Background: Regardless of its causes, acute lung injury is characterized pathophysiologically by increased pulmonary arterial pressure and the protein-rich edema. Many inflammatory mediators are known to be involved in the pathogenesis of acute lung injury, including oxygen free radicals (OFR). But the changes in pulmonary capillary pressure in the OFR-induced acute lung injury is not clear. While the pulmonary edema characterized by the movement of fluid and solutes is dependent on the pressure gradient and the alveolar-capillary permeability, the role of pulmonary capillary pressure in the development of pulmonary edema is also not well understood. Method: Male Sprague-Dawley rats were divided into 5 groups: normal control (n=5), xanthine/xanthine oxidase (X/XO)-treated group (n=7), catalase-pretreated group (n=5), papaverine-pretreated group (n=7), and indomethacin-pretreated group (n=5). In isolated perfused rat lungs, the sequential changes in pulmonary arterial pressure, pulmonary capillary pressure by double occlusion method, and lung weight as a parameter of pulmonary edema were determined. Results: Pulmonary arterial pressure and pulmonary capillary pressure were increased by X/XO. This increase was significantly attenuated by catalase and papaverine, but indomethacin did not prevent the X/XO-induced increase. Lung weight gain was also observed by X/XO perfusion. It was prevented by catalase. Papaverine did not completely block the increase, but significantly delayed the onset. Indomethacin had no effect on the increase in lung weight. Conclusion: These data suggest that increased pulmonary capillary pressure by OFR may aggravate pulmonary edema in the presence of increased alveolar-capillary permeability and this may not be mediated by cyclooxygenase metabolites.
Extracorporeal circulation leads to functional disorder and structural damage of organs, especially hematologic and pulmonary system, mainly by sequestration of neutrophils and deposition of macrophages at lung. Then, proteases are secreted, which insult vascular basement membrane of pulmonary capillary and alveolar septa of the lung. Among these, the most important protease at lung is elastase, because major component of lung is elastin. For prevention of lung injury, inactivators or antidotes to elastase should be necessary and Alpha 1-Proteinase Inhibitor is the elastase inactivator. Clinical experimental study was carried out to investigate the immediate postoperative change of serum Alpha 1-PI level following cardiopulmonary bypass for 20 heart cases [congenital 16 cases, acquired 4 cases] and 10 control [subtotal gastrectomy] cases. Also preliminary study was performed for 31 cases of open heart patients. The results were as follows: l. Immediate postoperative serum levels of Alpha 1-PI was significantly decreased at open heart surgery group [P< 0.005], but not decreased at control group. 2. There were no significant difference in change of serum Alpha 1-PI level between and membrane and bubble oxygenator group.Z 3. There were no significant difference in changes of serum Alpha 1-PI level between CHD and AHD. Alpha 1-PI is consumed at lung during cardiopulmonary bypass and increase after operation compensatedly and protect multiple organic damage especially lung. Therefore, Alpha 1-PI can be indicator for evaluation of prevention and treatment of pump-lung syndrome.
Objective: To investigate the protective effect of quercetin on radiation induced lung injury (RILI) and related mechanisms. Materials and Methods: Mice treated with radiation and/or quercetin were sacrificed at 1-8 weeks after irradiation under anesthesia. Lung tissues were collected for histological examination. Immunohistochemistry (IHC) and Western blotting were performed to detect the protein expression of nuclear factor-${\kappa}B$ ($NF-{\kappa}B$) and Mitogen-activated protein kinases (MAPK) pathway. Results: Hematoxylin and eosin (HE) staining showed that radiation controls displayed more severe lung damage than quercetin groups, either high or low dose. Results of IHC and Western blotting demonstrated the expression level of $NF-{\kappa}B$ to be decreased and that of an inhibitor of $NF-{\kappa}B$ ($I{\kappa}b-{\alpha}$) to be increased by the quercetin intervention compared with the radiation control group. Numbers of JNK/SAPK, p38 and p44/p42 positive inflammatory cells were decreased in the radiation+quercetin injection group (P<0.05). Conclusions: Quercetin may play a radio-protective role in mice lung via suppression of $NF-{\kappa}B$ and MAPK pathways.
Huh, Jin Won;Hong, Sang Bum;Kim, Mi Jung;Lim, Chae-Man;Koh, Younsuck
Tuberculosis and Respiratory Diseases
/
v.62
no.2
/
pp.105-112
/
2007
Background: Oxidative stress may play an important role in the pathogenesis of endotoxin-induced acute lung injury (ALI). This study evaluated the therapeutic effect of ${\alpha}$-lipoic acid, a nonenzymatic antioxidant, in a rat model of lipopolysaccharide (LPS) induced ALI. Materials and Methods: ALI was induced in Sprague-Dawley rats by instilling LPS (E.coli, 3mg/Kg) into the trachea. The rats were classified into the control, control+${\alpha}$-lipoic acid, LPS, and LPS+${\alpha}$-lipoic acid groups.The lung lavage neutrophil count, cytokine-induced neutrophil chemoattractant (CINC), lung myeloperoxidase (MPO), and cytokine concentrations (TNF-${\alpha}$, IL-$1{\beta}$, IL-6 and IL-10) were measured at 2 h and 6 h after LPS administration. Results: The total cell and neutrophil counts of the LPS+${\alpha}$-lipoic acid groups were significantly lower than the LPS groups. The protein concentration in the BAL fluid was similar in the LPS groups and LPS+${\alpha}$-lipoic acid groups. The TNF-${\alpha}$, IL-$1{\beta}$, and IL-6 concentrations in the BAL fluid were not decreased by the ${\alpha}$-lipoic acid treatment in the LPS treated rats. Conclusions: Although ${\alpha}$-lipoic acid decreased the level of LPS-induced neutrophil infiltration into the lung, it could not attenuate the LPS-induced ALI at the dose administered in this study.
Purpose: The present study will identify risk factors for aspiration in severe trauma patients by comparing patients who showed a sign of aspiration lung disease on chest computed tomography (CT) and those who did not. Methods: We conducted a retrospective review of the Korean Trauma Data Bank between January 2014 and December 2019 in a single regional trauma center. The inclusion criteria were patients aged ≥18 years with chest CT, and who had an Injury Severity Score ≥16. Patients with Abbreviated Injury Scale (AIS)-chest score ≥1 and lack of medical records were excluded. General characteristics and patient status were analyzed. Results: 425 patients were included in the final analysis. There were 48 patients showing aspiration on CT (11.2%) and 377 patients showing no aspiration (88.7%). Aspiration group showed more endotracheal intubation in the ER (p=0.000) and a significantly higher proportion of severe Glasgow Coma Scale (GCS) (p=0.000) patients than the non-aspiration group. In AIS as well, the median AIS head score was higher in the aspiration group (p=0.046). Median oxygen saturation was significantly lower in the aspiration group (p=0.002). In a logistic regression analysis, relative to the GCS mild group, the moderate group showed an odds ratio (OR) for aspiration of 2.976 (CI, 1.024-8.647), and the severe group showed an OR of 5.073 (CI, 2.442-10.539). Conclusions: Poor mental state and head injury increase the risk of aspiration. To confirm for aspiration, it would be useful to perform chest CT for severe trauma patients with a head injury.
Koh, Youn-Suck;Hybertson, Brooks M.;Jepson, Eric K.;Kim, Mi-Jung;Lee, In-Chul;Lim, Chae-Man;Lee, Sang-Do;Kim, Dong-Soon;Kim, Won-Dong;Repine, John E.
Tuberculosis and Respiratory Diseases
/
v.43
no.3
/
pp.308-322
/
1996
Background : Neutrophils are considered to play critical roles in the development of acute respiratory distress syndrome. Histamine, which is distributed abundantly in lung tissue, increases the rolling of neutrophills via increase of P-selectin expression on the surface of endothelial cells and is known to have some interrelationships with IL-1, IL-8 and TNF-$\alpha$. We studied to investigate the effect of the histamine on the acute lung injury of the rats induced by intratracheal insufflation of TNF-$\alpha$ which has less potency to cause lung injury compared to IL-1 in rats. Methods : We intratracheally instilled saline or TNF(R&D, 500ng), IL-1(R&D, 50ng)or histamine of varius dose(1.1, 11 and $55\;{\mu}g/kg$) with and without TNF separately in Sprague-Dawley rats weighing 270-370 grams. We also intratracheally treated IL-1(50ng) along with histamine($55\;{\mu}g/kg$). In cases, there were synergistic effects induced by histamine on the parameters of TNF-induced acute lung injury, antihistamines(Sigma, mepyramine as a $H_1$ receptor blockade and ranitidine as a $H_2$ receptor blockade, 10 mg/kg in each)were co-administered intravenously to the rats treated TNF along with histamine($1.1\;{\mu}g/kg$) intratraeheally. Then after 5 h we measured lung lavage neutrophil numbers, lavage cytokine-induced neutrophil chemoattractants(CINC), lung myeloperoxidase activity(MPO) and lung leak. We also intratracheally insufflated TNF with/without histamine($11\;{\mu}g/kg$), then after 24 h measured lung leak in rats. Statistical analyses were done by Kruskal-Wallis nonparametric ANOVA test with Dunn's multiple comparison test or by Mann-Whitney U test. Results : We found that rats given TNF, histamine alone(11 and $55\;{\mu}g/kg$), and TNF with histamine(l.1, 11, and $55\;{\mu}g/kg$) intratracheally had increased (p<0.05) lung MPO activity compared with saline-treated control rats. TNF with histamine $11\;{\mu}g/kg$ had increased MPO activity (P=0.0251) compared with TNF-treated rats. TNF and TNF with histamine(1.1, 11, and $55\;{\mu}g/kg$) intratracheally had all increased (p<0.05) lung leak, lavage neutophil numbers and lavage CINC activities compared with saline. TNF with histamine $1.1\;{\mu}g/kg$ had increased (p=0.0367) lavage neutrophil numbers compared with TNF treated rats. But there were no additive effect of histamine with TNF compared with TNF alone in acute lung leak on 5 h and 24 h in rats. Treatment of rats with the $H_1$ and $H_2$ antagonists resulted in inhibitions of lavage neutrophil accumulations and lavage CINC activity elevations elicited by co-treated histamine in TNF-induced acute lung injury intratracheally in rats. We also found that rats given IL-1 along with histamine intratracheally did not have increase in lung leak compared with IL-1 treated rats. Conclusion : Histamine administered intratracheally did not have synergistic effects on TNF-induced acute lung leak inspite of additive effects on increase in MPO activity and lavage neutrophil numbers in rats. These observations suggest that instilling histamine intratracheally would not play synergistic roles in neutrophil-mediated acute lung injury in rats.
Kim, Seong-Eun;Kim, Dug-Young;Na, Bo-Kyung;Lee, Young-Man
Applied Microscopy
/
v.33
no.1
/
pp.1-16
/
2003
As is well known that N-nitroso-N-methylurethane (NNNMU) causes acute lung injury (ALI) in experimental animals. And ALI caused by NNNMU is very similar to ARDS in human being in its pathology and progress. In its context, we investigated the pathogenetic mechanism of ARDS associated with oxidative stress by neutrophils in Sprague-Dawley rat model of NNNMU-induced ALI. NNNMU had increased lung weight/body weight ratio (L/B ratio), lung myeloperoxidase (MPO) activity, protein content and number of neutrophils in bronchoalveolar fluid (BALF) compared with those of control rat (p<0.001, respectively). In contrast, the amount of pulmonary surfactant in BALF was decreased by NNNMU (p<0.001). Morphologically, light microscopic examination denoted pathological findings such as formation of hyaline membrane, infiltration of neutrophils and perivascular cuffing in the lungs of NNNMU-treated rats. In addition, ultrastructural changes such as the necrosis of endothelial cells, swelling and vacuolization of lamellar bodies of alveolar type II cells, and the degeneration of pulmonary surfactant were identified after treatment of NNNMU. Very interestingly, cerium chloride electron microscopic cytochemistry showed that NNNMU had increased the production of cerrous-peroxide granules in the lung, which signified the increased production of hydrogen peroxide in the lung. Collectively, we conclude that NNNMU causes acute lung leak by the mechanism of neutrophilic oxidative stress of the lung.
Kim, Young-Whan;Yoo, Chul-Gyu;Jeong, Ki-Ho;Choi, Hyung-Seok;Lee, Hyuk-Pyo;Han, Sung-Koo;Shim, Young-Soo;Kim, Keun-Youl;Han, Yong-Chol
Tuberculosis and Respiratory Diseases
/
v.38
no.4
/
pp.357-371
/
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.
Journal of the Korean Society of Physical Medicine
/
v.5
no.4
/
pp.597-604
/
2010
Purpose : This study investigated the effects of air stacking exercise on respiratory ability of patients with cervical cord injury. Methods : The subjects of this study were 30 patients with cervical cord injury were randomly placed in an experimental group(n=15) and a control group(n=15), respectively. Basic therapeutic exercise(ROM exercise, stretching exercise, strengthening exercise) were conducted twice a day for 30 minutes each time in all subjects and air stacking exercise was additionally conducted on the experimently group only. Air stacking exercise was conducted for 4 weeks, twice a day, 5 times a week and repeated 10 to 15 times each time. Lung capacity, MIC and, peak cough flow were measured and evaluated. Results : The results showed that FEV1, FVC, MIC, UPCF and APCF were significantly increased(p<.05), but FEV1/FVC didn't show the significant differences in an experimental group. In a control group, the findings showed that FEV1, FVC were increased significantly(p<.05) while FEV1/FVC, MIC, UPCF, and APCF didn't show the significant differences.There were significant differences in FEV1, FVC, MIC, and APCF between a experimental group and a control group in the results of Pulmonary Function Test after conducting the pulmonary rehabilitation. However, no significant differences were found in FEV1/FVC, and UPCF between a experimental and a control group(p>.05). Conclusion : air stacking exercise has positive effects on the improvements of cough functions and that of pulmonary functions such as lung volume, lung elasticity in patients with cervical cord injury.
Park, Dong-Uk;Park, Soyoung;Park, Ju-Hyun;Park, Jihoon;Hong, Soo-Jong;Paek, Domyung
Journal of Environmental Health Sciences
/
v.46
no.2
/
pp.128-135
/
2020
Objective: The objectives of this study are to report the number of humidifier disinfectant (HD) associated health problems, including HD associated lung injury (HDLI), by year. This data was analyzed by the type of HD and HD brand. Methods: A total of 530 patients registered with the national program on HD through its third round were distributed based on the year when they developed their first health problem including HDLI (N=221). The distribution of health problems at diagnosis was clinically evaluated in order to examine the association between their lung injury and the use of HD. Results: The number of HD associated victims and HDLI patients was found to rise sharply from 2008 to 2011, with a peak in 2011. This trend was found not only for HD brands containing polyhexamethylene guanidine phosphate (PHMG), but also chloromethylisothiazolinone/methylisothiazolinone (CMIT/MIT). The number of patients who responded as developing health problems in the specific year was 35 for 2008, 51 for 2009, 108 for 2010 and 182 for 2011. Other types of HD brands and HD chemicals did not follow the trend of abrupt increase in HD associated patients since 2008. Conclusion: This study found the number of HD associated victims and HDLI patients who used HD brands containing PHMG sharply increased starting in 2008. A significant change in the process of manufacturing PHMG can be suspected with the abrupt rise in HD associated patients in specific years.
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