• Tuberculosis and Respiratory Diseases
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• v.52 no.4
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• pp.355-366
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• 2002

Background : The heat shock protein (HSP) 70 families are known to protect cells against the irreversible tissue injury induced by stress and to induce the recovery of cell function during stress. Heat pretreatment was reported to decrease the acute lung injury (ALI) of rats induced by lipopolysaccharide (LPS). However, the role of heat shock with LPS co-treatmenton ALI is unclear. The purpose of this study was to investigate the effect of heat treatment, which was given immediately after the beginning of ALI induced by LPS intratracheally administered in rats. Methods : Either saline (saline group) or LPS was intratracheally instilled without heat treatment (LPS group). In addition, heat was conducted 18 hours prior to the instillation of LPS (pre-treatment group) and conducted immediately after instillation of LPS (co-treatment group). Six hours after the LPS or saline treatment, blood, bronchoalveolar lavage (BAL) fluid and lung tissue samples were obtained. The myeloperoxidase (MPO) activity and the heat shock protein expression in the lung tissue, the differential counts of the polymorphonuclear leukocytes (PMN) in the BAL fluids, and the LDH, protein, $IL-1{\beta}$, $TNF-{\alpha}$ and IL-10 levels in BAL fluid and serum were measured. Results : 1) The MPO activity, the differential PMN counts in the BAL fluid, BAL fluid and serum cytokines were higher in the LPS, the heat pre-treatment and co-treatment group than those of the saline group (p value <0.05). 2) The MPO activity and the protein level in the BAL fluid from the heat co-treatment group were similar to those of the LPS group. 3) The serum $TNF-{\alpha}$ level of the heat co-treatment group was significantly higher than that of the LPS group (p=0.01). Conclusion : Heat shock response administered immediately after a LPS instillation did not attenuate the ALI in this model.

• Tuberculosis and Respiratory Diseases
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• v.48 no.4
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• pp.478-486
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• 2000

Background : In acute lung injury, alveolar macrophages play a pivotal role in the inflammatory process during the initiation phase and in the reconstruction and fibrosis process during the later phase. Recently, it has been proven that alveolar macrophages are constituted by morphologically, biochemically and immunologically heterogenous cell subpopulations. The possibility of alterations to these characteristics of the alveolar macrophage population during lung disease has been raised. To investigate such a possibility a hyperoxic rat lung model was made to check the distributional and morphological changes of rat alveolar macrophage subpopulation in acute hyperoxic lung injury. Method : Alveolar macrophage were lavaged from normal and hyperoxic lung injury rats and separated by discontinuous gradients of percoll. After cell counts of each density fraction were accessed, the morphomeric analysis of alveolar macrophages was performed on cytocentrifuged preparations by transmission electron micrograph. Result : 1. The total alveolar macrophage cell count significantly increased up to 24 hours after hyperoxic challenge (normal control group $171.6{\pm}24.1{\times}10^5$, 12 hour group $194.8{\pm}17.9{\times}10^5$, 24 hour group $207.6{\pm}27.1{\times}10^5$, p<0.05). oHoHH However the 48 hour group ($200.0{\pm}77.8{\times}10^5$) did not show a significant difference. 2. Alveolar septal thickness significantly increased up to 24 hours after hyperoxic challenge(normal control group $0.7{\pm}0.2{\mu}m$, 12 hour group $1.5{\pm}0.4{\mu}m$, 24 hour group $2.3{\pm}0.4{\mu}m$, p<0.05). However the 48 hour group did not show further change ($2.5{\pm}0.4{\mu}m$). Number of interstitial macrophage markedly increased at 24 hour group. 3. Hypodense fraction(fraction 1 and fraction 2) of alveolar macrophage showed a significant increase following hyperoxic challenge ($\beta=0.379$.$\beta=0.694$. p<0.05) ; however, fraction 3 was rather decreased following the hyperoxic challenge($\beta=0.815$. p<0.05), and fraction 4 showed an irregular pattern. 4. Electron microscopic observation of alveolar macrophage from each fraction revealed considerable morphologic heterogeneity. Cells of the most dense subfraction(fraction 4) were small, round, and typically highly ruffled with small membrane pseudopods. Cells of the least dense fraction (fraction 1) were large and showed irregular eccentric nucleus and high number of heterogenous inclusions. Conclusion : In conclusion, these results suggest that specific hypodense alveolar macrophage subpopulation may play a an important role in an acute hyperoxic lung injury model But further study, including biochemical and immunological function of these subpopulations, is needed.

• Journal of the Korean Society of Radiology
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• v.82 no.6
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• pp.1581-1588
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• 2021

Electronic cigarette (e-cigarette) or vaping product use-associated lung injury (EVALI) has emerged as a social issue as e-cigarette use is rapidly increasing worldwide and is related to many deaths in the United States. To our knowledge, this is the first case report of EVALI in South Korea of a 24-year-old man with acute respiratory symptoms and a history of e-cigarette use. Chest CT revealed diffuse bilateral ground-glass opacities with subpleural sparing, airspace consolidation, and centrilobular micronodules as typical patterns of EVALI with organizing pneumonia and diffuse alveolar damage. Infection was excluded with meticulous laboratory examinations, and the patients' illnesses were not attributed to other causes. EVALI was diagnosed by meeting the diagnostic criteria with consistent clinico-radiologic findings through a multidisciplinary approach. Radiologists should have good knowledge of EVALI radiologic findings and play a cardinal role in the proper diagnosis and management of EVALI.

• Tuberculosis and Respiratory Diseases
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• v.55 no.2
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• pp.188-197
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• 2003

Background : Smoke inhalation injury is an important determinant of mortality in burn patients. The early detection of inhalation injury in burn patients is important because the incidence of respiratory failure after inhalation injury was known to be high, with hypoxemia, pneumonia, and prolonged ventilatory support being commonplace. Acute carbon monoxide poisoning was one feature of smoke inhalation. The purpose of our study were to investigate the clinical characteristics of burn patients whose initial arterial carboxyhemoglobin (COHb) level had been elevated, to assess the clinical impact of COHb for smoke inhalation injury. Methods : Among 1,416 burn patients had been admitted at our institution from August 1, 2001 to July 31, 2002, 39 patients whose initial arterial COHb level have been more than 5% were included. We compared clinical scoring system for inhalation injury, percent total body surface area (%TBSA) burn, initial chest X-ray findings, APACHE II scores and SAPS II scores between survivors (n=27) and non-survivors (n=12) retrospectively. Results : COHb level were 9.7(5.71% and 10.3(8.81% in survivors and in non-survivors (p>0.05). Mean %TBSA burn of survivors and non-survivors were $16.6{\pm}17.8%$ and $60.7{\pm}28.8%$ (p<0.001). We did not find any difference in clinical scoring system, initial chest X-ray findings in survivors and in non-survivors. But %TBSA burn, APACHE II and SAPS II scores were high in non-survivors than in survivors significantly. Important factors associated with death were %TBSA burn, APACHE II scores, SAPS II scores, and the most important factor in predicting mortality was %TBSA burn. Conclusion : Burn patients with elevated initial arterial COHb level showed poor prognosis, but further study may be performed to know that the effect of COHb on prognosis in burn patients accompanying smoke inhalation.

• Journal of Trauma and Injury
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• v.24 no.1
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• pp.12-17
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• 2011

Purpose: A rib fracture secondary to blunt thoracic trauma continues to be an important injury with significant complications. Unfortunately, there are no definite treatment guidelines for severe multiple rib fractures. The purpose of this study was to evaluate the result of early operative stabilization and to find the risk factors of surgical fixation in patients with bilateral multiple rib fractures or flail segments. Methods: From December 2005 to December 2008, the medical records of all patients who underwent operative stabilization of ribs for severe multiple rib fractures were reviewed. We investigated patients' demographics, preoperative comorbidities, underlying lung disease, chest trauma, other associated injuries, number of surgical rib fixation, combined operations, perioperative ventilator support, and postoperative complications to find the factors affecting the mortality after surgical treatment. Results: The mean age of the 96 patients who underwent surgical stabilization for bilateral multiple rib fractures or flail segments was 56.7 years (range: 22 to 82 years), and the male-to-female ratio was 3.6:1. Among the 96 patients, 16 patients (16.7%) underwent reoperation under general or epidural anesthesia due to remaining fracture with severe displacement. The surgical mortality of severe multiple rib fractures was 8.3% (8/96), 7 of those 8 patients (87.5%) dying from acute respiratory distress syndrome or sepsis. And the other one patient expired from acute myocardial infarction. The risk factors affecting mortality were liver cirrhosis, chronic obstructive pulmonary disease, concomitant severe head or abdominal injuries, perioperative ventilator care, postoperative bleeding or pneumonia, and tracheostomy. However, age, number of fractured ribs, lung parenchymal injury, pulmonary contusion and combined operations were not significantly related to mortality. Conclusion: In the present study, surgical fixation of ribs could be carried out as a first-line therapeutic option for bilateral rib fractures or flail segments without significant complications if the risk factors associated with mortality were carefully considered. Furthermore, with a view of restoring pulmonary function, as well as chest wall configuration, early operative stabilization of the ribs is more helpful than conventional treatment for patients with severe multiple rib fractures.

• Journal of Chest Surgery
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• v.45 no.4
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• pp.236-241
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• 2012

Background: Prolonged usage of extracorporeal membrane oxygenation (ECMO) may induce multi-organ failure. This study is aimed to evaluate prognostic factors in the patients with ECMO. Also, the prognosis of ECMO with Kidney Injury Network Scoring system is studied. Materials and Methods: From May 2005 to July 2011, 172 cases of ECMO were performed. The cases of perioperative use of ECMO were excluded. Renal failure patient and younger than 15 years old one were also excluded. As a result, 26 cases were enrolled in this study. Male patients were 15 (57.7%), and mean age was $56.57{\pm}17.03$ years old. Demographic data, ECMO parameters, weaning from ECMO, and application of continuous renal replacement therapy are collected and Acute Kidney Injury Network (AKIN) scores were evaluated just before ECMO and day 1, day 2 during application of ECMO. Results: Venoarterial ECMO was applied in 22 cases (84.6%). The reasons for applications of ECMO were cardiac origin in 21 (80.8%), acute respiratory distress syndrome in 4, and septic shock in 1 case. Successful weaning from ECMO was achieved in 15 cases (57.7%), and survival discharge rate was 9 cases (34.6%). Mean duration of application of ECMO was $111.39{\pm}54.06$ hours. In univariate analysis, myocarditis was independent risk factors on weaning failure. Using the receiver operating characteristic curve, level of hemoglobin on 24 hours after ECMO, and base excess on 48 hours after ECMO were showed more than 0.7. AKIN score was not matched the prognosis of the patients with ECMO. Conclusion: In our study, the prognosis of the patients with myocarditis was poor. Hemoglobin level at first 24 hours, and degree of acidosis at 48 hours were useful methods in relating with prognosis of ECMO. AKIN scoring system was not related with the prognosis of the patients. Further study for prognosis and organ injury during application ECMO may be needed.

• Tuberculosis and Respiratory Diseases
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• v.44 no.6
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• pp.1332-1342
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• 1997

Background : Acute pulmonary injury by paraquat are caused by multiple mechanisms including direct injury with oxygen free radicals and several mediators released from inflammatory cells. In order to clarify whether vitamin E could reduce tissue damages induced by intraperitoneal administration of paraquat and to investigate the pathogenetic mechanisms of paraquat-induced pulmonary injury, vitamin E as a free radical scavenger was administered. Method : Rats were divided into three groups (group 1 : control, group 2 : paraquat treated group, group 3 : paraquat and vitamin E treated group). Animals were sacrificed on day 1, day 2, day 3, and day 8 after the administration of saline, paraquat, or paraquat/vitamin E. Results : Treatment with vitamin E decreased the death rate of rats treated with paraquat. Comparing with control group ($1.37{\times}10^6/ml$), mean total cell counts recovered from the lavage fluid from animals treated with paraquat($1.65{\times}10^6/ml$) were increased(p=0.06). Magnitudes of increment of the total cell counts on the Day 8 in the vitamin E treated group were smaller than those of the animals treated with paraquat alone. The neutrophils began to appear in significant amounts in the lavage fluid on Day 8 after the administration of paraquat(37.0+12.7%). A significant decreasing neutrophil concentration at Day 8 was observed in the paraquat/vitamin E treated group(20.6+13.4%). Histologically the degree of pulmonary fibrosis was most prominent in the paraquat treated group while diffuse alveolar damage was continuously observed in the paraquat/vitamin E treated group and extensive interstitial lymphocytic infiltration was seen in the paraquat/vitamin E treated group. The paraquat/vitamin E treated group showed the less histologic changes. Conclusion : In this study vitamin E acting as a scavenger of neutrophil-derived free radicals and suppressant of lipid peroxidation, seemed to be the effective antioxidant in the inhibition of paraquat-induced pulmonary injury.

• Journal of Life Science
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• v.19 no.7
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• pp.878-885
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• 2009

Serum ferritin levels are elevated in subjects with acute lung injury (ALI), and abnormalities in plasma and lung iron chemistry have also been demonstrated in ALI and acute respiratory distress syndrome (ARDS). Stress-inducible heme oxygenase-1 (HO-1), as well as ferritin, had shown anti-inflammatory actions. Biomarkers for early detection in patients who are likely to develop ARDS would give several therapeutic chances to the patients. In order to verify the predictability in severe hemorrhage-induced ALI in rats, we measured serum ferritin and HO-1 concentrations before and after hemorrhage. Severe hemorrhages significantly increased the number of leukocytes in bronchoalveolar lavage (BAL) fluid and lung tissue myeloperoxidase activity. Both serum ferritin and HO-1 levels increased following hemorrhage, but ferritin levels were elevated earlier than HO-1. In BAL cell immunohistochemical studies, ferritin and HO-1 expressions increased after hemorrhage and localized in the cytoplasm of leukocytes. These findings suggest that inflammatory leukocytes in BAL fluid can secrete ferritin and HO-1, and serum ferritin levels might be more valid factor in predicting ARDS than HO-1 levels in hemorrhage-induced ALI.

• Tuberculosis and Respiratory Diseases
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• v.60 no.4
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• pp.451-463
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• 2006

Background : Reactive oxygen species (ROS) take center stage as executers in ventilator-induced lung injury (VILI). The protein with DNA-damage scanning activity, poly (ADP-ribose) polymerase-1 (PARP1), signals DNA rupture and participates in base-excision repair. Paradoxically,overactivation of PARP1 in response to massive genotoxic injury such as ROS can induce cell death through ${\beta}$ -nicotinamide adenine dinucleotide ($NAD^+$) depletion, resulting in inflammation. The purpose of this study is to investigate the role of PARP1 and the effect of its inhibitor in VILI. Methods : Forty-eight male C57BL/6 mice were divided into sham, lung protective ventilation(LPV), VILI, and PARP1 inhibitor (PJ34)+VILI (PJ34+VILI) groups. Mechanical ventilator setting for the LPV group was $PIP\;15cmH_2O$ + $PEEP\;3cmH_2O$ + RR 90/min + 2 hours. The VILI and PJ34+VILI groups were ventilated on a setting of $PIP\;40cmH_2O$ + $PEEP\;0cmH_2O$ + RR 90/min + 2 hours. As a PARP1 inhibitor for the PJ34+VILI group, 20 mg/Kg of PJ34 was treated intraperitoneally 2 hours before mechanical ventilation. Wet-to-dry weight ratio and acute lung injury (ALI) score were measured to determine the degree of VILI. PARP1 activity was evaluated by using an immunohistochemical method utilizing biotinylated NAD. Myeloperoxidase (MPO) activity and the concentration of inflammatory cytokines such as tumor necrosis factor $(TNF)-{\alpha}$, interleukin $(IL)-1{\beta}$, and IL-6 were measured in bronchoalveolar lavage fluid (BALF). Results : In the PJ34+VILI group, PJ34 pretreatment significantly reduced the degree of lung injury, compared with the VILI group (p<0.05). The number of cells expressing PARP1 activity was significantly increased in the VILI group, but significantly decreased in the PJ34+VILI group (p=0.001). In BALF, MPO activity, $TNF-{\alpha}$, $IL-1{\beta}$, and IL-6 were also significantly lower in the PJ34+VILI group (all, p<0.05). Conclusion : PARP1 overactivation plays a major role in the mechanism of VILI. PARP1 inhibitor prevents VILI, and decreases MPO activity and inflammatory cytokines.

• Tuberculosis and Respiratory Diseases
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• v.61 no.4
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• pp.374-383
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• 2006

Background: Ethyl pyruvate (EP) is a derivative of pyruvate that has recently been identified by both various in vitro and in vivo studies to have antioxidant and anti-inflammatory effects. The aim of this study was to determine the effect of EP on lipopolysaccharide (LPS)-induced acute lung injury (ALI). Methods: 5 weeks old, male BALB/c mice were used. ALI was induced by an intratracheal instillation of LPS 0.5mg/Kg/$50{\mu}L$ of saline. The mice were divided into the control, LPS, EP+LPS, and LPS+EP groups. In the control group, balanced salt solution was injected intraperitoneally 30 minutes before or 9 hours after the intratracheal instillation of saline. In the LPS group, a balanced salt solution was also injected intraperitoneally 30 minutes before or 9 hours after instillation the LPS. In the EP+LPS group, 40mg/Kg of EP was injected 30 minutes before LPS instillation. In the LPS+EP group, 40mg/Kg of EP was injected 9 hours after LPS instillation. The TNF-$\alpha$ and IL-6 concentrations in the bronchoalveolar lavage fluid (BALF), and that of NF-$\kappa$B in the lung tissue were measured in the control, LPS and EP+LPS groups at 6 hours after instillation of saline or LPS, and the ALI score and myeloperoxidase (MPO) activity were measured in all four groups 24 and 48 hours after LPS instillation, respectively. Results: The TNF-$\alpha$ and IL-6 concentrations were significantly lower in the EP+LPS group than in the LPS group (p<0.05). The changes in the concentration of these inflammatory cytokines were strongly correlated with that of NF-$\kappa$B (p<0.01). The ALI scores were significantly lower in the EP+LPS and LPS+EP groups compared with the LPS group (p<0.05). In the EP+LPS group, the MPO activity was significantly lower than the LPS group (p=0.019). Conclusion: EP, either administered before or after LPS instillation, has protective effects against the pathogenesis of LPS-induced ALI. EP has potential theurapeutic effects on LPS-induced ALI.