• Journal of Trauma and Injury
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• v.28 no.3
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• pp.104-107
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• 2015

Purpose: Nitric oxide (NO) is a vasodilator and inhaled NO (iNO) is used in acute respiratory distress syndrome (ARDS) to improve alveolocapillary gas exchange. The mechanism to improve oxygenation is likely to redistribute blood flow from unventilated areas to ventilated areas. Though improvement of oxygenation, iNO therapy has not been shown to improve mortality and considered as only rescue therapy in severe hypoxemia. We conducted the study to investigate an efficacy of iNO in trauma patients with severe hypoxemia. Methods: We reviewed the trauma patients who underwent iNO therapy retrospectively from 2010 to 2014. Degree of hypoxemia was represented as $PaO_2/FiO_2$ ratio (PFR) and the severity of patient was represented with sequential organ failure assessment (SOFA) score. Patients were divided into the survivor group and non-survivor group according to the 28-day mortality. Results: A total of 20 patients were enrolled. The mortality of 28-day was 40%. There were no significant differences between survivor and non-survivor group in age, sex, severity of injury, PFR and SOFA score. There was significant difference in initiation time of iNO after injury (p=0.047). Maximum combinations of sensitivity and specificity for timing of iNO therapy were observed using cut-off of 3-day after injury with a sensitivity of 88% and specificity of 75%. Conclusion: Though iNO therapy does not influence the mortality, iNO therapy may decrease the mortality caused by respiratory failure in the early phase of trauma.

• Journal of Physiology & Pathology in Korean Medicine
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• v.25 no.1
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• pp.55-64
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• 2011

The object of this study was to observe the effects of Scutellariae Radix (SR) aqueous extracts on lipopolysaccharide (LPS)-induced rat acute lung injury. Five different dosages of SR extracts were orally administered once a day for 28 days before LPS treatments, and then 5 hours after lipopolysaccharide treatment, all rats were sacrificed. 8 groups, each of 16 rats per group were used in the present study. Changes on the body weights, lung weights, pulmonary transcapillary albumin transit, arterial gas parameters (pH, $PaO_2$ and $PaCO_2$) bronchoalveolar lavage fluid (BALF) protein, lactate dehydrogenase (LDH) and proinflammatory cytokines tumor necrosis factor-${\alpha}$ (TNF-${\alpha}$), interleukin-1${\beta}$ (IL-1${\beta}$) contents, total cell numbers, neutrophil and alveolar macrophage ratios, lung malondialdehyde (MDA), myeloperoxidase (MPO), proinflammatory cytokine TNF-${\alpha}$ and IL-1${\beta}$ contents were observed with histopathology of the lung, changes on luminal surface of alveolus (LSA), thickness of alveolar septum, number of polymorphonuclear neutrophils (PMNs). The results were compared with a potent antioxidant ${\alpha}$-lipoic acid, 60 mg/kg, in which the effects on LPS-induced acute lung injury were already confirmed. The results obtained in this study suggest that over 125 mg/kg of SR extracts showed favorable effects on the LPS-induced acute lung injury, and 250 mg/kg of SR extracts resembling acute respiratory distress syndrome mediated by their antioxidant and anti-inflammatory effects and .as similar to ${\alpha}$-lipoic acid in the present study. Therefore, it is expected that SR will be showed favorable effects on the acute respiratory distress syndrome.

• Journal of Trauma and Injury
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• v.32 no.3
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• pp.136-142
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• 2019

Purpose: Near drowning refers to immediate survival after asphyxia due to submersion or immersion in water, which is a crucial public safety problem worldwide. Acute lung injury or acute respiratory distress syndrome (ARDS) is a common complication of near drowning. The purpose of this study was to investigate the feasibility and effectiveness of noninvasive nasal positive pressure ventilation (NINPPV). Methods: This retrospective study was conducted at a tertiary emergency department. NINPPV was administered for moderate ARDS caused by submersion or immersion in patients who were older than 18 years, from January 2015 to December 2018. We collected the demographic (age, sex, length of hospital stay, and outcome), laboratory (arterial blood gas, lactate, oxygen saturation, partial pressure of oxygen divided by the fraction of inspired oxygen, complete blood count, blood urea nitrogen, and creatinine), and clinical data (acute lung injury index and ventilator failure) of the patients. A statistical analysis was performed using Statistical Package for the Social Sciences version 20.0 for Windows. Results: NINPPV treatment was provided to 57 patients for near drowning, 45 of whom (78.9%) were successfully treated without complications; in 12 (21.1%), treatment was changed to invasive mechanical ventilation within 48 hours due to ARDS or acute kidney injury. NINPPV treatment was successful in 31 (75.6%) out of 41 sea-water near drowning patients. They were more difficult to treat with NINPPV compared with the fresh-water near drowning patients (p<0.05). Conclusions: NINPPV would be useful and feasible as the initial treatment of moderate ARDS caused by near drowning.

• Tuberculosis and Respiratory Diseases
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• v.54 no.5
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• pp.522-531
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• 2003

Background : Hemorrhagic shock and trauma are two of the most common causes of acute lung injury. The activation of cyclooxygenase is one of the important causes of acute lung injury. This study investigated the effect of aspirin, a well-known cyclooxygenase inhibitor, on severe hemorrhage-induced acute lung injury in rats. Methods : The hemorrhagic shock was induced by withdrawing blood; 20ml/kg of B.W., through the femoral artery in 5 min. The mean arterial pressure was recorded through the femoral artery on a polygraph. Results : In the present investigation, the lung tissue myeloperoxidase activity, protein contents and leukocyte counts, in bronchoalveolar lavage fluid, increased significantly 2 and 24 h after the hemorrhage induction. Although the decreased mean arterial pressure spontaneously recovered, acute lung injury occurred after severe hemorrhage. These changes were effectively prevented by a single intravenous injection of aspirin (10 mg/kg of B.W.) 30 min before the hemorrhage. Conclusion : These results suggest that severe hemorrhage-induced acute lung injury is mediated, in part, by the activation of cyclooxygenase. Furthermore, pretreatment of aspirin in acute lung injury-prone patients, or prophylactic treatment of aspirin to the patients with precipitating conditions, could be helpful in the prevention of acute lung injury.

• Tuberculosis and Respiratory Diseases
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• v.40 no.4
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• pp.436-441
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• 1993

Human lung injury caused by the inhalation of nitrogen dioxide($NO_2$) has been reported in occupational situations other than agriculture, including arc welding, production of nitric acid or explosives, and blasting operations. Nitrogen dioxide reacts with the water in the respiratory tract to form nitric acid. The nitrates and nitrites formed from dissociation of nitric acid cause extensive local and systemic tissue damage. We present two cases of acute lung injury due to accidental inhalation of $NO_2$ gas in occupational situtions with a review of the literature.

• Journal of Life Science
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• v.11 no.3
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• pp.259-265
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• 2001

Mercury vapor inhalation-induced acute respiratory failure(ARF) has been reported to be fatal. This study was designed to observe the possible mechanism of inhaled mercury vapor poisoning in the respiratory system. Sixty percent of rats(12/20) exposed to mercury vapor were dead within 72 hours of exposure whereas all the rats(20/20) exposed to mercury vapor combined with dithiothreitol(DTT) vapor survived. The histological observation showed that ARF was a direct cause of the death induced by mercury vapor inhalation, which was significantly circumvented by DTT vapor. Cyclic AMP mediated chloride secretion was inhibited by luminal side but not serosal side sulfhydryl blocking agents (Hf$^{2+}$ $\rho$-chloromercuribenzoic acid or $\rho$-chloromercuriphenyl sulfonic acid) in a dose-dependent manner in a primary cultured rat airway monolayer. The inhibitory component of cAMP induced chloride secretion was completely restored by luminal side DTT(0.5mM). these results suggest that the oxidized form(Hg$^{2+}$) of mercury vapor(Hg0) contribute to ARF and subsequent death. The finding is important as it can provide important information regarding emergency manipulation of ARF patients suffering from by mercury vapor poisoning.ing.

• Tuberculosis and Respiratory Diseases
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• v.70 no.6
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• pp.482-489
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• 2011

Background: Based on the assertion that apocynin diminishes acute lung injury (ALI) by inhibition of NADPH oxidase, the effect of apocynin was tested in interleukin-$1{\alpha}$ (IL-1)-induced ALI in rats. Methods: IL-1 was insufflated into the trachea of Sprague-Dawley rats to induce ALI, and apocynin (8 mg/kg) was given intravenously for inhibition of NADPH oxidase. In addition, we determined whether apocynin inhibited generation of superoxide anions from isolated human neutrophils. Five hours after IL-1 instillation, lung injury parameters, expression of cytosolic phospholipase A2 (cPLA2) by cells from bronchoalveolar lavage (BAL), an index of oxidative stress in lung tissues (${\gamma}$-glutamyltranspeptidase, activity), and ultrastructure of alveolar type II (AT II) cells were evaluated. Results: Apocynin decreased the generation of free radicals from phorbol myristate (PMA)-activated neutrophils in vitro, but did not ameliorate ALI. IL-1 induced enhancement of the expression of cPLA2 on neutrophils was not altered by apocynin. Conclusion: Apocynin induced suppression of the generation of superoxide anions from neutrophils by inhibition of NADPH oxidase does not attenuate IL-1-induced ALI in rats.

• Journal of Trauma and Injury
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• v.24 no.2
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• pp.155-158
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• 2011

Mechanical ventilation is usually the treatment of choice for severe respiratory failure associated with trauma. However, in case of severe hypoxia, mechanical ventilation may not be sufficient for gas exchange in lungs. Patients with Acute Respiratory Distress Syndrome (ARDS) undergo difficulties in oxygen and carbon dioxide exchange. Extracorporeal Membrane Oxygenation (ECMO) is the ideal therapeutic option for those patients with severe traumatic injuries. ECMO allows lungs to reserve their functions and decreases further lung injuries while increasing survival rate at the same time. We report two cases of patients with traumatic ARDS and Multiple Organ Failure including compromised heart function. The preservation of lung function was successful using ECMO therapy.

• Tuberculosis and Respiratory Diseases
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• v.71 no.2
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• pp.97-105
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• 2011

Background: It was hypothesized that the immunomodulating effects of moxifloxacin contribute to ameliorate oleic acid (OA)-induced acute lung injury (ALI) by suppression of cytosolic phospholipase A2 (cPLA2). This was based on observations from experiments on rats associated with neutrophilic respiratory burst, cPLA2 activity, and expressions of cPLA2, $TNF{\alpha}$, and COX-II in the lung. Methods: ALI was induced by intravenous injection of OA in male Sprague-Dawley rats. Five hours after OA injection, protein content in bronchoalveolar lavage (BAL), lung myeloperoxidase (MPO) activity, and numbers of BAL neutrophils were measured. As an index of oxidative stress-induced lung injury, the content of malondialdehyde (MDA) in lung tissues was also determined. Lung histology, immunohistochemistry and determination of activity of cPLA2 in lung tissues were carried out. In addition, Western blotting of $TNF{\alpha}$ and COX-II in lung tissues was performed. Results: The accumulation of neutrophils in the lungs was observed after OA injection. BAL protein was increased along with neutrophilic infiltration and migration by OA. Moxifloxacin decreased all of these parameters of ALI and ameliorated ALI histologically. The increased malondialdehyde (MDA) in the lung by OA was also decreased by moxifloxacin. Moxifloxacin not only suppressed cPLA2 expression in the lungs and neutrophils but also decreased cPLA2 activity in lung tissues of rats given OA. The enhanced expressions of $TNF{\alpha}$ and COX-2 in the lung tissues of rats given OA were also suppressed by moxifloxacin. Conclusion: Moxifloxacin inhibited cPLA2 and down-regulated $TNF{\alpha}$ and COX-2 in the lungs of rats given OA, which resulted in the attenuation of inflammatory lung injury.

• Journal of Environmental Health Sciences
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• v.38 no.6
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• pp.451-459
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• 2012

Background: In Korea, a healthy 36-year-old man developed acute interstitial pneumonitis soon after inhaling a waterproofing spray which he had applied at home to his outdoor jacket. Objectives: The objectives of this study were to review cases of varying degrees of respiratory toxicity and poisoning in connection with the use of waterproofing spray and summarize major reasons for cases of poisoning. Methods: We searched articles reporting on a combination of a waterproofing agent and/or respiratory symptoms, including acute respiratory syndrome, lung injury, pneumonia, pulmonary toxicity, and respiratory disease. Results: We reviewed a number of cases of varying degrees of respiratory toxicity and poisoning resulting from inhalation of waterproofing spray containing fluorocarbon co-polymer, solvents and propellants reported in a variety of countries. The literature searches concluded that among the ingredients of waterproofing agents, fluorinated polymer may cause acute respiratory health effects. Conclusion: Environmental policy should be implemented in order to prevent consumers from using household and industrial products including waterproofing agents. In addition, a national surveillance system should be created to collect cases of poisoning caused by the use of consumer products.