Pulmonary oedema in isolated lung lobe after inhalation injury

Pulmonary oedema was produced in isolated lung lobes with steam and provided direct continuous measurements of transudation as it occurred. Transvascular flux (Q_f) and weight gain (G_w) of the lobe increased immediately and the transudation reached its peak within half an hour after inhalation injury. Studies of protein content, colloid osmotic pressure of bronchial exudate and water content of lung, reconfirmed the increase in pulmonary capillary permeability. Marked haemoconcentration was revealed. Plasma leaked 113g (25 per cent), plasma protein leaked 1.96g (9.7 per cent) during the experiment. Based on the measured arterial pressure (P_a), vein pressure (P_v), arterial occlusion (P_ao), venous occlusion (P_vo), double occlusion (P_do) and blood flow through the lobe (Q_t), the total vascular (R_t), arterial (R_a), middle compartment (R_mid) and venous (R_v) resistances were calculated. All the resistances were increased and the Q_t showed a decrease after inhalation injury.     

A comparison of effects of thermal injury and smoke inhalation on bacterial translocation

Thermal injury as well as smoke inhalation injury results in serious morbidity and high mortality. In a chronic ovine model, we studied the development of bacterial translocation to the mesenteric lymph node, liver, spleen, kidney, and lung following: 1) sham injury (N = 6), 2) cutaneous thermal injury (N = 5), 3) cotton smoke inhalation injury (N = 4), 4) combined thermal injury and smoke inhalation injury (N = 7). Cardiac output, mean arterial pressure, and plasma protein concentration were maintained within 10% of preinjury values. Urine output was maintained above 1 ml/kg/hour with fluid and plasma resuscitation. A wide-beam ultrasonic flow probe was chronically implanted to allow serial measurement of cephalic mesenteric arterial blood flow throughout the 48-hour experimental period. Sheep were sacrificed 48 hours following injury for quantitative organ culture of mesenteric lymph node, liver, spleen, kidney, and lung. Measurements of mesenteric blood flow demonstrated a decrease to 48 +/- 8%, 80 +/- 5%, and 64 +/- 9% of preinjury levels in sheep receiving thermal injury, smoke inhalation injury, and combination injury, respectively. The sham animals maintained mesenteric blood flow at 102 +/- 7% of control levels. Thermal injury, as well as combination thermal and smoke inhalation injury, resulted in higher levels of translocation than smoke inhalation injury alone.     

重度蒸汽吸入性损伤后组织氧合的变化

采用蒸汽吸入造成实验犬急性肺损伤，探讨伤后心输出量（ＣＯ）、氧供量（ＤＯ_２）、氧耗量（ＶＯ_２）、氧摄取率（ＥＲＯ_２）、动脉和混合静脉血氧分压（ＰａＯ_２和ＰｖＯ_２）、动脉和混合静脉血氧饱和度（ＳａＯ_２和ＳｖＯ_２）、肺泡氧分压（Ｐ_ＡＯ_２）以及肺泡－动脉氧分压差（Ｐ_（Ａ－ａ）Ｏ_２）等变化。结果表明，蒸汽吸入４ｈ内，ＣＯ、Ｄ０_２、ＰａＯ_２、ＰｖＯ_２、ＳａＯ_２、ＳｖＯ_２、ＰＡＯ_２和ｐＨ值均显著下降（Ｐ＜０．０１）、Ｐ_（Ａ－ａ）Ｏ_２、ＥＲＯ_２和ＰａＣＯ_２均显著升高（Ｐ＜０．０１和０．０５），ＶＯ_２则无显著变化。提示，蒸汽吸入性损伤后２～４ｈ即可出现组织缺氧，其直接原因是组织灌注和供氧不足。     

Hemodynamic sequelae of combined arteriovenous injury in an experimental canine hindlimb model: Venous ligation vs. repair

The hemodynamic effects of combined venoarterial injury and stasis were studied in the hindlimbs of 10 dogs. Femoral arterial blood flow and pressure, peripheral venous pressure, and peripheral resistance were measured after the restoration of blood flow following venoarterial injury and a 4-hour period of occlusion for up to 72 hours. In one limb of each animal both the artery and vein were repaired, whereas only the artery was repaired in the other limb and the vein was ligated. Arterial blood flow was similar in both groups but was significantly diminished from baseline for the first 30 minutes after restoration of blood flow, but then it became significantly reduced in the limbs with venous ligation when compared with values in those with venous repair. By 72 hours the flow on both sides returned to control values. Peripheral venous hypertension and edema occurred in all 10 limbs with venous ligation and persisted for the 72-hour experimental period. In the 10 limbs with venous repair, edema occurred in four and venous hypertension in none. The peripheral resistance was elevated on both sides; this elevation persisted for 75 minutes and then dropped to control values. None of the repaired arteries and only one repaired vein thrombosed during the experiment. Combined venous and arterial occlusion for 4 hours reduced both the amount of arterial flow and its subsequent rate of increase compared with changes seen after release of an actue venous occlusion. The rate of increase was enhanced by repair of the affected venous segment compared with simple venous ligation.Supported by the William Beaumont Hospital Research Institute and Department of Surgery, RI-91-41RM.Presented at the Sixteenth Annual Meeting of the Midwestern Vascular Surgical Society, Cleveland, Ohio, September 11–12, 1992.     

Extravascular lung water changes following smoke inhalation and massive burn injury

During a 3-year period (1984 through 1987), 40 patients with smoke inhalation, cutaneous burns, or a combination of both injuries were studied. Injuries were assigned to the three categories on the basis of bronchoscopic findings and clinical history. Eleven patients had simultaneously sustained a common smoke-inhalation injury without burns while trapped in a burning ship; twelve patients had massive cutaneous burns over 50% of the total body surface area (TBSA); and seventeen patients had cutaneous burns over more than 30% of the TBSA and inhalation injury. Colloid oncotic pressure was maintained with salt-poor albumin infusion. Central venous pressure, arterial saturation, inspired oxygen, arterial pressure, and urine output were continuously monitored. Extravascular lung water (EVLW) and cardiac output were measured by the double indicator (thermal dye dilution) technique. EVLW remained normal throughout the study period in the group of patients with burns alone. In the first 24 hours after injury, EVLW increased in both groups with smoke injury and remained elevated for more than 48 hours after injury in patients with smoke injury only. The group with both smoke-inhalation and burn injuries showed an early increase in EVLW, which returned to normal by 28 hours after injury and which remained normal until 5 days after injury. The EVLW level then increased again until the end of the study period. In this study, lung edema formation is attributed to the toxic effect of smoke inhalation.     

Reduction of resuscitation fluid volumes in severely burned patients using ascorbic acid administration: a randomized, prospective study

HYPOTHESIS: High-dose ascorbic acid (vitamin C) therapy (66 mg/kg per hour) attenuates postburn lipid peroxidation, resuscitation fluid volume requirements, and edema generation in severely burned patients. STUDY DESIGN AND SETTING: A prospective, randomized study at a university trauma and critical care center in Japan. SUBJECTS AND METHODS: Thirty-seven patients with burns over more than 30% of their total body surface area (TBSA) hospitalized within 2 hours after injury were randomly divided into ascorbic acid and control groups. Fluid resuscitation was performed using Ringer lactate solution to maintain stable hemodynamic measurements and adequate urine output (0.5-1.0 ml/kg per hour). In the ascorbic acid group (n = 19; mean burn size, 63% +/- 26% TBSA; mean burn index, 57 +/- 26; inhalation injury, 15/ 19), ascorbic acid was infused during the initial 24-hour study period. In the control group (n = 18; mean burn size, 53% +/- 17% TBSA; mean burn index, 47 +/- 13; inhalation injury, 12/18), no ascorbic acid was infused. We compared hemodynamic and respiratory measurements, lipid peroxidation, and fluid balance for 96 hours after injury. Two-way analysis of variance and Tukey test were used to analyze the data. RESULTS: Heart rate, mean arterial pressure, central venous pressure, arterial pH, base deficit, and urine outputs were equivalent in both groups. The 24-hour total fluid infusion volumes in the control and ascorbic acid groups were 5.5 +/- 3.1 and 3.0 +/- 1.7 mL/kg per percentage of burn area, respectively (P<.01). In the first 24 hours, the ascorbic acid group gained 9.2% +/- 8.2% of pretreatment weight; controls, 17.8% +/- 6.9%. Burned tissue water content was 6.1 +/- 1.8 vs 2.6 +/- 1.7 mL/g of dry weight in the control and ascorbic acid groups, respectively (P<.01). Fluid retention in the second 24 hours was also significantly reduced in the ascorbic acid group. In the control group, the ratio of PaO2 to fraction of inspired oxygen at 18, 24, 36, 48, and 72 hours after injury was less than that of the ascorbic acid group (P<.01). The length of mechanical ventilation in the control and ascorbic acid groups was 21.3 +/- 15.6 and 12.1 +/- 8.8 days, respectively (P<.05). Serum malondialdehyde levels were lower in the ascorbic acid group at 18, 24, and 36 hours after injury (P<.05). CONCLUSIONS: Adjuvant administration of high-dose ascorbic acid during the first 24 hours after thermal injury significantly reduces resuscitation fluid volume requirements, body weight gain, and wound edema. A reduction in the severity of respiratory dysfunction was also apparent in these patients.     

高渗氯化钠羟乙基淀粉注射液输注对急性颅内高压伴失血性休克犬脑组织病理学及氧自由基的影响

目的 观察高渗氯化钠羟乙基淀粉40注射液(HSH)在犬急性颅内高压伴失血性休克模型中恢复循环血容量、减轻脑组织水肿和降低脑组织氧自由基含量的作用.方法 健康杂种犬20只,采用硬膜外球囊注水和动脉放血的方法复制急性颅内高压伴失血性休克模型.动物随机分为羟乙基淀粉溶液组(HES组),乳酸盐林格液组(RL组),7.5%氯化钠溶液组(HS组)和高渗氯化钠羟乙基淀粉40注射液组(HSH组),在休克后1 h分别输入相应液体.监测平均动脉压(MAP)、中心静脉压(CVP)、心率(HR)、颅内压(ICP),检测脑组织丙二醛(MDA)含量、超氧化物歧化酶(SOD)活力,脑组织标本行病理学检查.结果 复苏后4组液体均能有效地升高MAP(P<0.05),但HES组和RL组的ICP上升明显(P<0.05),复苏后2 h,HS组的MAP开始下降(P<0.05).至复苏后4 h,仅HSH组能维持理想的MAP及较低的ICP,HSH组脑组织氧自由基含量较其他组明显减少(P<0.05).病理学检查显示复苏后4 h,HSH组的脑组织损伤较其他组轻.结论 高渗氯化钠羟乙基淀粉40注射液可有效地复苏失血性休克,降低ICP及氧自由基的生成,减轻脑组织缺血/再灌注的损伤.     

液体复苏对严重脓毒症及脓毒性休克患者的治疗作用研究

目的评价液体复苏手段对严重脓毒症或脓毒性休克的治疗作用。方法通过液体复苏使20例严重脓毒症或脓毒性休克患者达到如下治疗目标：中心静脉压8—12mmHg（机械通气者12—15mmHg）、平均动脉压65～90mmHg、混合静脉血氧饱和度〉70％。测定达标前后血流动力学、组织灌注、血管内皮细胞功能的变化。结果液体复苏达标后,肺动脉楔压明显升高（P〈0．01）,心指数及体循环阻力指数增加（P〈0．01）,肺循环阻力指数下降（P〈0．01）,左心室做功指数上升（P〈0．01）;组织灌注指标中动脉血乳酸（ABL）在复苏后下降（P〈0．01）,胃黏膜二氧化碳分压与动脉血二氧化碳分压差（Pg—aCO2）在复苏后明显下降（P〈0．01）,血管内皮细胞功能中内皮素及血管性假血友病因子在液体复苏后下降（P〈0．05）。结论液体复苏早期达标可改善严重脓毒症或脓毒性休克患者血流动力学和组织灌注并可减轻血管内皮细胞的损伤,是一种有效的治疗方式。     

Measurement of extravascular lung water in sheep during colloid and crystalloid resuscitation from smoke inhalation

The pathophysiology of pulmonary inhalation injury, a major cause of morbidity and mortality from fires, is poorly understood. To examine the effects of colloid and crystalloid resuscitation on extravascular lung water (EVLW) during a standard smoke inhalation injury, we subjected 12 sheep to 8 minutes of cool pine smoke inhalation. The animals were then resuscitated to a pulmonary capillary wedge pressure (PCWP) of 10 +/- 1.5 mm Hg with either lactated Ringer's solution or plasma protein derivative. EVLW, cardiac output, vascular resistance, colloid oncotic pressure (COP), arterial and pulmonary artery pressures, PCWP, and blood gases were monitored during 4 hours of resuscitation. In colloid-treated animals, EVLW increased from 8.3 +/- 1.2 to 11.1 +/- 0.9 ml/kg with injury; it increased only to 12.5 +/- 1.3 ml/kg during resuscitation. In crystalloid-treated animals, EVLW increased from 8.0 +/- 1.0 to 10.3 +/- 0.8 ml/kg with injury and further increased to 17.4 +/- 1.6 ml/kg during resuscitation, a level significantly higher than that in the colloid group (P less than 0.05). The increases in EVLW were associated with progressive hypoxia, which was worse in the crystalloid group. In the crystalloid group, COP decreased from 27.3 +/- 0.9 to 14.2 +/- 0.4 mm Hg and intravascular driving force (COP-PCWP) dropped from 17.6 to 3.26 +/- 1.5 mm Hg; COP and COP-PCWP were maintained in the colloid group. These data demonstrate that supporting serum COP minimizes the increase in EVLW with smoke inhalation injury and suggests that smoke inhalation does not lead to a dramatic increase in alveolar capillary membrane permeability to protein.     

Traumatic shock and head injury: effects of fluid resuscitation on the brain

The effects of resuscitation of traumatic-hemorrhagic shock on the brain are unknown. Traumatic shock in sheep (fracture/crush injury, 2-hr hemorrhage to 40 mm Hg) was followed by resuscitation to baseline mean arterial pressure. Two groups without brain injury were resuscitated with lactated Ringer's (LR1, n = 7) or albumin (ALB1, n = 6). Focal brain injury was added in two further groups (LR2, n = 6; ALB2, n = 6). Hemodynamics, intracranial pressure (ICP), EEG, and colloid osmotic pressure (COP) were followed. Brain water (BW) and cerebral blood volume (CBV) were compared to those of controls (C, n = 7). Results: ICP rose in all groups. Animals without brain injury did not have increased brain water. Below are results for brain-injured animals after resuscitation (mean +/- SEM). (table; see text) Maintaining COP during initial resuscitation does not minimize cerebral edema: the effects of LR and ALB were similar in this setting. Focal brain injury causes edema but does not cause large increases in ICP with initial resuscitation.     

Thermal filament continuous thermodilution cardiac output delayed response limits its value during acute hemodynamic instability.

BACKGROUND: It has been suggested that measurement of continuous cardiac output (CCO) is an advancement in the management of critically ill patients. Our objective was to determine the accuracy of CCO during the rapid hemodynamic changes induced by hemorrhage and resuscitation. METHODS: In 12 anesthetized dogs (20.2+/-0.9 kg), pulmonary artery blood flow, our "gold standard" cardiac output, was measured with an sonographic flowprobe, whereas CCO, intermittent bolus cardiac output (ICO), and mixed venous oxygen saturation were measured with a thermodilution fiberoptic pulmonary artery catheter with a thermal filament. A graded hemorrhage (20 mL/min) was produced to a mean arterial pressure of 40 mm Hg, which was maintained at this level for 30 minutes. Total shed blood volume (701+/-53 mL) was retransfused at a rate of 40 mL/min, over 30 minutes, after which a massive hemorrhage (100 mL/min) was produced over 10 minutes. RESULTS: Hemorrhage induced significant decreases in mean arterial pressure, mixed venous oxygen saturation, and oxygen delivery, which were all restored during early resuscitation. However, CCO showed a delayed response after hemorrhage and resuscitation, compared with pulmonary blood flow, throughout the study (r = 0.549), matching only at baseline and at the end of both graded hemorrhage and resuscitation periods. There was a good correlation between ICO and pulmonary artery blood flow (r = 0.964) and no significant differences between them throughout the study. CONCLUSION: CCO has a delayed response during acute hemodynamic changes induced by hemorrhage and resuscitation. When sudden changes in mean arterial pressure or in mixed venous oxygen saturation are detected, cardiac output must be estimated by the standard bolus thermodilution technique, not by CCO.     

Intracranial venous hypertension and the effects of venous outflow obstruction in a rat model of arteriovenous fistula

A model of rat arteriovenous fistula (AVF) was created using a proximal common carotid artery to distal external jugular vein anastomosis. Anatomical dissections revealed that the external jugular vein is the primary vessel draining intracranial venous blood. Physiological measurements were made with the AVF open and closed, and during venous outflow occlusion of the contralateral external jugular vein. Opening the AVF increased torcular pressure from 6.5 +/- 0.6 to 13.5 +/- 1.1 mm Hg and decreased mean arterial pressure from 82.7 +/- 1.8 to 62.8 +/- 1.8 mm Hg (both P less than .05), decreasing cerebral perfusion pressure from 76.2 +/- 1.7 to 49.3 +/- 2.2 mm Hg (P less than .05). Middle cerebral artery blood flow velocity (MCA BFV) decreased from 6.8 +/- 1.1 to 4.2 +/- 0.7 cm/s (P less than 0.05). In rats with an AVF, occlusion of venous outflow increased torcular pressure to 34.8 +/- 3.1 mm Hg (P less than 0.05), MCA BFV decreased to 1.8 +/- 0.5 cm/s (P less than 0.05), and severe ischemic changes were seen on the electroencephalogram. Under this condition, torcular pressure and systemic arterial pressure had a positive linear relationship (P less than 0.05), whereas in control rats torcular pressure and arterial pressure had no relationship. Restoration of cerebral perfusion pressure by release of venous outflow occlusion and AVF closure transiently increased MCA BFV to 69% above baseline (P less than 0.05). Histological examination 1 week after permanent venous outflow occlusion revealed venous infarction, subarachnoid hemorrhage, and severe brain edema in rats with an AVF but not in control rats without an AVF. This model of cerebrovascular steal with venous hypertension reproduces both hemodynamic and hemorrhagic complications of human AVF and emphasizes the importance of venous outflow obstruction and venous hypertension in the pathophysiology of these lesions.     

Positive end-expiratory pressure accelerates lung water accumulation in high surface tension edema

The effect of positive end expiratory pressure (PEEP) on the rate of lung water accumulation with high surface tension pulmonary edema was examined. Alveolar surface tension was elevated by inhalation of 15 mg/kg of the aerosolized detergent dioctyl sodium sulfosuccinate (OT). Hemodynamic measurements, blood gases, and colloid oncotic pressures were recorded in anesthesized dogs for 2 hours after surfactant displacement and elevation of PEEP to 10 cm H2O pressure (group II; n = 10). These data were compared with those of an identical protocol that used only 5 cm H2O PEEP (group I; n = 10). Pulmonary extravascular water volume (PEWV) was measured gravimetrically at the end of the experiment. OT inhalation resulted in an immediate fall in Pao2 and rise in venous admixture (QVa/QT), with little change in colloid oncotic pressure or left atrial pressure. In group I, Pao2 and QVa/QT did not improve significantly over 2 hours, whereas both returned to near baseline in group II. PEWV was elevated in group I compared with normal PEWV (historic controls; n = 11) (6.1 +/- 0.07 - 3.6 +/- 0.01 ml/gm dry lung; p less than 0.01); however, PEWV in group II (9.1 +/- 1.0 ml/gm dry lung; p less than 0.01) was greater than in both group I and historic controls. These data indicate that high alveolar surface tension induces pulmonary edema and PEEP accelerates this edema formation.     

Oxothiazolidine Carboxylate Provides Protection against Hepatocellular Injury Seen after Porta <Emphasis Type="Bold">Hepatis Occlusion (Pringle Maneuver) under Hypovolemic Conditions</Emphasis>

Abstract The sensitivity of liver to warm ischemia has always been a concern for surgeons. To monitor the ischemia and/or reperfusion injury after the Pringle maneuver (occlusion of porta hepatis) in livers subjected to hemorrhage, blood pressure, blood pH, base deficit (BE), serum alanine aminotransferase (ALT), serum and liver malondialdehyde (MDA), and liver glutathione (GSH) levels were measured. MDA is a by-product of oxidant induced lipid peroxidation, and GSH is an endogenous antioxidant. The effect of lactated Ringer’s (LR) resuscitation with or without the addition of 2-oxothiazolidine-4-carboxylate (OTC), a cysteine prodrug (enhancing glutathione production) on liver injury, if any, were investigated. Rats in the sham group (n = 8) and five other groups (n = 8) underwent femoral artery and vein catheterization and laparotomy. The hemorrhage group was bled 30% of their blood volume and the ischemia group underwent occlusion of the porta hepatis 30 minutes. The hemorrhage-ischemia (HI), LR, and OTC groups underwent both hemorrhage and occlusion. The LR and OTC groups, 30 minutes after hemorrhage, received either LR resuscitation (equivalent to three times the shed blood) or LR resuscitation plus IV OTC (100 mg/kg before clamping and 100 mg/kg after de-clamping). Porta hepatis occlusion in the presence of hypovolemia (HI group) caused an increase in serum ALT, plasma MDA, liver MDA, and base deficit and a decrease in blood pH levels. LR resuscitation lowered only MDA (plasma and liver) and base deficit but did not reduce ALT and increase blood pH. Although liver GSH did not change, OTC kept all parameters at control levels. OTC prevents the deleterious effects of total hepatic inflow occlusion under hypovolemic conditions, but this does not occur through enhancement liver glutathione production. OTC may protect the liver by accelerating hepatic glutathione turnover, but further studies are needed to explain its mechanism of action.     

Hemodynamic Response of Modified Fluid Gelatin Compared with Lactated Ringer's Solution for Volume Expansion in Emergency Resuscitation of Hypovolemic Shock Patients: Preliminary Report of a Prospective, Randomized Trial

The objective of this study was to compare the cardiac and hemodynamic responses to a rapid infusion of 1000 ml of modified fluid gelatin (group A) or 1000 ml of lactated Ringer's solution (group B) in emergency room patients suffering from shock. This prospective, randomized, open, noncrossover study was performed at a medical center university hospital in a surgical resuscitation room in the emergency department. The subjects were 34 patients with either hypovolemic or neurogenic shock who were admitted to the emergency room. A resuscitation protocol according to Advanced Trauma Life Support (ATLS) with an additional central venous line or Swan-Ganz catheters for hemodynamic monitoring was used. Physical parameters and hemodynamic variables were measured at baseline and 15 minutes, 30 minutes, and 1 hour after the infusion of each fluid. In both groups the mean arterial blood pressure (MAP), systolic and diastolic pressure, central venous pressure (CVP), and pulmonary artery occlusion pressure (PAOP) increased significantly. The CVP and PAOP increased significantly more in the modified fluid gelatin resuscitation group. In patients with traumatic or neurogenic shock due to acute volume deficiency, there was significantly better hemodynamic improvement, judged by CVP and PAOP measurements using the modified fluid gelatin for volume replacement than with lactated Ringer's solution during the first hour of resuscitation.     

Effects of lobar pulmonary blood flow on the evolution of oleic acid lung injury in dogs

We studied the effects of interruption of the pulmonary blood flow to the left diaphragmatic lung lobe on the evolution of canine oleic acid lung injury. We compared the morphology and edema of the left diaphragmatic lobe, whose pulmonary artery was ligated immediately after oleic acid injury, with the right diaphragmatic lobe, in which the blood supply was intact. The injury plus ligation resulted in hypoxemia and pulmonary hypertension with PaO2 falling from 98 +/- 4 to 72 +/- 21 torr (P less than 0.05) and pulmonary artery pressure increasing from 11 +/- 3 to 18 +/- 4 mm Hg (P less than 0.05). Animals were sacrificed 48 hr following the injury. Morphological examination of right and left lobes showed no consistent differences although wet/dry ratios indicated significantly greater edema (P less than 0.01) for the right diaphragmatic lobes (7.66 +/- 1.23) than the left (6.80 +/- 0.59). Both right and left lobes were substantially more edematous than our laboratory normal value of 4.74 +/- 0.54 (P less than 0.001 for both). We conclude that interruption of pulmonary arterial blood flow protects against edema formation in oleic acid injury but does not alter the morphologic evolution of the injury.     

Experimental study on lung injury following severe burn. Early changes in function and hemodynamics and morphologic changes in the lung of dogs with burns

This study investigated the pulmonary and hemodynamic dysfunction and morphologic changes after major burns. Full-thickness burns, 40% TBSA were produced in 9 dogs. Respiratory Rate (RR), airway resistance (Raw), effective compliance (Ec), lung impedance Zo (LIZo), pulmonary arterial pressure (PAP), pulmonary arterial wedge pressure (PAWP), blood gas monitoring, light and electron microscopic studies were performed. Following burns, RR, Raw, PAP and PAWP increased and Ec, LIZo, RaCO2 and PaO2 decreased significantly while morphologic evidence of endothelial and interstitial edema was associated with significant cellular infiltration of lung tissue, especially by leukocytes, showing evidence of degranulation. This results shown that a 40% TBSA burn without inhalation injury can produce lung injury similarly to adult respiratory distress syndrome. This lung injury is characterized by increasing pulmonary capillary permeability. Ec and LIZo monitoring may help to early diagnose of lung injury after major burns.     

Hemodynamic and metabolic effects of resuscitation in an uncontrolled hemorrhage model of severe rat liver injury

Purpose: The benefits of fluid resuscitation have become controversial for noncompressible uncontrolled hemorrhage. The effect of delayed access to definitive care is an additional confounding variable. Rural and military environments often entail delayed access to surgical care, and current recommendations are for ongoing fluid resuscitation to a normal blood pressure during transport. This approach has been proposed to increase survival time, at the expense of increased blood loss. This study was designed to evaluate the hemodynamic and metabolic response to resuscitation in a rat model of severe liver injury and uncontrolled hemorrhage over 4 hours.MethodsAll animals (N = 21, 275 ± 15 g), underwent a reproducible excision of the median hepatic lobe. The animals received either no resuscitation (NR) or 40°C lactated Ringer’s solution at 1 ml/min, starting at 2.5 minutes after the injury (LR). The end point of resuscitation was a return to the immediate preinjury mean arterial pressure (MAP). Total blood loss, MAP, survival time, fluid volume infused, serum lactate, arterial blood gasses, intra-abdominal pressure, and hematocrit were measured preinjury and at 4 hours or death.ResultsBlood loss was greater (p < 0.01) in the LR group (37.8 ± 13.5 ml/kg) than in the NR group (15.9 ± 5.9). Final Pao₂ was lower (p < 0.01) in the LR group (55.0 ± 21.5 mm Hg) than in the NR group (92.2 ± 17). No differences were noted between groups in the amount of hepatic median lobe excised (60% ± 7%), overall survival time (86.3 ± 66.0 min), MAP nadir (35.2 ± 0.7 mm Hg at 1.9 ± 0.7 min postinjury), final pH (7.04 ± 0.14), final base excess (−16.5 ± 4.5 mmol/l), final intra-abdominal pressure (2.2 ± 1.4 mm Hg), and final serum lactate (6.8 ± 4.0 mmol/l).ConclusionsIn this model of uncontrolled hemorrhage from a solid organ, fluid resuscitation provided no survival or metabolic advantage, serving only to increase blood loss and decrease Pao₂. Vigorous resuscitation may not provide benefit when significant injury and prolonged transport times are combined.     

Oxygen transport dynamics after resuscitation with a conjugated hemoglobin solution

HYPOTHESIS: Pyridoxalated hemoglobin polyoxyethylene conjugate (PHP), a hemoglobin-based oxygen carrier, is effective in restoring hemodynamic balance and oxygen delivery after moderate hemorrhage but may be less effective in off-loading oxygen at the tissue level. DESIGN: Before-after trial. SETTING: Animal research laboratory of an academic institution. PARTICIPANTS: Ten female Yorkshire swine. INTERVENTIONS: Anesthetized swine underwent a 25% controlled hemorrhage followed by resuscitation with crystalloid plus either shed blood or PHP. Hemodynamic parameters, including heart rate, mean arterial pressure, mean pulmonary arterial pressure, and cardiac index were continuously monitored. Arterial and mixed venous blood samples were collected at baseline, after hemorrhage, after resuscitation, and every 15 minutes for 90 minutes after resuscitation. Oxygen delivery and consumption, oxygen extraction ratios, and percentage of contribution to oxygen delivery and consumption were determined in whole blood, red blood cells, and plasma by using a compartmentalized approach. MAIN OUTCOME MEASURES: Intergroup and intragroup comparisons were performed for hemodynamic parameters and oxygen transport dynamics. RESULTS: Heart rate returned closer to baseline levels in the PHP group (P<.05) and mean pulmonary arterial pressure was transiently elevated after infusion of PHP (P =.028), but otherwise no significant differences in hemodynamic balance were observed. The extraction ratio from the red blood cells in the PHP group more than doubled, whereas the extraction ratio from plasma remained constant. The percentage of contribution of plasma, including PHP, to oxygen delivery exceeded 20% (P <.05), but the relative contribution to oxygen consumption did not markedly change from baseline. CONCLUSIONS: Pyridoxalated hemoglobin polyoxyethylene conjugate is at least as effective as shed blood in restoring hemodynamic balance and oxygen delivery after moderate hemorrhage. There is a disproportionately low contribution from plasma to oxygen consumption, which suggests that PHP may act as an oxygen sink in moderate anemia.     

Alpha1-acid-glycoprotein protects against trauma-hemorrhagic shock

BACKGROUND: Recent studies have shown that the acute phase protein alpha(1)-acid-glycoprotein (AAG) directly modifies endothelial cell responsiveness and is a crucial factor for maintaining endothelial barrier function. We hypothesized that the addition of AAG to the resuscitation fluid will prevent edema formation, increases circulating blood volume, and reduces tissue inflammation following soft tissue trauma and hemorrhagic shock. MATERIALS AND METHODS: Male Sprague-Dawley rats (338 +/- 28 g) underwent a 5-cm midline laparotomy (i.e., induction of soft tissue trauma) and were bled to and maintained at a mean arterial pressure of 35 mm Hg for 90 min. The rats were then resuscitated with four times the shed blood volume with Ringer's lactate containing 200 mg/kg AAG or the same amount of albumin. At 6 h after resuscitation, organ wet-to-dry weight ratios and circulating blood volume (Evans blue dilution) were determined. Neutrophil accumulation (myeloperoxidase activity, MPO) and tissue lipid peroxidation (thiobarbituric acid reactive substances) were also measured in the lungs, liver, and intestine. RESULTS: Administration of AAG during the resuscitation significantly increased circulating blood volume and reduced edema formation, neutrophil accumulation, and lipid peroxidation. Interestingly, concomitant plasma IL-6 levels increased while TNF-alpha levels were not significantly affected. CONCLUSIONS: Since addition of AAG to the resuscitation fluid increased circulating blood volume, reduced edema formation, and neutrophil accumulation following trauma and hemorrhagic shock, supplementation of this acute phase protein appears to be a potential adjunct to prevent capillary leakage in patients undergoing major traumatic injury.