• Tuberculosis and Respiratory Diseases
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• v.48 no.4
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• pp.513-521
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• 2000

Background : TNF may play an important role(central mediator) in the development of an acute respiratory distress syndrome. Since TNF induced lung injury in the acute respiratory distress syndrome and abnormalities in surfactant function have been described in acute respiratory distress syndrome, the authors investigated the effects of TNF on the regulation of surfactant protein A, B and C mRNA accumulation. Methods : The effects of TNF on gene expression of surfactant protein A, B, and C were analyzed using filter hybridization, 12 and 24 hours after intravenous injection of TNF in rats. Results : 1. The accumulation of SP-A mRNA in the TNF treated group (12 and 24 hours after TNF injection) was significantly decreased by 22.9% and 27.4%, respectively, compared to the control group (P<.025, P<.025). 2. The accumulation of SP-B mRNA in 24 hours after TNF treated group was significantly decreased by 20.5% compared to that of the control group(P<.01). 3. The accumulation of SP-C mRNA in 12 hours after TNF treated group was significantly decreased by 31% the compared to that of the control group(P<.01). Conclusions : These findings indicate the marked inhibitory effects of tumor necrosis factor on surfactant proteins expression in vivo. This finding. in turn, supports the idea of inhibitory effects of tumor necrosis factor on surfactant proteins expression as it relates to pathogenesis of acute respiratory distress syndrome.

• 대한상한금궤의학회지
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• v.13 no.1
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• pp.21-44
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• 2021

Objective : This study aimed to assess the preventive effect of Bupleuri Radix aqueous extracts (BR) and red koji-fermented BR (fBR) in lipopolysaccharide (LPS)-induced acute lung injury in a rat model. Methods : Rats were administered 30, 60, or 120 mg/kg/day of fBR for 28 days before LPS treatments. All rats were sacrificed 5 h after LPS treatment (500 ㎍/head, intratracheal instillation). Body weights, lung weights, pulmonary transcapillary albumin transit, arterial gas parameters (pH, partial pressure [Pa] of O2, PaCO2), bronchoalveolar lavage fluid (BALF) protein, lactate dehydrogenase (LDH), tumor necrosis factor-α (TNF-α), interleukin-1β (IL-1β), total cell numbers, neutrophil/alveolar macrophage ratios, lung malondialdehyde (MDA), and myeloperoxidase (MPO) were measured. In addition, histopathological changes including the luminal surface of alveoli (LSA), thickness of alveolar septum, and number of polymorphonuclear neutrophils (PMNs) were checked. Results : LPS injection led to increases in lung weights, pulmonary transcapillary albumin transit, BALF protein, LDH, TNF-α and IL-1β contents, total cells, neutrophil and alveolar macrophage ratios, lung MDA, MPO, alveolar septum thickness, and PMNs, and decreases in PaCO2 and pH of arterial blood and LSA. However, these LPS-induced acute lung injuries were inhibited by pretreatment of 30, 60, and 120 mg/kg of fBR. The most favorable effects were seen with 30 mg/kg fBR as compared with 60 mg/kg of α-lipoic acid and BR. Conclusions : fBR showed preventive effects on LPS-induced acute lung injury, which resembles acute respiratory distress syndrome. The mechanisms of action were likely via antioxidant and anti-inflammatory means.

• The Korean Journal of Physiology and Pharmacology
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• v.2 no.5
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• pp.617-628
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• 1998

In order to understand the pathogenetic mechanism of adult respiratory distress syndrome (ARDS), the role of phospholipase A2 (PLA2) in association with oxidative stress was investigated in rats. $Interleukin-1{\alpha}\;(IL-1,\;50\;{\mu}g/rat)$ was used to induce acute lung injury by neutrophilic respiratory burst. Five hours after IL-1 insufflation into trachea, microvascular integrity was disrupted, and protein leakage into the alveolar lumen was followed. An infiltration of neutrophils was clearly observed after IL-1 treatment. It was the origin of the generation of oxygen radicals causing oxidative stress in the lung. IL-1 increased tumor necrosis factor (TNF) and cytokine-induced neutrophil chemoattractant (CINC) in the bronchoalveolar lavage fluid, but mepacrine, a PLA2 inhibitor, did not change the levels of these cytokines. Although IL-1 increased PLA2 activity time-dependently, mepacrine inhibited the activity almost completely. Activation of PLA2 elevated leukotriene C4 and B4 (LTC4 and LTB4), and 6-keto-prostaglandin $F2{\alpha}\;(6-keto-PGF2{\alpha})$ was consumed completely by respiratory burst induced by IL-1. Mepacrine did not alter these changes in the contents of lipid mediators. To estimate the functional changes of alveolar barrier during the oxidative stress, quantitative changes of pulmonary surfactant, activity of gamma glutamyltransferase (GGT), and ultrastructural changes were examined. IL-1 increased the level of phospholipid in the bronchoalveolar lavage (BAL) fluid, which seemed to be caused by abnormal, pathological release of lamellar bodies into the alveolar lumen. Mepacrine recovered the amount of surfactant up to control level. IL-1 decreased GGT activity, while mepacrine restored it. In ultrastructural study, when treated with IL-1, marked necroses of endothelial cells and type II pneumocytes were observed, while mepacrine inhibited these pathological changes. In histochemical electron microscopy, increased generation of oxidants was identified around neutrophils and in the cytoplasm of type II pneumocytes. Mepacrine reduced the generation of oxidants in the tissue produced by neutrophilic respiratory burst. In immunoelectron microscopic study, PLA2 was identified in the cytoplasm of the type II pneumocytes after IL-1 treatment, but mepacrine diminished PLA2 particles in the cytoplasm of the type II pneumocyte. Based on these experimental results, it is suggested that PLA2 plays a pivotal role in inducing acute lung injury mediated by IL-1 through the oxidative stress by neutrophils. By causing endothelial damage, functional changes of pulmonary surfactant and alveolar type I pneumocyte, oxidative stress disrupts microvascular integrity and alveolar barrier.

• Tuberculosis and Respiratory Diseases
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• v.71 no.6
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• pp.470-475
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• 2011

So far more than 350 drugs have been reported to be the cause for lung injury and the incidence tends to increase. Although infiltrative lung disease is the most common pattern of drug-induced lung injury, it can appear in the form of alveolar changes, vasculitis and other injury. Herbal medicine also has been known as a cause for interstitial pneumonitis, but it is difficult to identify the key herbal medicine because of the complex components of the contents. Till date, there is no report of pneumonitis caused by golden thread. Here we report a case of a 54-year-old male who developed interstitial pneumonitis with acute liver injury caused by herbal medicine made from golden thread.

• Tuberculosis and Respiratory Diseases
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• v.62 no.3
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• pp.223-226
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• 2007

Tetrafluoroethylene is a colorless gas that can be used to synthesize a variety of fluoride compounds by polymerization (e.g., Teflon). Fluoride compounds have many applications in industry. There are several reports of inhalation injury from the pyrolytic product of fluoride compounds. When the polymer is heated under the conditions of inadequate ventilation, the fumes can cause polymer fume fever or pulmonary edema which manifested as symptoms such as fever, chill, profuse sweating, cough and dyspnea. However there are no reports of a direct lung injury caused by tetrafluoroethylene. We report a case of a 27-year-old male presented with acute lung injury after inhaling concentrated tetrafluoroethylene. He complained of cough and dyspnea after the accidental inhalation of tetrfluoroethylene at his workplace. The symptoms improved without any complications after conservative treatment with oxygen and steroid.

• Tuberculosis and Respiratory Diseases
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• v.60 no.1
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• pp.83-91
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• 2006

Background : For unknown reasons, the serum ferritin concentrations are higher in patients with acute lung injury. A pretreatment with aspirin reduces the acute lung injury in rats subjected severe hemorrhage, and increases the rate of ferritin synthesis in vitro. This study investigated the effect of aspirin on the serum ferritin changes in rats subjected to severe hemorrhage. Methods : Hemorrhagic shock was induced by withdrawing blood (20 ml/kg of B.W.) through the femoral artery for 5 min. The rats were pretreated with aspirin (10 mg/kg, i.v.) 30 min before hemorrhage. Results : The protein content and leukocyte count in the bronchoalveolar lavage fluid, lung tissue myeloperoxidase activities were significantly higher after hemorrhage. The aspirin pretreatment prevented these changes. The serum and lavage fluid ferritin concentrations were elevated higher after hemorrhage. These were also attenuated by the aspirin pretreatment. Conclusion : The changes in the serum and lung lavage ferritin level might be closely related to the severity of hemorrhage-induced acute lung injury. Therefore, the serum and lavage ferritin concentrations can be a useful biomarker for patients with precipitating conditions.

• Tuberculosis and Respiratory Diseases
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• v.45 no.4
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• pp.888-895
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• 1998

Malaria is one of the most common infectious diseases in the world. Plasmodium falciparum, accounting for nearly all malaria mortality, kills an estimated 1 to 2 million persons yearly and has several features that make it deadlist of malarias. While cerebral malaria is the most common presentation of severe disease, acute lung injury associated with malaria is uncommon but serious and fatal complication. We report two cases of severe malaria with ARDS and multi-organ failure. All two patients traveled to foreign countries, Kenya, Papua New Guinea where choroquine-resistant malaria is distributed. The first case, which developed cerebral malaria, hypoglycemia, multi-organ failure, and ARDS, treated with quinine and mechanical ventilator, but expired due to oxygenation failure. Autopsy showed acute necrotizing infiltration, diffuse eosinophilic fibrinoid deposits along the alveolar space, and alveolar macrophage with malaria pigment The second case also developed multi-organ failure, followed by ARDS, and was treated with quinine, exchange transfusion, plasmapheresis, and mechanical ventilator. He recovered with residual restrictive lung change after treatment.

• Tuberculosis and Respiratory Diseases
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• v.72 no.2
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• pp.177-181
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• 2012

Activated charcoal is an inert substance and it is used in standard therapy in patients with acute intoxication. Charcoal has some side effects such as pulmonary aspiration, gastrointestinal complications, and electrolyte abnormalities. Although aspiration of charcoal is a rare complication, it can cause fatal sequelae. We report a 69-year old man who developed acute respiratory failure associated with charcoal aspiration after management of glyphosate poisoning. The patient was drowsy and suffered severe vomiting during transport to our hospital. On arrival, acute respiratory failure was observed due to charcoal aspiration, but the clinical state was improved with repeated bronchoscopy with a bronchoalveolar lavage (BAL). We presumed that the aspirated charcoal was an important factor in evoking a lung injury. Early bronchoscopy with a BAL might be an effective method for eliminating charcoal from the lung, especially in the case of a large amount of aspiration, and be helpful in decreasing respiratory failure due to charcoal aspiration.

• Journal of Society of Preventive Korean Medicine
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• v.15 no.1
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• pp.49-69
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• 2011

Objective : The object of this study was to observe the effects of Lonicerae Flos (LF) aqueous extracts on lipopolysaccharide (LPS)-induced rat acute lung injury. Method : Five different dosages of LF extracts were orally administered once a day for 28 days before LPS treatments, and then all rats were sacrificed after 5 hour-treatment of LPS. Eight groups of 16 rats each were used in the present study. The following parameters caused by LPS treatment were observed ; 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 cytokines TNF-${\alpha}$ and IL-$1{\beta}$ contents. In addition, the histopathologic changes were observed in the lung in terms of luminal surface of alveolus, thickness of alveolar septum, number of polymorphonuclear neutrophils. Result : As results of LPS-injection, dramatical increases in lung weights, pulmonary transcapillary albumin transit increases, increases in $PaCO_2$, decreases in pH of arterial blood and $PaO_2$, increases of BALF protein, LDH, TNF-${\alpha}$ and IL-$1{\beta}$ contents, total cells, neutrophil and alveolar macrophage ratios, TNF-${\alpha}$ and IL-$1{\beta}$ contents increases were detected with decreases in LSA and increases of alveolar septum and PMNs numbers, respectively as compared with intact control. These are means that acute lung injuries (resembling acute respiratory distress syndrome) are induced by treatment of LPS mediated by inflammatory responses, oxidative stress and related lipid peroxidation in the present study. However, these LPS-induced acute lung injuries were inhibited by 28 days continuous pretreatment of 250 and 500mg/kg of LF extracts. Because of lower three dosages of LF treated groups, 31.25 and 62.5 and 125mg/kg did not showed any favorable effects as compared with LPS control, the effective dosages of LF in LPS-induced acute lung injuries in the present study, is considered as about 125mg/kg. The effects of 250mg/kg of LF extracts showed almost similar effects with ${\alpha}$-lipoic acid 60mg/kg in preventing LPS-induced acute lung injuries. Conclusion : It seems that LF play a role in protecting the acute respiratory distress syndrome caused by LPS.

• Tuberculosis and Respiratory Diseases
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• v.38 no.4
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• pp.357-371
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• 1991

To identify the pathogenetic role of reactive oxygen free radical-induced oxidation reaction in endotoxin-induced acute lung injury, we infused endotoxin into 8 domestic pigs; endotoxin only (n=3), pretreatment with dimethylthiourea (DMTU) (n=5). We observed the sequential changes in hemodynamic parameters, the concentration of plasma oxidized glutathione (GSSG) in pulmonary arterial and venous blood, and albumin content in bronchoalveolar lavage fluid (BALF). The results were as follows. 1) While cardiac output decreased, mean pulmonary arterial pressure, pulmonary vascular resistance, and alveolar-arterial oxygen difference increased over phase 1 (0-2 hr) and phase 2 (2-4.5 hr) by endotoxin, DMTU attenuated the above changes only during phase 2. 2) While the concentration of plasma GSSG increased significantly by endotoxin during phase 2, there were no significant differences between pulmonary arterial and venous GSSG contents during both phases. The increase in plasma GSSG content was attenuated by DMTU. 3) The content of BALF albumin was significantly lower in DMTU group than that of endotoxin group. These results suggest that reactive oxygen free radical-induced oxidation reaction may have an important pathogenetic role in endotoxin-induced acute lung injury in pigs, which seems to be greater during phase 2 rather than phase 1.