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Daniel L Traber - One of the best experts on this subject based on the ideXlab platform.
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Pathophysiological Basis of Smoke Inhalation
2020Co-Authors: Daniel L TraberAbstract:moke Inhalation injury is a serious health threat to victims of house fires, explosions, and other disasters involving fire and Smoke. The clinical symptoms and prognosis of Smoke Inhalation injury are often exacerbated by additional burn injury or bacterial infection (such as pneumonia). From our experience using an ovine model of Inhalation injury, we have found that the acute lung injury (ALI) resulting from a combination injury of Smoke Inhalation and burn injury or pneumonia is more severe than that resulting from Smoke Inhalation injury alone. We have also observed that a combination of Smoke Inhalation and pneumonia results in a severe septic response in sheep. We will review the pathophysiological aspects of Smoke Inhalation injury and note the various treatment strategies being currently investigated. Because of space limitations, this review will not discuss the pathophysiology of toxic gas Inhalation or oropharyngeal and/or tracheobronchial thermal injury. These topics are important issues to be considered elsewhere. Bronchial blood flow The lungs have two separate blood supplies (the systemic and the pulmonary), each of which can contribute to lung edema. Under normal conditions, the pulmonary blood supply is equivalent to the cardiac output, whereas the bronchial blood flow is ~1% of the cardiac output. After Inhalation injury, there is a marked increase in bronchial blood flow, which results in pulmonary edema. In an ovine Smoke Inhalation model, airway blood flow increases eightfold or more in the main stem bronchi after the injury, whereas cardiac output, and thus blood flow to the peripheral tissues, remains relatively unchanged (1). Bronchial blood flow enters into the pulmonary vasculature through various bronchopulmonary anastomoses. It has been suggested that the bronchial circulation plays a significant role in the spread of injury from the airway to the parenchyma. We have investigated the effect of bronchial artery ligation or ethanol injection after Inhalation injury in sheep (11) and have found that the decrease in gas exchange [PaO 2 /FiO 2 (P/F) ratio], the increase in lung lymph flow, and the lung wet/dry weight ratio were all improved by these bronchial artery occlusion techniques. Therefore, we have concluded that the bronchial circulation contributes to edema formation in the lung that occurs after ALI caused by Smoke Inhalation injury. This phenomenon has been confirmed by other investigators (4). There are several mediators involved in the regulation of bronchial circulation, including nitric oxide (NO), a potent vasodilator. It has been reported that NO synthase (NOS) inhibitors reduce the increase in bronchial blood flow. There may be other factors, such as neurotransmitters, involved in this phenomenon, but they are still under investigation.
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a murine model of sepsis following Smoke Inhalation injury
Biochemical and Biophysical Research Communications, 2010Co-Authors: Daniel L Traber, Matthias Lange, Atsumori Hamahata, Aimalohi Esechie, Collette Jonkam, Kamna Bansal, Yoshimitsu Nakano, Lillian D Traber, Perenlei EnkhbaatarAbstract:Abstract Acute lung injury (ALI) by Smoke Inhalation with subsequent pneumonia and sepsis represents a major cause of morbidity and mortality in burn patients. The aim of the present study was to develop a murine model of ALI and sepsis to enhance the knowledge of mechanistic aspects and pathophysiological changes in patients with these injuries. In deeply anesthetized female C57BL/6 mice, injury was induced by four sets of cotton Smoke using an Inhalation chamber. Afterward, live Pseudomonas aeruginosa (3.2 × 10 7 colony-forming units) was administered intranasally. The indicated dose of bacteria was determined based on the results of a dose–response study ( n = 47). The following study groups were monitored for survival over 96 h: (1) sham injury group, (2) only Smoke Inhalation group, (3) only bacteria group, and (4) Smoke Inhalation plus bacteria group. Each group included 10 mice. The survival rates were 100%, 90%, 30%, and 10%, respectively. The double hit injury was associated with excessive releases of pro-inflammatory cytokines in the plasma, and enhanced neutrophil accumulation, increased lipid peroxidation, and excessive formation of reactive nitrogen species in the lung. In mice receiving only Smoke Inhalation injury, no systemic cytokine release and increased lung tissue lipid peroxidation were observed. However, Smoke alone significantly increased neutrophil accumulation and formation of reactive nitrogen species in lung tissue. In conclusion, bacterial pneumonia is predominantly responsible for mortality and morbidity in this novel murine model of Smoke Inhalation and pulmonary sepsis. Reactive oxygen and nitrogen species mediate the severity of lung injury.
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pathophysiology management and treatment of Smoke Inhalation injury
Expert Review of Respiratory Medicine, 2009Co-Authors: Sebastian Rehberg, Marc O Maybauer, Perenlei Enkhbaatar, Dirk M Maybauer, Yusuke Yamamoto, Daniel L TraberAbstract:Smoke Inhalation injury continues to increase morbidity and mortality in burn patients in both the third world and industrialized countries. The lack of uniform criteria for the diagnosis and definition of Smoke Inhalation injury contributes to the fact that, despite extensive research, mortality rates have changed little in recent decades. The formation of reactive oxygen and nitrogen species, as well as the procoagulant and antifibrinolytic imbalance of alveolar homeostasis, all play a central role in the pathogenesis of Smoke Inhalation injury. Further hallmarks include massive airway obstruction owing to cast formation, bronchospasm, the increase in bronchial circulation and transvascular fluid flux. Therefore, anticoagulants, antioxidants and bronchodilators, especially when administered as an aerosol, represent the most promising treatment strategies. The purpose of this review article is to provide an overview of the pathophysiological changes, management and treatment options of Smoke Inhalation i...
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Pulmonary changes in a mouse model of combined burn and Smoke Inhalation-induced injury
Journal of Applied Physiology, 2008Co-Authors: Akio Mizutani, Kazunori Murakami, Perenlei Enkhbaatar, Aimalohi Esechie, Lillian D Traber, Hal K Hawkins, Donald J. Deyo, Takayuki Noguchi, Daniel L TraberAbstract:The morbidity and mortality of burn victims increase when burn injury is combined with Smoke Inhalation. The goal of the present study was to develop a murine model of burn and Smoke Inhalation inj...
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effect of inhaled nitric oxide on pulmonary vascular hyperpermeability in sheep following Smoke Inhalation
Burns, 2005Co-Authors: Perenlei Enkhbaatar, Marc O Maybauer, Dirk M Maybauer, David N. Herndon, Lillian D Traber, Yuji Kikuchi, Martin Westphal, Naoki Morita, Daniel L TraberAbstract:Abstract Smoke Inhalation increases mortality and morbidity in burn patients. We have reported that Smoke Inhalation increases lung lymph flow, an index of pulmonary transvascular fluid flux and decreases reflection coefficient, an index of microvascular permeability to protein. Nitric oxide has been reported to decrease microvascular permeability to protein. We hypothesize that inhaled nitric oxide decreases pulmonary microvascular hyperpermeability following Smoke Inhalation. Sheep were prepared for study with a chronic lung lymph fistula, Swan-Ganz, left atrial, and femoral arterial catheters. Occluders were placed on pulmonary veins to measure reflection coefficient. All animals were insufflated with 4 × 12 breaths of cotton Smoke. Sheep were randomly divided into two groups: NO (injured, treated with nitric oxide (40 ppm) Inhalation, n = 6) and control (injured, not treated, n = 6). Nitric oxide Inhalation was started 22 h after the insult. Control animals showed an increase in lung lymph flow, and lung water content. These changes were associated with marked increase in pulmonary microvascular resistance, pulmonary artery pressure, and decrease in reflection coefficient. Nitric oxide Inhalation ameliorated the above-mentioned pathological changes. The results suggest that nitric oxide Inhalation has potential for beneficial effect in the treatment of patients suffering from Smoke Inhalation.
Perenlei Enkhbaatar - One of the best experts on this subject based on the ideXlab platform.
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Safety of Nebulized Epinephrine in Smoke Inhalation Injury.
Journal of Burn Care & Research, 2017Co-Authors: Guillermo Foncerrada, Perenlei Enkhbaatar, David N. Herndon, Ronald P Mlcak, Francisco Lima, Robert P. Clayton, Oscar E SumanAbstract:: This pilot study was conducted to profile safety of nebulized racemic epinephrine when used as a therapy for Smoke Inhalation injury in severely burned children. We enrolled 16 patients who were 7 to 19 years of age ([mean ± SD], 12 ± 4 years) with burns covering more than 30% of the TBSA (55 ± 17%) and Smoke Inhalation injury, as diagnosed by bronchoscopy at burn center admission. Patients were randomized to receive either standard of care (n = 8), which consisted of nebulized acetylcysteine, nebulized heparin, and nebulized albuterol, or to receive standard of care plus nebulized epinephrine (n = 8). Primary endpoints were death, chest pain, and adverse changes in cardiopulmonary hemodynamics (arrhythmia, arterial blood pressure, electrocardiographic [ST segment] changes, and peak inspiratory pressure). Additional endpoints included total days on ventilator, pulmonary function, and physiological cardiopulmonary measurements at intensive care unit discharge. No adverse events were observed during or after the nebulization of epinephrine, and no deaths were reported that were attributable to the administration of nebulized epinephrine. The groups did not significantly differ with regard to age, sex, burn size, days on ventilator, pulmonary function, or cardiopulmonary fitness. Results of this pilot trial indicate epinephrine to be safe when administered to pediatric burn patients with Smoke Inhalation injury. Current data warrant future efficacy studies with a greater number of patients.
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pathophysiology research challenges and clinical management of Smoke Inhalation injury
The Lancet, 2016Co-Authors: Perenlei Enkhbaatar, David N. Herndon, Basil A. Pruitt, Oscar E Suman, Ronald P Mlcak, Steven E Wolf, Hiroyuki SakuraiAbstract:Summary Smoke Inhalation injury is a serious medical problem that increases morbidity and mortality after severe burns. However, relatively little attention has been paid to this devastating condition, and the bulk of research is limited to preclinical basic science studies. Moreover, no worldwide consensus criteria exist for its diagnosis, severity grading, and prognosis. Therapeutic approaches are highly variable depending on the country and burn centre or hospital. In this Series paper, we discuss understanding of the pathophysiology of Smoke Inhalation injury, the best evidence-based treatments, and challenges and future directions in diagnostics and management.
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a murine model of sepsis following Smoke Inhalation injury
Biochemical and Biophysical Research Communications, 2010Co-Authors: Daniel L Traber, Matthias Lange, Atsumori Hamahata, Aimalohi Esechie, Collette Jonkam, Kamna Bansal, Yoshimitsu Nakano, Lillian D Traber, Perenlei EnkhbaatarAbstract:Abstract Acute lung injury (ALI) by Smoke Inhalation with subsequent pneumonia and sepsis represents a major cause of morbidity and mortality in burn patients. The aim of the present study was to develop a murine model of ALI and sepsis to enhance the knowledge of mechanistic aspects and pathophysiological changes in patients with these injuries. In deeply anesthetized female C57BL/6 mice, injury was induced by four sets of cotton Smoke using an Inhalation chamber. Afterward, live Pseudomonas aeruginosa (3.2 × 10 7 colony-forming units) was administered intranasally. The indicated dose of bacteria was determined based on the results of a dose–response study ( n = 47). The following study groups were monitored for survival over 96 h: (1) sham injury group, (2) only Smoke Inhalation group, (3) only bacteria group, and (4) Smoke Inhalation plus bacteria group. Each group included 10 mice. The survival rates were 100%, 90%, 30%, and 10%, respectively. The double hit injury was associated with excessive releases of pro-inflammatory cytokines in the plasma, and enhanced neutrophil accumulation, increased lipid peroxidation, and excessive formation of reactive nitrogen species in the lung. In mice receiving only Smoke Inhalation injury, no systemic cytokine release and increased lung tissue lipid peroxidation were observed. However, Smoke alone significantly increased neutrophil accumulation and formation of reactive nitrogen species in lung tissue. In conclusion, bacterial pneumonia is predominantly responsible for mortality and morbidity in this novel murine model of Smoke Inhalation and pulmonary sepsis. Reactive oxygen and nitrogen species mediate the severity of lung injury.
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pathophysiology management and treatment of Smoke Inhalation injury
Expert Review of Respiratory Medicine, 2009Co-Authors: Sebastian Rehberg, Marc O Maybauer, Perenlei Enkhbaatar, Dirk M Maybauer, Yusuke Yamamoto, Daniel L TraberAbstract:Smoke Inhalation injury continues to increase morbidity and mortality in burn patients in both the third world and industrialized countries. The lack of uniform criteria for the diagnosis and definition of Smoke Inhalation injury contributes to the fact that, despite extensive research, mortality rates have changed little in recent decades. The formation of reactive oxygen and nitrogen species, as well as the procoagulant and antifibrinolytic imbalance of alveolar homeostasis, all play a central role in the pathogenesis of Smoke Inhalation injury. Further hallmarks include massive airway obstruction owing to cast formation, bronchospasm, the increase in bronchial circulation and transvascular fluid flux. Therefore, anticoagulants, antioxidants and bronchodilators, especially when administered as an aerosol, represent the most promising treatment strategies. The purpose of this review article is to provide an overview of the pathophysiological changes, management and treatment options of Smoke Inhalation i...
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Pulmonary changes in a mouse model of combined burn and Smoke Inhalation-induced injury
Journal of Applied Physiology, 2008Co-Authors: Akio Mizutani, Kazunori Murakami, Perenlei Enkhbaatar, Aimalohi Esechie, Lillian D Traber, Hal K Hawkins, Donald J. Deyo, Takayuki Noguchi, Daniel L TraberAbstract:The morbidity and mortality of burn victims increase when burn injury is combined with Smoke Inhalation. The goal of the present study was to develop a murine model of burn and Smoke Inhalation inj...
David N. Herndon - One of the best experts on this subject based on the ideXlab platform.
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Safety of Nebulized Epinephrine in Smoke Inhalation Injury.
Journal of Burn Care & Research, 2017Co-Authors: Guillermo Foncerrada, Perenlei Enkhbaatar, David N. Herndon, Ronald P Mlcak, Francisco Lima, Robert P. Clayton, Oscar E SumanAbstract:: This pilot study was conducted to profile safety of nebulized racemic epinephrine when used as a therapy for Smoke Inhalation injury in severely burned children. We enrolled 16 patients who were 7 to 19 years of age ([mean ± SD], 12 ± 4 years) with burns covering more than 30% of the TBSA (55 ± 17%) and Smoke Inhalation injury, as diagnosed by bronchoscopy at burn center admission. Patients were randomized to receive either standard of care (n = 8), which consisted of nebulized acetylcysteine, nebulized heparin, and nebulized albuterol, or to receive standard of care plus nebulized epinephrine (n = 8). Primary endpoints were death, chest pain, and adverse changes in cardiopulmonary hemodynamics (arrhythmia, arterial blood pressure, electrocardiographic [ST segment] changes, and peak inspiratory pressure). Additional endpoints included total days on ventilator, pulmonary function, and physiological cardiopulmonary measurements at intensive care unit discharge. No adverse events were observed during or after the nebulization of epinephrine, and no deaths were reported that were attributable to the administration of nebulized epinephrine. The groups did not significantly differ with regard to age, sex, burn size, days on ventilator, pulmonary function, or cardiopulmonary fitness. Results of this pilot trial indicate epinephrine to be safe when administered to pediatric burn patients with Smoke Inhalation injury. Current data warrant future efficacy studies with a greater number of patients.
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pathophysiology research challenges and clinical management of Smoke Inhalation injury
The Lancet, 2016Co-Authors: Perenlei Enkhbaatar, David N. Herndon, Basil A. Pruitt, Oscar E Suman, Ronald P Mlcak, Steven E Wolf, Hiroyuki SakuraiAbstract:Summary Smoke Inhalation injury is a serious medical problem that increases morbidity and mortality after severe burns. However, relatively little attention has been paid to this devastating condition, and the bulk of research is limited to preclinical basic science studies. Moreover, no worldwide consensus criteria exist for its diagnosis, severity grading, and prognosis. Therapeutic approaches are highly variable depending on the country and burn centre or hospital. In this Series paper, we discuss understanding of the pathophysiology of Smoke Inhalation injury, the best evidence-based treatments, and challenges and future directions in diagnostics and management.
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effect of inhaled nitric oxide on pulmonary vascular hyperpermeability in sheep following Smoke Inhalation
Burns, 2005Co-Authors: Perenlei Enkhbaatar, Marc O Maybauer, Dirk M Maybauer, David N. Herndon, Lillian D Traber, Yuji Kikuchi, Martin Westphal, Naoki Morita, Daniel L TraberAbstract:Abstract Smoke Inhalation increases mortality and morbidity in burn patients. We have reported that Smoke Inhalation increases lung lymph flow, an index of pulmonary transvascular fluid flux and decreases reflection coefficient, an index of microvascular permeability to protein. Nitric oxide has been reported to decrease microvascular permeability to protein. We hypothesize that inhaled nitric oxide decreases pulmonary microvascular hyperpermeability following Smoke Inhalation. Sheep were prepared for study with a chronic lung lymph fistula, Swan-Ganz, left atrial, and femoral arterial catheters. Occluders were placed on pulmonary veins to measure reflection coefficient. All animals were insufflated with 4 × 12 breaths of cotton Smoke. Sheep were randomly divided into two groups: NO (injured, treated with nitric oxide (40 ppm) Inhalation, n = 6) and control (injured, not treated, n = 6). Nitric oxide Inhalation was started 22 h after the insult. Control animals showed an increase in lung lymph flow, and lung water content. These changes were associated with marked increase in pulmonary microvascular resistance, pulmonary artery pressure, and decrease in reflection coefficient. Nitric oxide Inhalation ameliorated the above-mentioned pathological changes. The results suggest that nitric oxide Inhalation has potential for beneficial effect in the treatment of patients suffering from Smoke Inhalation.
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heparin nebulization attenuates acute lung injury in sepsis following Smoke Inhalation in sheep
Shock, 2002Co-Authors: Kazunori Murakami, David N. Herndon, Lillian D Traber, Roy Mcguire, Jeffrey M Jodoin, Lars J Bjertnaes, J Katahira, Frank C Schmalstieg, Hal K Hawkins, Daniel L TraberAbstract:ABSTRACTPseudomonas pneumonia is a common complication of Smoke Inhalation injury. Airway casts formed from clotted mucous occur frequently in this condition. A recent report shows that intravenous heparin improves oxygenation and reduces lung damage in a sheep model of Smoke Inhalation. We hypothes
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Effect of phenytoin on Smoke Inhalation injury in sheep
Shock, 1995Co-Authors: Kazuya Nishida, David N. Herndon, Lillian D Traber, Naoaki Matsumoto, Yuji Kikuchi, Daniel L TraberAbstract:: To determine whether the anti-inflammatory effects of phenytoin might reduce cardiopulmonary dysfunction we studied the effects of phenytoin treatment on acute lung injury induced by Smoke Inhalation. Twenty-one chronically instrumented sheep were observed for 24 h after Smoke Inhalation injury. Myocardial contractility was evaluated by left ventricular end-systolic pressure-diameter relationship (LVESPDR) with a pair of ultrasonic transducers and strain-gauge transducer. In the control group (n = 6), uninjured sheep were given a bolus of phenytoin (12.5 mg/kg). Smoke-insufflated sheep were divided into nontreatment (n = 7) and phenytoin (n = 8) groups. Phenytoin alone had no effects in uninjured sheep except an early rise in heart rate and LVESPDR. In the group given Smoke without treatment, there was a significant increase in pulmonary artery pressure and pulmonary vascular resistance index and a decrease in cardiac index. Pulmonary vascular changes were attenuated by treatment with phenytoin. Pulmonary transvascular fluid flux was evaluated by using a lung lymph fistula. LVESPDR fell in the Smoke group but not in the group given phenytoin. There was a marked increase in lung lymph flow with Smoke Inhalation but this phenomenon was not affected by phenytoin treatment. In conclusion, phenytoin treatment reduced early hemodynamic depression.
Chengbin Wang - One of the best experts on this subject based on the ideXlab platform.
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imbalance of th17 tregs in rats with Smoke Inhalation induced acute lung injury
Scientific Reports, 2016Co-Authors: Fan Zhang, Mianyang Li, Chengbin WangAbstract:T helper (Th) 17 cells and CD4+ CD25+ regulatory T (Treg) cells are supposed to be critically involved in regulating autoimmune and inflammatory diseases. The aim of this study was to investigate the Th17/Treg pattern in rats with gunpowder smog-induced acute lung injury. Wistar rats were equally randomized to three groups: normal control group, ALI 6 h group (Smoke Inhalation for 6 h) and ALI 24 h group (Smoke Inhalation for 24 h). We observed changes in cell counting in bronchoalveolar lavage fluid (BALF), alveolar-capillary membrane permeability and lung tissue pathology. Moreover, rats in ALI 6 h and ALI 24 h group showed increased expression of Th17 cell and related cytokines (IL-17 A, IL-6, TGF-β and IL-23). Meanwhile, Treg prevalence and related cytokines (IL-10, IL-2 and IL-35) were decreased. Consequently, the ratio of Th17/Treg was higher after Smoke Inhalation. Additionally, Th1 cell decreased while Th2 cell increased at 6 h and 24 h after Smoke Inhalation. In conclusion, Th17/Treg imbalance exists in rats with Smoke Inhalation-induced acute lung injury, suggesting its potential role in the pathogenesis of this disease.
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Imbalance of Th17/Tregs in rats with Smoke Inhalation-induced acute lung injury
Scientific Reports, 2016Co-Authors: Fan Zhang, Mianyang Li, Chengbin WangAbstract:T helper (Th) 17 cells and CD4+ CD25+ regulatory T (Treg) cells are supposed to be critically involved in regulating autoimmune and inflammatory diseases. The aim of this study was to investigate the Th17/Treg pattern in rats with gunpowder smog-induced acute lung injury. Wistar rats were equally randomized to three groups: normal control group, ALI 6 h group (Smoke Inhalation for 6 h) and ALI 24 h group (Smoke Inhalation for 24 h). We observed changes in cell counting in bronchoalveolar lavage fluid (BALF), alveolar-capillary membrane permeability and lung tissue pathology. Moreover, rats in ALI 6 h and ALI 24 h group showed increased expression of Th17 cell and related cytokines (IL-17 A, IL-6, TGF-β and IL-23). Meanwhile, Treg prevalence and related cytokines (IL-10, IL-2 and IL-35) were decreased. Consequently, the ratio of Th17/Treg was higher after Smoke Inhalation. Additionally, Th1 cell decreased while Th2 cell increased at 6 h and 24 h after Smoke Inhalation. In conclusion, Th17/Treg imbalance exists in rats with Smoke Inhalation-induced acute lung injury, suggesting its potential role in the pathogenesis of this disease.
Lillian D Traber - One of the best experts on this subject based on the ideXlab platform.
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a murine model of sepsis following Smoke Inhalation injury
Biochemical and Biophysical Research Communications, 2010Co-Authors: Daniel L Traber, Matthias Lange, Atsumori Hamahata, Aimalohi Esechie, Collette Jonkam, Kamna Bansal, Yoshimitsu Nakano, Lillian D Traber, Perenlei EnkhbaatarAbstract:Abstract Acute lung injury (ALI) by Smoke Inhalation with subsequent pneumonia and sepsis represents a major cause of morbidity and mortality in burn patients. The aim of the present study was to develop a murine model of ALI and sepsis to enhance the knowledge of mechanistic aspects and pathophysiological changes in patients with these injuries. In deeply anesthetized female C57BL/6 mice, injury was induced by four sets of cotton Smoke using an Inhalation chamber. Afterward, live Pseudomonas aeruginosa (3.2 × 10 7 colony-forming units) was administered intranasally. The indicated dose of bacteria was determined based on the results of a dose–response study ( n = 47). The following study groups were monitored for survival over 96 h: (1) sham injury group, (2) only Smoke Inhalation group, (3) only bacteria group, and (4) Smoke Inhalation plus bacteria group. Each group included 10 mice. The survival rates were 100%, 90%, 30%, and 10%, respectively. The double hit injury was associated with excessive releases of pro-inflammatory cytokines in the plasma, and enhanced neutrophil accumulation, increased lipid peroxidation, and excessive formation of reactive nitrogen species in the lung. In mice receiving only Smoke Inhalation injury, no systemic cytokine release and increased lung tissue lipid peroxidation were observed. However, Smoke alone significantly increased neutrophil accumulation and formation of reactive nitrogen species in lung tissue. In conclusion, bacterial pneumonia is predominantly responsible for mortality and morbidity in this novel murine model of Smoke Inhalation and pulmonary sepsis. Reactive oxygen and nitrogen species mediate the severity of lung injury.
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Pulmonary changes in a mouse model of combined burn and Smoke Inhalation-induced injury
Journal of Applied Physiology, 2008Co-Authors: Akio Mizutani, Kazunori Murakami, Perenlei Enkhbaatar, Aimalohi Esechie, Lillian D Traber, Hal K Hawkins, Donald J. Deyo, Takayuki Noguchi, Daniel L TraberAbstract:The morbidity and mortality of burn victims increase when burn injury is combined with Smoke Inhalation. The goal of the present study was to develop a murine model of burn and Smoke Inhalation inj...
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effect of inhaled nitric oxide on pulmonary vascular hyperpermeability in sheep following Smoke Inhalation
Burns, 2005Co-Authors: Perenlei Enkhbaatar, Marc O Maybauer, Dirk M Maybauer, David N. Herndon, Lillian D Traber, Yuji Kikuchi, Martin Westphal, Naoki Morita, Daniel L TraberAbstract:Abstract Smoke Inhalation increases mortality and morbidity in burn patients. We have reported that Smoke Inhalation increases lung lymph flow, an index of pulmonary transvascular fluid flux and decreases reflection coefficient, an index of microvascular permeability to protein. Nitric oxide has been reported to decrease microvascular permeability to protein. We hypothesize that inhaled nitric oxide decreases pulmonary microvascular hyperpermeability following Smoke Inhalation. Sheep were prepared for study with a chronic lung lymph fistula, Swan-Ganz, left atrial, and femoral arterial catheters. Occluders were placed on pulmonary veins to measure reflection coefficient. All animals were insufflated with 4 × 12 breaths of cotton Smoke. Sheep were randomly divided into two groups: NO (injured, treated with nitric oxide (40 ppm) Inhalation, n = 6) and control (injured, not treated, n = 6). Nitric oxide Inhalation was started 22 h after the insult. Control animals showed an increase in lung lymph flow, and lung water content. These changes were associated with marked increase in pulmonary microvascular resistance, pulmonary artery pressure, and decrease in reflection coefficient. Nitric oxide Inhalation ameliorated the above-mentioned pathological changes. The results suggest that nitric oxide Inhalation has potential for beneficial effect in the treatment of patients suffering from Smoke Inhalation.
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heparin nebulization attenuates acute lung injury in sepsis following Smoke Inhalation in sheep
Shock, 2002Co-Authors: Kazunori Murakami, David N. Herndon, Lillian D Traber, Roy Mcguire, Jeffrey M Jodoin, Lars J Bjertnaes, J Katahira, Frank C Schmalstieg, Hal K Hawkins, Daniel L TraberAbstract:ABSTRACTPseudomonas pneumonia is a common complication of Smoke Inhalation injury. Airway casts formed from clotted mucous occur frequently in this condition. A recent report shows that intravenous heparin improves oxygenation and reduces lung damage in a sheep model of Smoke Inhalation. We hypothes
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Effects of an L-selectin antibody on the pulmonary and systemic manifestations of severe Smoke Inhalation injuries in sheep.
Journal of Burn Care & Rehabilitation, 2000Co-Authors: Paul J. Schenarts, Lillian D Traber, Frank C Schmalstieg, Hal K Hawkins, Hans G. Bone, Daniel L TraberAbstract:: Sheep were treated with either lymphocyte adhesion molecule (LAM)1-3, an antibody against L-selectin, (40 mg 1 hour before Smoke Inhalation and 35 mg 24 hours after Smoke Inhalation; n = 6) or equivalent volumes of 0.9% saline solution (n = 6). After the Smoke Inhalation injuries, the PaO2/FIO2 ratio declined in both groups until 40 hours after the injuries, when a trend toward improvement was noted in the group that received LAM1-3. Lung lymph flow increased in both groups until 36 hours after the Smoke Inhalation injuries and then significantly decreased in the group that received LAM1-3. Forty-eight hours after the Smoke Inhalation injuries, there was a significant decrease in the ratio of wet-dry lung weight and in preservation of the reflection coefficient in the group that received LAM1-3 (P < .05). Histopathologic examination showed no differences between the groups in the pulmonary morphology associated with Smoke Inhalation. A reduction in splanchnic blood flow was noted in the control group (P < .05); this reduction was attenuated by treatment with LAM1-3. The delayed pulmonary effects and improved splanchnic blood flow suggested that LAM1-3 attenuated the development of a systemically induced secondary lung injury rather than of the primary lung injury associated with Smoke Inhalation.
