardized liver injury into two groups: early resuscitation (ER, n = 9) and delayed resuscitation (DR, n = 9). The ER and DR groups were resuscitated with hypertonic saline dextran (HSD) 20 min and 40 min after the injury, respectively. Mean arterial pressure (MAP), cardiac output (CO), and arterial blood gases were measured in addition to vascular blood flow rates in the aorta, hepatic artery and portal vein. The duration of follow-up was 100 min. RESULTS: MAP decreased from 112 +/- 4 to 23 +/- 2 mmHg (P < 0.05) during 20 min after the injury. Bolus infusion of HSD significantly elevated MAP, CO, and flow rates in the aorta, portal vein and common hepatic artery in both groups. Portal vein flow remained relatively high during the shock. Intra-abdominal bleeding (ER, 701 +/- 42 mL; DR 757 +/- 78 mL) and the mortality rate (ER 44%; DR 33%) did not differ between the groups 100 min after injury (P > 0.05). Aortic flow, portal vein flow, common hepatic artery flow, MAP, CO, PaO(2), PaCO(2), base deficit, pH, hemoglobin measurements, and the volume of blood shed into the intraperitoneal cavity did not affect survival in the Cox regression analysis. CONCLUSIONS: Early versus delayed fluid infusion with HSD resulted in a comparable hemodynamic response and survival 100 min after injury. No rebleeding was observed.     

Hypertonic saline dextran resuscitation fails to improve cardiac function in neonatal and senescent burned guinea pigs.

Our previous studies suggested that the greater diminution in burn-induced cardiac contractile function which occurs in young and elderly subjects compared with adult subjects is related to differences in intracellular calcium availability to the myofilaments. We recently showed that improved cardiac function after hypertonic saline dextran (HSD) resuscitation from burn injury in adults was related to enhanced intracellular calcium content. In the study presented here, 126 hearts isolated from neonatal, adult, and senescent guinea pigs were used to evaluate age-related differences in cardiac contractile response to HSD resuscitation from burn injury. Scald burn was induced in 30 adult, 18 neonatal, and 30 senescent guinea pigs; within each age group, half of the burned animals were resuscitated with lactated Ringer's (Parkland formula, 4 mL/kg/% burn for 24 hours); half received an initial bolus of HSD (4 mL/kg, IV) plus lactated Ringer's (1 mL/kg/% burn for 24 hours). An additional 16 animals from each age group served as sham burn controls.(ABSTRACT TRUNCATED AT 250 WORDS)     

Burn resuscitation with two doses of 4 mL/kg hypertonic saline dextran provides sustained fluid sparing: a 48-hour prospective study in conscious sheep

BACKGROUND: The large fluid volumes usually required for burn resuscitation can be suppressed for 8 to 12 hours by intravenous infusion of 4 mL x kg(-1) hypertonic saline dextran (HSD) 1 hour after burn. We hypothesized that a double (8 mL x kg(-1)) dose of HSD or two repeated doses of 4 mL x kg(-1) could enhance or prolong the volume sparing. METHODS: We produced a full-thickness flame burn covering 40% of the body surface on 18 anesthetized sheep. One hour after the burn, the animals were awake and resuscitated with either (1) lactated Ringer's solution (LR) only, (2) 8 mL x kg(-1) HSD followed by LR, or (3) 4 mL x kg(-1) HSD followed by LR, with a second dose of 4 mL x kg(-1) HSD administered when net fluid accumulation increased to 20 mL x kg(-1). For all regimens, infusion rates were adjusted to produce a urine output of 1 to 2 mL x kg(-1) x h(-1). RESULTS: Animals resuscitated with only LR required fluid volumes identical to that predicted by the Parkland formula for the first 12 hours. Infusion of 8 mL x kg(-1) HSD initially created a net fluid loss (urine output > infused volume), followed by a rebound fluid requirement eventually equaling that of animals treated with LR only. Animals treated with two separate doses of 4 mL x kg(-1) HSD generally did not experience a net fluid loss or a rebound fluid requirement. Also in the HSD x 2 group, peak and net fluid accumulation was less than that of the other two groups from 18 hours through 48 hours, although the difference was not significant. CONCLUSION: An initial 4 mL x kg(-1) dose of HSD reduces fluid requirements early after burn, and a second dose administered after an appropriate interval may prolong volume sparing through 48 hours. An 8 mL x kg(-1) continuously infused initial dose was without prolonged fluid sparing effect. The volume-sparing effect of HSD is thus dependent on all of the following: dose, dosing interval, and infusion rate.     

Hypertonic saline dextran resuscitation of thermal injury.

Burn treatment requires large volumes of crystalloid, which may exacerbate burn-induced cardiopulmonary dysfunction. Small-volume hypertonic saline dextran (HSD) resuscitation has been used for effective treatment of several types of shock. In this study isolated coronary perfused guinea pig hearts were used to determine if HSD improved left ventricular contractile response to burn injuries. Parameters measured included left ventricular pressure (LVP) and maximal rate of LVP rise (+dP/dt max) and fall (-dP/dt max) at a constant preload. Third-degree scald burns comprising 45% of total body surface area (burn groups, N = 75), or 0% for controls (group 1, N = 25) were produced using a template device. In group 2, 25 burned guinea pigs were not fluid resuscitated and served as untreated burns; 20 burns were resuscitated with 4 mL lactated Ringer's (LR) solution/kg/% burn for 24 hours (group 3); additional burn groups were treated with an initial bolus of HSD (4 mL/kg, 2400 mOsm, sodium chloride, 6% dextran 70) followed by either 1, 2, or 4 mL LR/kg/% burn over 24 hours (groups 4, 5, and 6, respectively). Untreated burn injury significantly impaired cardiac function, as indicated by a fall in LVP (from 88 +/- 3 to 68 +/- 4 mmHg; p = 0.01) and +/- dP/dt max (from 1352 +/- 50 to 1261 +/- 90 and from 1150 +/- 35 to 993 +/- 59; p = 0.01, respectively) and a downward shift of LV function curves from those obtained from control hearts. Compared to untreated burns, hearts from burned animals treated with LR alone showed no significant improvement in cardiac function. However hearts from burned animals treated with HSD + 1 mL LR/kg/% burn had significantly higher LVP (79 +/- 4 vs. 68 +/- 4 mmHg, p = 0.01) and +/- dP/dt max (+dP/dt: 1387 +/- 60 vs. 1261 +/- 90 mmHg/sc, p = 0.01; -dP/dt: 1079 +/- 50 vs. 993 +/- 59 mmHg/sc, p = 0.01) than hearts from untreated burned animals and generated left ventricular function curves comparable to those calculated for hearts from control animals. Mortality 24 hours after burn was 29% for untreated burns was 0% for control animals, as well as for groups treated with the Parkland formula or HSD plus 1 or 2 mL/kg/% burn lactated Ringer's. The only deaths after treatment occurred in those animals given HSD plus 4 mL/kg/% burn, Parkland formula (17% mortality).(ABSTRACT TRUNCATED AT 400 WORDS)     

Small-volume resuscitation with hypertonic saline dextran solution

Small-volume hypertonic resuscitation has been proposed as an effective means for restoration of cardiovascular function after hemorrhage at the scene of an accident. We evaluated the cardiovascular, metabolic, and neurohumoral response of resuscitation after hemorrhage using 200 ml of 2400 mosm sodium chloride, 6% dextran 70. Unanesthetized adult sheep were bled to maintain mean arterial pressure at 50 mm Hg for 3 hours, shed blood volume = 42 +/- 7 ml/kg. The sheep were then treated with a single bolus infusion of hypertonic saline dextran (n = 7) or normal saline solution (control group, n = 7) and then observed for a 30-minute period of simulated patient transport during which no additional fluid was given. Hypertonic saline dextran caused rapid restoration of blood pressure and cardiac output within 2 minutes of infusion. Cardiac output remained at or above baseline level, while both O2 consumption and urine output increased to above baseline level during the 30 minutes of simulated patient transport. By comparison 200 ml of normal saline solution caused only a small increase in blood pressure and no improvement in cardiac output or oxygen consumption. After this 30-minute period, both groups were given lactated Ringer's solution as needed to return and maintain cardiac output at its baseline value. The volume of lactated Ringer's solution required to maintain cardiac output was less in the hypertonic group, 371 +/- 168 ml, only one sixth that of the control group, 2200 +/- 814 ml. In summary after 3 hours of hypovolemia, a small volume of hypertonic saline dextran, about 4 ml/kg, fully restored cardiovascular and metabolic function for at least 30 minutes and significantly lowered the total volume requirements of resuscitation.     

Blood loss after fluid resuscitation with isotonic or hypertonic saline for the initial treatment of uncontrolled hemorrhage induced by spleen rupture

BACKGROUND: It has been suggested that fluid resuscitation for the prehospital management of hypotensive trauma victims increases bleeding. In a model of uncontrolled hemorrhage induced by complete splenic laceration with a hilar vascular injury, we hypothesized that small-volume hypertonic saline or large-volume lactated Ringer's solution may provide sustained hemodynamic benefits despite promoting increases in intra-abdominal bleeding. METHODS: Forty anesthetized, spontaneously breathing dogs (18 +/- 1 kg) underwent laparotomy. A suture line was placed around the spleen to produce a splenic rupture with hilar vascular injury by pulling the exteriorized lines after incision closure. Intra-abdominal blood loss was measured directly, immediately after the animal was killed. Dogs were randomly assigned to four groups (n = 10 per group): Untreated controls were killed 20 (CT20) or 40 (CT40) minutes after splenic rupture to measure blood loss directly. Treatment groups received (20 minutes after spleen rupture) lactated Ringer's (LR), 33 mL/kg over 15 minutes, or 7.5% NaCl/6% dextran 70 (HSD), 4 mL/kg over 4 minutes. Blood loss was measured 40 minutes after spleen rupture. RESULTS: Mean arterial pressure dropped from an average value of 103 +/- 3 mm Hg to 67 +/- 5 mm Hg during the first 20 minutes and was partially restored afterward in all groups, with no significant differences between them. No resuscitation was associated with low cardiac output, whereas HSD restored and LR overshot baseline cardiac output. Intra-abdominal blood loss was 30 +/- 4, 38 +/- 4, 43 +/- 5, and 42 +/- 5 mL/kg for groups CT20, CT40, HSD, and LR, respectively, with no statistical significance between groups. CONCLUSION: No-fluid resuscitation in uncontrolled hemorrhage from splenic rupture resulted in a low-flow state, whereas resuscitation with small volumes of HSD or large volumes of LR produced hemodynamic benefits without significant increases in bleeding.     

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.     

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。     

A comparison of several hypertonic solutions for resuscitation of bled sheep

Small volumes (4 ml/kg) of 2400 mOsm NaCl restore cardiac output and mean arterial pressure to 80% of baseline after hemorrhage (65% of blood volume) in unanesthetized sheep. An equal volume of normal saline is less effective. To identify an optimal hypertonic solution, we screened six 2400 mOsm solutions in 18 randomized experiments in 8 sheep: NaCl, NaHCO3, NaCl/sodium acetate, NaCl/mannitol, NaCl/6% Dextran 70, and glucose. Cardiovascular function, as determined by cardiac output and mean arterial pressure, was restored best with NaCl, NaCl/NaAc, and NaCl/Dex. These three solutions were then evaluated using 18 sheep in 36 experiments. Following a 1-hr baseline period, the sheep were bled to a mean arterial pressure of 50 mm Hg for 2 hr. One of the solutions was then given in a volume of 4 ml/kg over 2 min and the sheep were monitored for 3 hr. Within 3 min of the infusion, cardiac output increased to greater than 100% of baseline for all three solutions. The NaCl-Dex solution sustained a significantly higher cardiac output over the 3-hr observation period than the other solutions. Plasma volume increased for all solutions following infusion. NaCl-Dex maintained plasma volume significantly better than the other solutions. As a further control, an isotonic solution of 6% Dextran 70 in normal saline was studied. It was not as effective as the hypertonic NaCl-Dex in maintaining cardiac output, mean arterial pressure, or plasma volume. Osmolality increased 10% (309 to 326 mOsm/kg H2O), plasma [NA] increased 7% (151 to 161 meq/liter), and plasma [K] decreased from 3.9 to 2.6 meq/liter following the hypertonic infusions. The sheep appeared to tolerate these electrolyte changes well. We conclude that a single bolus infusion of 2400 mOsm NaCl with 6% Dextran 70 best resuscitates sheep that have been subjected to a moderate degree of hemorrhagic shock compared to several other solutions. Its beneficial effects are caused in part by a sustained reestablishment of plasma volume. More studies are needed to document the safety of dextran in the clinical setting of hemorrhagic shock. Small volumes of hypertonic solutions may be valuable in the initial fluid resuscitation of patients in hemorrhagic shock.     

The dynamics of vascular volume and fluid shifts of lactated Ringer's solution and hypertonic-saline-dextran solutions infused in normovolemic sheep

Infusions of hyperosmotic-hyperoncotic solutions such as hypertonic saline dextran (HSD) are used in Europe for resuscitation of traumatic shock and perioperative volume support as an adjunct to conventional isotonic crystalloids. Whereas plasma volume expansion of HSD has been measured at single time points after the intravascular volume expansion, the detailed time course of fluid shifts during and after infusions have not been reported. We compared the time course of volume expansion during and after 30-min infusions of 4 mL/kg HSD and 25 mL/kg lactated Ringer's solution (LR) in normovolemic conscious splenectomized sheep. Peak plasma volume (Evans blue and hemoglobin dilution) expansion was similar for HSD (7.8 +/- 0.9 mL/kg) and the larger sixfold volume of LR (7.2 +/- 0.5 mL/kg). However, 30 min after the 30-min infusion (T60), plasma expansion remained larger after HSD (5.1 +/- 0.9 mL/kg) than after LR (1.7 +/- 0.6 mL/kg). Both solutions caused an equivalent diuresis. Intravascular volume expansion efficiency (VEE), defined as milliliter plasma expansion/milliliter fluid infused at 0 (T30), 30 (T60), and 60 (T90) min after infusion ended was 1.8, 1.3, and 0.8, respectively for HSD, whereas LR provided a VEE of only 0.27, 0.07, and 0.07. The relative expansion efficiency of HSD versus LR, calculated as the ratio (VEE(HSD)/VEE(LR)), was 7-fold that of LR at the end of infusion T30, and 20-fold at T60, but decreased to 9-fold by T120. Intravascular volume dynamic studies of different volume expanders in animals and patients may provide anesthesiologists with a new tool for monitoring the effectiveness of fluid therapy. IMPLICATIONS: Hypertonic saline dextran (HSD) is a new plasma expander recently approved for clinical use in Europe. We compared the plasma volume expansion of HSD versus lactated Ringers (LR) in normovolemic sheep. After a 30 min infusion, HSD was 7 times as effective at expanding volume as an equal volume of LR, but for the next 90 minutes the relative effectiveness of HSD increased to 10-20 times.     

Inhibition of CD18-dependent neutrophil adherence reduces organ injury after hemorrhagic shock in primates

Neutrophil adherence or aggregation may be important in the development of organ injury after hemorrhagic shock. Monoclonal antibody (MAb) 60.3 prevents both adherence and aggregation. Therefore we investigated MAb 60.3 treatment in prevention of organ injury after hemorrhagic shock in rhesus monkeys (Macaca mulatta). We performed esophagogastroscopy and placed catheters to measure cardiac output, mean arterial pressure, arterial blood gases, and urine output. Blood was removed to decrease CO to 30% of baseline for 90 minutes. Just before resuscitation, MAb 60.3 (2 mg/kg) or saline solution (control) was administered intravenously. Monitoring and fluid resuscitation continued for 24 hours, with lactated Ringer's solution given as a maintenance infusion (4 ml/kg/hr) plus additional lactated Ringer's solution to maintain CO at preshock levels. Esophagogastroscopy was repeated 24 hours after shock. There were two deaths in the control group at about 72 hours and none in the MAb 60.3 group. MAb 60.3-treated animals required less fluid (9.6 +/- 8.8 ml/kg vs 263.8 +/- 225.7 ml/kg), gained less weight (0.08 +/- 0.11 kg vs 0.70 +/- 0.37 kg), and maintained a higher hematocrit level (35.0% +/- 1.0% vs 26.9% +/- 4.9%). All five control animals had gastritis; MAb 60.3-treated animals had none (p less than 0.05; Fisher's exact test). Inhibition of neutrophil adherence or aggregation with MAb 60.3 at the time of resuscitation reduces fluid requirements and gastric injury in monkeys after hemorrhagic shock.