Perflubron
(Synonyms: 全氟溴辛烷,Perfluorooctyl bromide; PFOB) 目录号 : GC38936Perflubron (1-Bromoperfluorooctane, Perfluorooctyl bromide, Oxygent, PFOB) exhibits anti-inflammatory activity thus decreases cytokine production in human alveolar macrophages. Perflubron also attenuates oxidative damage to both biological and nonbiological systems which is independent of its anti-inflammatory properties.
Cas No.:423-55-2
Sample solution is provided at 25 µL, 10mM.
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Perflubron (1-Bromoperfluorooctane, Perfluorooctyl bromide, Oxygent, PFOB) exhibits anti-inflammatory activity thus decreases cytokine production in human alveolar macrophages. Perflubron also attenuates oxidative damage to both biological and nonbiological systems which is independent of its anti-inflammatory properties.
[1] M J Thomassen, et al. Crit Care Med. 1997 Dec;25(12):2045-7. [2] Alexandre T Rotta, et al. Pediatr Crit Care Med. 2003 Apr;4(2):233-8.
Cas No. | 423-55-2 | SDF | |
别名 | 全氟溴辛烷,Perfluorooctyl bromide; PFOB | ||
Canonical SMILES | FC(F)(F)C(F)(F)C(F)(F)C(F)(F)C(F)(F)C(F)(F)C(F)(F)C(F)(Br)F | ||
分子式 | C8BrF17 | 分子量 | 498.96 |
溶解度 | DMSO : 16 mg/mL | 储存条件 | Store at -20°C |
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1 mg | 5 mg | 10 mg | |
1 mM | 2.0042 mL | 10.0208 mL | 20.0417 mL |
5 mM | 0.4008 mL | 2.0042 mL | 4.0083 mL |
10 mM | 0.2004 mL | 1.0021 mL | 2.0042 mL |
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给药剂量 | mg/kg | 动物平均体重 | g | 每只动物给药体积 | ul | 动物数量 | 只 | |||
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2.
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Perflubron decreases inflammatory cytokine production by human alveolar macrophages
Crit Care Med 1997 Dec;25(12):2045-7.PMID:9403756DOI:10.1097/00003246-199712000-00023.
Objective: To determine whether inflammatory cytokine production by stimulated human alveolar macrophages is affected by Perflubron exposure. Design: Controlled laboratory investigation of alveolar macrophage function in vitro. Setting: Research laboratory. Subjects: Cultured alveolar macrophages obtained by bronchoalveolar lavage from eleven normal volunteers. Interventions: Endotoxin-stimulated alveolar macrophages were treated with Perflubron. Measurements and main results: Alveolar macrophages were stimulated for 1 hr with lipopolysaccharide and then treated with Perflubron for 23 hrs. Cell-free supernatants were collected and cytokines were assayed by enzyme-linked immunosorbent assay. Tumor necrosis factor-alpha, interleukin-1, and interleukin-6 were stimulated by lipopolysaccharide (endotoxin) and all of these cytokines were significantly (p < .05) inhibited by Perflubron. Cell viability was not affected by Perflubron. Basal cytokine concentrations from unstimulated alveolar macrophages were not altered by Perflubron. Conclusions: Exposure of stimulated human alveolar macrophages to Perflubron in vitro decreases cytokine production. This observation suggests that Perflubron may have anti-inflammatory activity.
Perflubron dosing affects ventilator-induced lung injury in rats with previous lung injury
Crit Care Med 2007 Feb;35(2):561-7.PMID:17205026DOI:10.1097/01.CCM.0000253396.86212.8C.
Objectives: Randomized controlled trials of partial liquid ventilation in acute respiratory distress syndrome have been negative. Reasons for this failure may reside in the use of too large doses of perfluorocarbon. The objective was to evaluate whether various doses of Perflubron affect ventilation-induced injury in edematous lungs in different ways. Design: Prospective, controlled animal study. Setting: Research laboratory of a university. Subjects: Male Wistar rats weighing 300+/-20 g. Interventions: Separate groups of rats were injected with alpha-naphtylthiourea to produce mild permeability pulmonary edema. They were then given 0, 7 (low), 13 (moderate), or 20 mL/kg (near functional residual capacity) Perflubron doses and mechanically ventilated with a large (33 mL/kg) tidal volume for 15 mins. Measurements and main results: 125I-albumin distribution space was used to assess lung microvascular permeability. Quasi-static respiratory system pressure-volume curves were analyzed. Administration of low and moderate Perflubron doses significantly improved respiratory mechanics and reduced the ventilator-induced permeability alterations to the level observed in rats that were not ventilated. By contrast, a Perflubron dose that was near functional residual capacity increased end-inspiratory plateau pressure and aggravated the permeability alterations due to high tidal volume ventilation. Conclusions: Near functional residual capacity but not low Perflubron dose worsens ventilation-induced lung injury of preinjured lungs. This may provide some explanation for the negative results of the recent clinical trials, and it stresses the importance of the amount of Perflubron used for partial liquid ventilation.
Perflubron residua: 12 years following therapy
Pediatr Radiol 2009 Apr;39(4):393-5.PMID:19189093DOI:10.1007/s00247-008-1139-8.
Partial liquid ventilation therapy utilizing perfluorocarbons has been used for patients with severe respiratory distress. Perfluorocarbons such as Perflubron have been demonstrated to clear from the lungs shortly after therapy. We present a 13-year-old boy with residual Perflubron in his lungs, 12 years following therapy with Perflubron. The imaging features are important to recognize as these patients return for additional care and imaging.
Perfluorooctyl bromide (Perflubron) attenuates oxidative injury to biological and nonbiological systems
Pediatr Crit Care Med 2003 Apr;4(2):233-8.PMID:12749658DOI:10.1097/01.PCC.0000059729.21375.D0.
Objective: To examine whether perfluorooctyl bromide (Perflubron) is capable of protecting biological and nonbiological systems against oxidative damage through a mechanism independent of its known anti-inflammatory property. Design: A controlled, in vitro laboratory study. Setting: Research laboratory of a health sciences university. Subjects: Rat pulmonary artery endothelial cell cultures (biological system) and linoleic acid in sodium dodecyl sulfate micelles (nonbiological system). Interventions: Rat pulmonary artery endothelial cells labeled with dichlorofluorescein diacetate and incubated with Perflubron or culture media (control) were exposed to H2O2. H2O2-induced fluorescence of dichlorofluorescein diacetate was measured as an index of intracellular oxidative stress. In another experiment, linoleic acid in sodium dodecyl sulfate micelles was exposed to various concentrations of the azo initiator 2,2'-diazo-bis-(2-amidinopropane) dihydrochloride (2, 4, 20, and 50 mM) in the presence or absence of Perflubron. Malondialdehyde measurements were obtained as a marker of oxidative damage to linoleic acid. Measurements and main results: Cell monolayers incubated with Perflubron exhibited 66.6% attenuation in intracellular fluorescence compared with controls (p < .05). Linoleic acid in sodium dodecyl sulfate micelles incubated with Perflubron and exposed to 2, 4, 20, or 50 mM of 2,2'-diazo-bis-(2-amidinopropane) dihydrochloride showed less evidence of lipid peroxidation as indicated by lower malondialdehyde measurements at 240 mins (10.6%, 16%, 41%, and 14.2%, respectively) compared with controls. Conclusions: Perflubron attenuates oxidative damage to both biological and nonbiological systems. This newly recognized property of Perflubron is independent of its anti-inflammatory properties.
Perflubron emulsion delays blood transfusions in orthopedic surgery. European Perflubron Emulsion Study Group
Anesthesiology 1999 Nov;91(5):1195-208.PMID:10551568DOI:10.1097/00000542-199911000-00009.
Background: Fluorocarbon emulsions have been proposed as temporary artificial oxygen carriers. The aim of the present study is to compare the effectiveness of Perflubron emulsion with the effectiveness of autologous blood or colloid infusion for reversal of physiologic transfusion triggers. Methods: A multinational, multicenter, randomized, controlled, single-blind, parallel group study was performed in 147 orthopedic patients. Patients underwent acute normovolemic hemodilution with colloid to a target hemoglobin of 9 g/dl with an inspiratory oxygen fraction (FIO2) of 0.40. Patients were then randomized into one of four treatment groups after having reached any of the protocol-defined transfusion triggers including tachycardia (heart rate > 125% of posthemodilution rate or > 110 bpm), hypotension (mean arterial pressure < 75% of posthemodilution level or < or = 60 mmHg), elevated cardiac output (> 150% of posthemodilution level) or decreased mixed venous oxygen partial pressure (PVO2; < 38 mmHg). Treatments in the four groups were 450 ml autologous blood harvested during acute normovolemic hemodilution given at FO2 = 0.40; 450 ml colloid at FIO2 = 1.0; 0.9 g/kg Perflubron emulsion with colloid (total = 450 ml) at FIO2 = 1.0; and 1.8 g/kg Perflubron emulsion with colloid (total = 450 ml) at FIO2 = 1.0. The primary endpoint was duration of transfusion-trigger reversal. A secondary end-point was percentage of transfusion-trigger reversal. Results: Perflubron emulsion was well tolerated with no serious adverse event attributed to drug treatment. Duration of reversal was longest in the 1.8 g/kg Perflubron group (median, 80 min; 95% confidence interval, 60-100 min; P = 0.014 vs. autologous blood, P < 0.001 vs. colloid) followed by the 0.9 g/kg Perflubron group (median, 59 min; 95% confidence interval, 40-90 min), the autologous blood group (median, 55 min; 95% confidence interval, 30-70 min) and the colloid group (median, 30 min; 95% confidence interval, 27-60 min). Percentage of reversal was also highest in the 1.8 g/kg Perflubron group (97%; P < 0.001 vs. autologous blood; P = 0.014 vs. colloid), followed by 0.9 g/kg Perflubron (82%), colloid (76%), and autologous blood (60%). Conclusions: Perflubron emulsion (1.8 g/kg) combined with 100% oxygen ventilation is more effective than autologous blood or colloid infusion in reversing physiologic transfusion triggers.