摘要:

ObjectiveTo investigate whether pulmonary compliance and gas exchange will be sustained during ``total'' perfluorocarbon liquid ventilation followed by ``partial'' perfluorocarbon liquid ventilation when compared with gas ventilation in the setting of the acute respiratory distress syndrome (ARDS).Study DesignA prospective, controlled, laboratory study.SettingA university research laboratory.SubjectsTen sheep, weighing 12.7 to 25.0 kg.InterventionsLung injury was induced in ten young sheep, utilizing a right atrial injection of 0.07 mL/kg of oleic acid followed by saline pulmonary lavage. Bijugular venovenous extracorporeal life support access, a pulmonary artery catheter, and a carotid artery catheter were placed. When the alveolar-arterial O2gradient was more than equals 600 torr and PaO2less than equals 50 torr (less than equals 6.7 kPa) with an FIO2of 1.0, extracorporeal life support was instituted. For the first 30 mins on extracorporeal life support, all animals were ventilated with gas. Animals were then ventilated with equal tidal volumes of 15 mL/kg during gas ventilation (n equals 5) over the ensuing 2.5 hrs, or with total liquid ventilation for 1 hr, followed by partial liquid ventilation for 1.5 hrs (total/partial liquid ventilation, n equals 5).Measurements and Main ResultsAn increase in physiologic shunt (gas ventilation equals 69 plus minus 11%, total/partial liquid ventilation equals 71 plus minus 3%) and a decrease in static total pulmonary compliance measured at 20 mL/kg inflation volume (gas ventilation equals 0.48 plus minus 0.03 mL/cm H2O/kg, total/partial liquid ventilation equals 0.50 plus minus 0.17 mL/cm H2O/kg) were observed in both groups with induction of lung injury. Physiologic shunt was significantly reduced during total and partial liquid ventilation when compared with physiologic shunt observed in the gas ventilation animals (gas ventilation equals 93 plus minus 8%, total liquid ventilation equals 45 plus minus 11%, p less than .001; gas ventilation equals 95 plus minus 3%, partial liquid ventilation equals 61 plus minus 12%, p less than .001), while static compliance was significantly increased in the total, but not the partial liquid ventilated animals when compared with the gas ventilated group (gas ventilation equals 0.43 plus minus 0.03 mL/cm H2O/kg, total liquid ventilation equals 1.13 plus minus 0.18 mL/cm H2O/kg, p less than .001; gas ventilation equals 0.41 plus minus 0.02 mL/cm H2O/kg, partial liquid ventilation equals 0.47 plus minus 0.08, p equals .151). In addition, the extracorporeal life support flow rate required to maintain adequate oxygenation was significantly lower in the total/partial liquid ventilation group when compared with that of the gas ventilation group (gas ventilation equals 89 plus minus 7 mL/kg/min, total liquid ventilation equals 22 plus minus 10 mL/kg/min, p less than .001; gas ventilation equals 91 plus minus 12 mL/kg/min, partial liquid ventilation equals 41 plus minus 11 mL/kg/min, p less than .001). Lung biopsy light microscopy demonstrated a marked reduction in alveolar hemorrhage, lung fluid accumulation, and inflammatory infiltration in the total/partial liquid ventilation animals when compared with the gas ventilation animals.ConclusionsIn a model of severe ARDS, pulmonary gas exchange is improved during total followed by partial liquid ventilation. Pulmonary compliance is improved during total, but not during partial liquid ventilation. Total followed by partial liquid ventilation was associated with a reduction in alveolar hemorrhage, pulmonary edema, and lung inflammatory infiltration.(Crit Care Med 1996; 24:1001-1008)

ISSN:0090-3493    

出版商:OVID    

年代:1996

数据来源: OVID

摘要:

ObjectivesTo test the hypothesis that selective brain cooling could be performed in an infant model of cardiac arrest and resuscitation without changing core temperature and to study its acute effects on regional organ blood flow, cerebral metabolism, and systemic hemodynamics.DesignProspective, randomized, controlled study.SettingResearch laboratory at a university medical center.SubjectsFourteen healthy infant piglets, weighing 3.5 to 6.0 kg.InterventionsPiglets were anesthetized and mechanically ventilated, and had vascular catheters placed. Parietal cortex (superficial brain), caudate nucleus (deep brain), esophageal, and rectal temperatures were monitored. All animals underwent 6 mins of cardiac arrest induced by ventricular fibrillation, 6 mins of external cardiopulmonary resuscitation (CPR), defibrillation, and 2 hrs of reperfusion. Normal core temperature (rectal) was regulated in all animals. In seven control animals (group 1), brain temperature was not manipulated. In seven experimental animals (group 2), selective brain cooling was begun during CPR, using a cooling cap filled with minus 30 degrees C solution. Selective brain cooling was continued for 45 mins of reperfusion, after which passive rewarming was allowed. Regional blood flow (microspheres) and arterial and sagittal sinus blood gases were measured prearrest, during CPR, and at 10 mins, 45 mins, and 2 hrs of reperfusion.Measurements and Main ResultsRectal temperature did not change over time in either group. In group 1, brain temperature remained constant except for a decrease of 0.6 degrees C at 10 mins of reperfusion. In group 2, superficial and deep brain temperatures were lowered to 32.8 plus minus 0.7 (SEM) degree C and 34.9 plus minus 0.4 degrees C, respectively, by 15 mins of reperfusion. Superficial and deep brain temperatures were further lowered to 27.8 plus minus 0.8 degrees C and 31.1 plus minus 0.3 degrees C, respectively, at 45 mins of reperfusion. Both temperatures returned to baseline by 120 mins. Cerebral blood flow was not different between groups at any time point, although there was a trend for higher flow in group 2 at 10 mins of reperfusion (314% of baseline) compared with group 1 (230% of baseline). Cerebral oxygen uptake was lower in group 2 than in group 1 (69% vs. 44% of baseline, p equals .02) at 45 mins of reperfusion. During CPR, aortic diastolic pressure was lower in group 2 than in group 1 (27 plus minus 1 vs. 23 plus minus 1 mm Hg, p equals .007). Myocardial blood flow during CPR was also lower in group 2 (80 plus minus 7 vs. 43 plus minus 7 mL/min/100 g, p equals .002). Kidney and intestinal blood flows were reduced during CPR in both groups; however, group 2 animals also had lower intestinal flow vs. group 1 at 45 and 120 mins of reperfusion.ConclusionsSelective brain cooling by surface cooling can be achieved rapidly in an infant animal model of cardiac arrest and resuscitation without changing core temperature. Brain temperatures known to improve neurologic outcome can be achieved by this technique with minimal adverse effects. Because of its ease of application, selective brain cooling may prove to be an effective, inexpensive method of cerebral resuscitation during pediatric CPR.(Crit Care Med 1996; 24:1009-1017)

ISSN:0090-3493    

出版商:OVID    

年代:1996

数据来源: OVID

摘要:

ObjectiveTo investigate the acute effects of experimental fat embolism on splanchnic and peripheral perfusion and oxygenation in pigs.DesignRandomized, controlled trial.SettingAnimal laboratory.SubjectsEighteen domestic pigs, weighing 25 to 31 kg.InterventionsThe 18 pigs were randomized to either the fat embolism or control groups. Nine anesthetized and mechanically ventilated pigs were intracavally infused with a 10% allogeneic bone marrow suspension at a dose of 100 mg/kg over 5 mins (the fat embolism group); nine control pigs received normal saline in the same volume and speed (control group).Measurements and Main ResultsMean pulmonary arterial pressure, pulmonary vascular resistance, and pulmonary shunt increased, and PaO2decreased immediately after the bone marrow suspension infusion. In the fat embolism animals, oxygen delivery decreased, oxygen content difference widened, and total oxygen consumption remained high, indicating enhanced oxygen extraction. Further, superior mesenteric artery blood flow and mesenteric oxygen delivery decreased, while intramucosal pH in the small bowel was stable. Subcutaneous PO2decreased in both groups, whereas transcutaneous PO2decreased only in the animals receiving bone marrow suspension. Skin red cell flux showed no significant changes.ConclusionsThe present model of fat embolism results in significant impairment in systemic oxygenation. Despite this fact, the intestinal oxygenation remains unaffected probably due to sufficient compensatory mechanisms. Transcutaneous PO2measurements may provide a useful index for early detection of fat embolism.(Crit Care Med 1996; 24:1018-1024)

ISSN:0090-3493    

出版商:OVID    

年代:1996

数据来源: OVID

摘要:

ObjectiveTo evaluate the efficacy of treating sepsis-induced adult respiratory distress syndrome (ARDS) by instillation of exogenous surfactant in a porcine endotoxin model.DesignProspective trial.SettingLaboratory at a university medical center.SubjectsFifteen hybrid pigs, weighing 15 to 20 kg.InterventionsPigs were anesthetized and surgically prepared for hemodynamic and lung function measurements. Animals were randomized into three groups: a control group (group I; n equals 4) that received sham Escherichia coli lipopolysaccharide (endotoxin); an endotoxin group (group II; n equals 6) that received endotoxin (25 micro gram/kg); and an endotoxin plus surfactant (Infasurf, ONY, Amherst, NY) instillation group (group III; n equals 5) that received endotoxin (25 micro gram/kg) followed by surfactant (100 mg/kg) instillation; all groups were studied for 6 hrs after the start of endotoxin injection. At necropsy, lung water and surfactant function (Wilhelmy balance) were measured and the right middle lung lobe was fixed for histologic analysis. Surfactant function was expressed as the surface tension at the minimum trough area.Measurements and Main ResultsSurfactant treatment (group III) significantly (p less than .05) decreased venous admixture (group III equals 41.5 plus minus 9.1%; group II equals 61.6 plus minus 4.7%), PaCO2(group III equals 46.6 plus minus 1.3 torr [6.2 plus minus 0.2 kPa]; group II equals 54.4 plus minus 2.6 torr [7.25 plus minus 0.34 kPa]), and surface tension minimum (group III equals 8.8 plus minus 1.8 dyne/cm; group II equals 20.0 plus minus 2.0 dyne/cm), as compared with endotoxin without treatment (group II) 6 hrs after endotoxin infusion. However, surfactant instillation did not significantly improve PaO2(group III equals 62.8 plus minus 6.8 torr [8.4 plus minus 0.9 kPa]; group II equals 50.3 plus minus 3.7 torr [6.7 plus minus 0.49 kPa]) or reduce the amount of pulmonary edema (group III equals 7.1 plus minus 0.39 ratio; group II equals 6.8 plus minus 0.24 ratio) seen 6 hrs following endotoxin injection. Histologic analysis showed that endotoxin caused edema accumulation around airways and pulmonary vessels, and a large increase in the number of marginated leukocytes with or without surfactant treatment. Surfactant treatment significantly increased the total number of leukocytes in the pulmonary parenchyma.ConclusionsWe conclude that endotoxin caused lung injury typical of ARDS as demonstrated by pulmonary edema, an increase in PaCO2and a decrease in PaO sub 2, a decrease in static lung compliance, and inhibition of surfactant function. Exogenous surfactant treatment effected only moderate improvements in lung function (i.e., reduced venous admixture and restored surfactant function) in this sepsis-induced ARDS model.(Crit Care Med 1996; 24:1025-1033)

ISSN:0090-3493    

出版商:OVID    

年代:1996

数据来源: OVID

摘要:

ObjectiveTo test the hypothesis that the effects of intravenous injection of latex particles would demonstrate the contribution of phagocytosis by mononuclear phagocytes to the development of Escherichia coli-induced acute lung injury in neutropenic guinea pigs.DesignProspective, controlled, experimental study. Intravenously injected the latex particles into 41 guinea pigs to investigate the contribution of the phagocytosis in acute lung injury.SubjectsForty-one guinea pigs.InterventionsForty-one guinea pigs were divided into five experimental groups: a saline group (n equals 9); an endotoxin group (n equals 10) receiving 2 mg/kg of intravenous E. coli endotoxin; a latex group (n equals 7) receiving 2 times 109/kg of intravenous polystyrene latex (mean diameter 3.19 micro meter); an endotoxin plus latex group (n equals 8); and an E. coli group (n equals 7) receiving 2 times 109live E. coli/kg.Measurements and Main ResultsThe lung wet/dry ratio was increased in the live E. coli-treated guinea pigs (6.71 plus minus 0.16 [SEM], p less than .01) as compared with the saline control (5.40 plus minus 0.16), whereas the ratio was not increased in the endotoxin (5.52 plus minus 0.14) or latex (5.58 plus minus 0.20) groups. However, the lung wet/dry ratio was greater in the endotoxin plus latex group (6.11 plus minus 0.16, p less than .05) than in the saline control. The125I albumin lung tissue/plasma ratio was greater in the E. coli (2.00 plus minus 0.29, p less than .01) and endotoxin plus latex (0.84 plus minus 0.12, p less than .05) groups than in the saline group (0.18 plus minus 0.07), whereas no increases were observed in the endotoxin group (0.22 plus minus 0.10) and the latex (0.34 plus minus 0.13) group. More than 40% of the injected radiolabeled latex was observed to have accumulated in the reticuloendothelial system (liver and spleen), in both the saline control (40.1 plus minus 2.3%, n equals 4) and endotoxin (57.3 plus minus 6.8%, n equals 5) groups, with 2.6 plus minus 1.5% and 3.1 plus minus 1.7% in the lungs for the saline control and the endotoxin groups, respectively. The percent deposition of radiolabeled latex in the liver was greater in the endotoxin group (51.7 plus minus 3.8%, p less than .05) than in the saline group (37.6 plus minus 5.9%).ConclusionsThese findings suggest that, in neutropenic guinea pigs: a) the combination of endotoxin and latex particles induces acute lung injury; and b) the phagocytic properties of mononuclear phagocytes in the reticuloendothelial system augment endotoxin-induced pulmonary responses and may play a role in the development of live E. coli-induced acute lung injury.(Crit Care Med 1996; 24:1034-1040)

ISSN:0090-3493    

出版商:OVID    

年代:1996

数据来源: OVID

摘要:

ObjectiveTo investigate the mechanism by which activated leukocytes induce gastric mucosal lesions, we examined whether granulocyte elastase is involved in the formation of such lesions in a rat model of hemorrhagic shock.DesignProspective, randomized, controlled study.SettingResearch laboratory at a university medical center.SubjectsMale Wistar rats, weighing 220 to 280 g.InterventionsAnimals were subjected to hemorrhagic shock by phlebotomy. ONO-5046, a granulocyte elastase inhibitor (300 mg/kg ip), was administered 30 mins before or after phlebotomy. The effects of antithrombotic substances and tranexamic acid on hemorrhagic shock-induced gastric mucosal lesions also were examined. The effects of granulocyte elastase on the thrombomodulin activity and35S-glycosaminoglycan content of endothelial cells were examined, using cultured human umbilical vein endothelial cells.Measurements and Main ResultsThree hours after phlebotomy, linear gastric mucosal erosions were observed. Formation of these lesions, as evaluated by the total linear length, was attenuated significantly by posttreatment as well as pretreatment of animals with ONO-5046. Administration of antithrombin III and an inactive factor Xa derivative, a selective inhibitor of thrombin generation, significantly prevented gastric mucosal lesion formation, while tranexamic acid, an inhibitor of thrombolysis, significantly worsened lesion formation. When incubated with cultured endothelial cells, granulocyte elastase markedly decreased the endothelial thrombomodulin activity and glycosaminoglycan content. These effects of granulocyte elastase were significantly decreased by ONO-5046.ConclusionsThese observations strongly suggest that granulocyte elastase plays an important role in the pathogenesis of hemorrhagic shock-induced gastric mucosal lesions. Additionally, endothelial cell injury induced by granulocyte elastase may eventually lead to microthrombus formation, which in turn could be an important etiologic factor leading to ischemia in gastric mucosal lesion formation.(Crit Care Med 1996; 24:1041-1046)

ISSN:0090-3493    

出版商:OVID    

年代:1996

数据来源: OVID

摘要:

ObjectiveIn order to determine whether gabexate mesilate, a synthetic protease inhibitor with anticoagulant properties, is useful for the treatment of adult respiratory distress syndrome, we examined its effect on endotoxin-induced pulmonary vascular injury in rats.DesignProspective, randomized, controlled study.SettingResearch laboratory at a university medical center.SubjectsMale Wistar rats (180 to 220 g).InterventionsAnimals received intravenous infusions of endotoxin (5 mg/kg iv) or saline (control). Pulmonary vascular injury was assessed 6 hrs after administration of endotoxin in terms of the increase in vascular permeability. Rats received gabexate mesilate (10 mg/kg ip), heparin, antithrombin III, an inactive derivative of activated factor X (a selective inhibitor of thrombin generation), or N-[2-[4-(2,2-dimethyl-propionyloxy) phenyl-sulfonylamino] benzoyl] aminoacetic acid (ONO-5046) (a potent granulocyte elastase inhibitor) 30 mins before endotoxin administration. Leukocytopenia was induced by administration of methotrexate. The effects of gabexate mesilate on the function of activated neutrophils and the production of tumor necrosis factor-alpha (TNF-alpha) by endotoxin-stimulated monocytes were examined in vitro using neutrophils and monocytes prepared from healthy human volunteers.Measurements and Main ResultsPulmonary vascular permeability was determined by measuring the vascular leakage of intravenously administered125I-labeled bovine serum albumin. Intravenous administration of endotoxin significantly increased pulmonary vascular permeability. Gabexate mesilate significantly inhibited pulmonary vascular injury observed 6 hrs after the administration of endotoxin. Pulmonary vascular injury was not attenuated by the administration of heparin, heparin plus antithrombin III, or the inactive derivative of activated factor X, but pulmonary vascular injury was significantly attenuated in animals with methotrexate-induced leukocytopenia and in those animals treated with N-[2-[4-(2,2-dimethyl-propionyloxy) phenylsulfonylamino] benzoyl] aminoacetic acid. Gabexate mesilate in concentrations of 10minus4 to 10minus3 M inhibited the release of granulocyte elastase and leukocyte aggregation stimulated by N-formyl-methionyl-leucyl-phenylalanine and the opsonized zymosan-activated production of superoxide radical by neutrophils in vitro. Gabexate mesilate significantly inhibited the endotoxin-induced increase in the serum concentration of TNF-alpha in vivo and, at a concentration of 10minus8 M, the production of TNF-alpha by endotoxin-stimulated monocytes in vitro.ConclusionOur findings suggest that gabexate mesilate attenuated endotoxin-induced pulmonary vascular injury mainly by inhibiting TNF-alpha production by monocytes, which may play a central role in sepsis-related lung injury.(Crit Care Med 1996; 24:1047-1053)

ISSN:0090-3493    

出版商:OVID    

年代:1996

数据来源: OVID

摘要:

ObjectiveTo study the efficacy of a low sodium hypertonic resuscitation fluid for resuscitation of severe hemorrhage in a pediatric animal, using the intraosseous route.DesignProspective, randomized, controlled animal study.SettingUniversity physiology laboratory.SubjectsSeventeen immature (6- to 9-wk-old) piglets, weighing 10.6 plus minus 0.4 kg, were studied under anesthesia.InterventionsA new 2400 mosm/L hypertonic fluid, ``Isosal'' was formulated with reduced (3.45%) sodium content compared with a 2400-mosm/L (7.5%) hypertonic saline solution. This formulation was accomplished by substituting glucose and mixed amino acids for sodium. Piglets were subjected to 1 hr of hemorrhage, reducing the cardiac output to 50% of baseline value. Resuscitation was carried out through the intraosseous route with an initial 6 mL/kg bolus of either hypertonic saline, Isosal, or lactated Ringer's solution. After the initial bolus, additional test fluid was given to maintain the cardiac output at baseline value for a 2-hr period.Measurements and Main ResultsTotal resuscitation volumes, hemodynamic variables, and electrolytes were measured. Intraosseous vascular access was easily established in all animals, and fluid resuscitation was carried out effectively through this route. Resuscitation volumes were significantly lower for both of the hypertonic fluids (12.7 plus minus 1.2 mL/kg for hypertonic saline, and 12.5 plus minus 1.7 mL/kg for Isosal solution) compared with lactated Ringer's solution (75.3 plus minus 11.6 mL/kg) (p equals .01). Both hypertonic saline and Isosal solution resulted in an immediate supranormal response in cardiac output that lasted 20 mins. In contrast, when lactated Ringer's solution was used, multiple boluses were required over a 20-min period to normalize cardiac output. Serum sodium was significantly higher in the hypertonic saline group compared with the Isosal or lactated Ringer's groups (p equals .001).ConclusionsIsosal solution was as effective as hypertonic saline in ``small volume'' resuscitation of severe hemorrhagic shock in a pediatric animal model through the intraosseous route, and produced significantly less hypernatremia when compared with hypertonic saline.(Crit Care Med 1996; 24:1054-1061)

ISSN:0090-3493    

出版商:OVID    

年代:1996

数据来源: OVID

摘要:

ObjectiveTo determine surfactant profiles of tracheal secretions in mechanically ventilated children with respiratory failure secondary to bacterial pneumonia, viral pneumonitis, adult respiratory distress syndrome (ARDS), and cardiopulmonary bypass.DesignProspective, cohort study.SettingTertiary, multidisciplinary, pediatric intensive care unit.PatientsOne hundred twenty pediatric patients with respiratory failure requiring mechanical ventilation.InterventionsRoutine tracheal aspirates were collected from children with bacterial pneumonia, viral pneumonitis, ARDS, postcardiopulmonary bypass, and a postsurgical control group. Samples were obtained on days 1, 2, 3, after every week of intubation and on the day of extubation.Measurements and Main ResultsThe tracheal aspirates were analyzed by high-performance liquid chromatography for lecithin/sphingomyelin ratios and by enzyme-linked immunosorbent assay for surfactant proteins A and B. Lung compliance and the oxygenation index were measured on each day of sample collection. On day 1, patients with bacterial pneumonia, viral pneumonitis, and ARDS had decreased lecithin/sphingomyelin ratios (p less than .001), and those patients with bacterial pneumonia and viral pneumonitis had decreased surfactant protein A/protein concentration (p less than .001). The lecithin/sphingomyelin ratios and surfactant protein A/protein concentration were significantly different among the groups (p less than .001), with the bacterial pneumonia and viral pneumonitis groups having higher lecithin/sphingomyelin ratios and increased surfactant protein concentrations before extubation. Pulmonary compliance was lower and the oxygenation index was higher than controls (p less than .001) in patients with bacterial pneumonia, viral pneumonitis, and ARDS. Pulmonary compliance was correlated weakly with lecithin/sphingomyelin ratio (r2equals .11, p less than .001) and surfactant protein A/protein concentration (r2equals .03, p less than .05). Surfactant protein B was similar in the diagnostic groups. Surfactant content in tracheal secretions from cardiopulmonary bypass patients was equivalent to controls.ConclusionAbnormal tracheal aspirate surfactant phospholipids and surfactant protein A were noted in children with bacterial pneumonia, viral pneumonitis, and ARDS, but not in children on cardiopulmonary bypass.(Crit Care Med 1996; 24:1062-1067)

ISSN:0090-3493    

出版商:OVID    

年代:1996

数据来源: OVID

摘要:

ObjectiveTo evaluate a portable scavenging system for nitric oxide and its oxides, designed for use on neonatal transport.DesignA prospective evaluation of the nitric oxide scavenging system, using a neonatal transport incubator ventilator and a test lung.SettingLaboratory of a tertiary care children's hospital.InterventionsThe scavenging system was tested, using a neonatal transport incubator with attached ventilator, ventilator circuit, and a neonatal test lung. Nitric oxide was administrated on the inspiratory limb, and nitric oxide and its oxides were measured in the expiratory gas after passing through the scavenger.Measurements and Main ResultsA modified scrubber assembly was filled with 50% activated charcoal and 50% aluminas potassium permanganate pellets[3]. Three wire meshes were placed before, in between, and after the two chemicals to facilitate gas flow. Using the maximum FIO2, with a nitric oxide concentration of 120 parts per million (ppm), the test lung continuous flow ventilation (FIO2of 0.86, peak inspiratory pressure of 30 cm H2O, positive end-expiratory pressure of 6 cm H2O, and respiratory rate of 60 breaths/min) was performed for 4 hrs with each of four freshly prepared scavenging systems. A fifth scavenging system was tested for a 12-hr period. The mean composition of the exhaled gases for 4 hrs were: nitric oxide 0.01 plus minus 0.03 (SD) ppm, nitric dioxide 0.06 plus minus 0.06 ppm, and other oxides 0.05 plus minus 0.09 ppm. After 12 hrs of 120 ppm of inhaled nitric oxide, the fifth scavenger system had undetectable nitric oxide, nitric dioxide, and other oxides in the exhaled gas. Normal room air contained between 0.0 and 0.03 ppm of nitric oxide, 0.0 and 0.02 ppm of nitric dioxide, and 0.0 and 0.02 ppm of other oxides.ConclusionNitric oxide, nitric dioxide, and other dioxides can be safely scavenged by this portable scavenging system, allowing safe administration of nitric oxide free from environmental contamination with nitric oxide and its oxides.(Crit Care Med 1996; 24:1068-1071)

ISSN:0090-3493    

出版商:OVID    

年代:1996

数据来源: OVID