Dong-Soon Kim

Hypothermia protects against endotoxin- induced acute lung injury in rats

AbstractnObjective. Hypothermia in humans and animals is known to decrease the number and function of circulating neutrophils. Because an activation of circulating neutrophils and their sequestration into the lung are important pathogenetic phenomena in endotoxin-associated lung injury, we conjectured that hypothermia could prevent this type of lung injury.nDesign and setting. Animal study at a university-affiliated research institute.nSubjects. Thirty-six Sprague-Dawley rats.nInterventions. After anesthesia, the rats were randomly assigned to normothermia (37°C, rectal temperature) or hypothermia (27°C), which was induced by surface cooling. After 1xa0h of stable temperature, the rats were administered intratracheal doses of lipopolysaccharide (LPS; 3xa0mg/kg) (normothermia-LPS; hypothermia-LPS) or an equivalent volume of normal saline (normothermia-saline; hypothermia-saline). The rectal temperature was maintained within ±1°C of the target temperature for 6xa0h after the intratracheal treatment.nMeasurements and results. Compared with the normothermia-LPS group, the neutrophil count in bronchoalveolar lavage (BAL) fluid (p=0.002) and the myeloperoxidase activity of lung tissues (p=0.002) of the hypothermia-LPS group were both lower. Compared with the normothermia-LPS group, the BAL interleukin-1β level of the hypothermia-LPS group was lower (p<0.001), whereas the BAL interleukin-10 level of the hypothermia-LPS group was higher (p=0.026). Compared with the normothermia-LPS group, the histologic scores for acute lung injury of the hypothermia-LPS group were lower (p=0.007).nConclusions. Hypothermia pretreatment decreased the pulmonary sequestration of neutrophils, induced a favorable balance between pro- and anti-inflammatory cytokines, and attenuated histologic injury in endotoxin-challenged rats.

The Risk of Obstructive Lung Disease by Previous Pulmonary Tuberculosis in a Country with Intermediate Burden of Tuberculosis

We evaluated the effects of previous pulmonary tuberculosis (TB) on the risk of obstructive lung disease. We analyzed population-based, the Second Korea National Health and Nutrition Examination Survey 2001. Participants underwent chest X-rays (CXR) and spirometry, and qualified radiologists interpreted the presence of TB lesion independently. A total of 3,687 underwent acceptable spirometry and CXR. Two hundreds and ninty four subjects had evidence of previous TB on CXR with no subjects having evidence of active disease. Evidence of previous TB on CXR were independently associated with airflow obstruction (adjusted odds ratios [OR] = 2.56 [95% CI 1.84-3.56]) after adjustment for sex, age and smoking history. Previous TB was still a risk factor (adjusted OR = 3.13 [95% CI 1.86-5.29]) with exclusion of ever smokers or subjects with advanced lesion on CXR. Among never-smokers, the proportion of subjects with previous TB on CXR increased as obstructive lung disease became more severe. Previous TB is an independent risk factor for obstructive lung disease, even if the lesion is minimal and TB can be an important cause of obstructive lung disease in never-smokers. Effort on prevention and control of TB is crucial in reduction of obstructive lung disease, especially in countries with more than intermediate burden of TB.

Measurement of Thermal Conductivity of TiO2 Thin Films Using 3ω Method

TiO2 film has been used in many industrial components such as laser filters, protection mirrors, chemical sensors, and optical catalysts. Therefore, the thermal properties of TiO2 thin films are important in, e.g., reducing the thermal conductivity of ceramic coatings in gas turbines and increasing the laser damage threshold of antireflection coatings. The thermal conductivity of four kinds of TiO2 thin films, prepared by dc magnetron sputtering, was measured using the 3ω method in the temperature range from 80 K to room temperature. The results showed that the thermal conductivity of TiO2 thin films strongly depends on the thickness and the microstructure of the films. The films with smaller grain size and thinner thickness have smaller thermal conductivities.

Hypothermia Attenuates Vascular Manifestations of Ventilator-Induced Lung Injury in Rats

Alveolar hemorrhage and pulmonary edema induced by mechanical ventilation are partly dependent on cardiac output. Because cardiac output is low during hypothermia, we hypothesized that hypothermia may protect against these vascular manifestations of ventilator-induced lung injury. Twenty-seven Sprague-Dawley rats were assigned to either normothermia (37 ± 1°C)-injurious ventilation (NT; n = 10), hypothermia (27 ± 1°C)- injurious ventilation (HT; n = 10), or nonventilated control (n = 7). The two ventilated groups were subjected to injurious ventilation of peak airway pressure 30 cm H2O with zero end-expiratory pressure for 20 min. Compared with the NT group, the hemorrhage/congestion score of the lung (11.2 ± 1.5 vs. 4.7 ± 1.6; p < 0.001) and the ratio of wet/dry lung weight (6.1 ± 0.8 vs. 5.0 ± 0.1; p = 0.046) of the HT group were lower. Compared with the NT group, protein concentration (3,471 ± 1,985 µg/ml vs. 1,374 ± 726 µg/ml; p = 0.003) and lactate dehydrogenase level (0.43 ± 0.22 U/ml vs. 0.18 ± 0.1 U/ml; p = 0.046) in bronchoalveolar lavage fluid of the HT group were lower. Whereas pressure-volume curve was shifted to the right in the NT group after injurious ventilation, it was not shifted in the HT group. In conclusion, hypothermia in rats attenuated the degrees of vascular manifestations and alveolar epithelial injuries induced by injurious ventilation, and preserved the mechanical properties of the lung.

Hypothermia inhibits cytokine release of alveolar macrophage and activation of nuclear factor κB in endotoxemic lung

ObjectiveWe have previously reported that endotoxin-induced neutrophil infiltration of the lung is lower during hypothermia than during normothermia. Because neutrophil infiltration of the lung is considered a downstream phenomenon following an activation of tissue macrophages, we examined the effects of induced hypothermia on the proximal aspects of acute lung injury, which involves alveolar macrophages and nuclear transcription of cytokine genes.Design and settingAnimal study in an institutional animal laboratory.SubjectsThirty-six Sprague-Dawley rats.InterventionsRats were assigned to the following groups: normothermia (37°C) with saline; hypothermia (27°C) with saline; normothermia with lipopolysaccharide; hypothermia with lipopolysaccharide. After 1xa0h of stable temperature rats were intraperitoneally given lipopolysaccharide or an equivalent volume of normal saline. The temperature of rats was maintained within ±1°C of the target temperature for the subsequent 2xa0h, after which rats were subjected to lung lavage.Measurements and resultsNeutrophil count, TNF-α, and IL-1β in lavage fluid were all higher with normothermia-LPS than in normothermia-saline. Neutrophil count, TNF-α, and IL-1β levels of lavage fluid were lower with hypothermia-LPS than with normothermia-LPS. TNF-α release from cultured alveolar macrophages and NF-κB activity in lung tissue were both lower with hypothermia-LPS than with normothermia-LPS. I-κBα level in lung tissue was lower with normothermia-LPS than with the normothermia-saline, whereas I-κBα level in lung tissue did not differ between normothermia-saline and hypothermia-LPS.ConclusionsInduced hypothermia suppressed the release of inflammatory cytokine from alveolar macrophages and NF-κB activation in endotoxemic lung.

The Clinical Efficacy of GOCA Scoring System in Patients with Acute Respiratory Distress Syndrome

To explore the following hypotheses: 1) Gas exchange, Organ failure, Cause, Associated disease (GOCA) score, which reflects both general health and the severity of lung injury, would be a better mortality predictor of acute respiratory distress syndrome (ARDS) than acute physiology and chronic health evaluation (APACHE II) or simplified acute physiology score (SAPS II), which are not specific to lung injury, and lung injury score (LIS) that focuses on the lung injury; 2) the performance of APACHE II and SAPS II will be improved when reinforced by LIS, we retrospectively analyzed ARDS patients (N=158) admitted to a medical intensive care unit for five years. The overall mortality of the ARDS patients was 53.2%. Calibrations for all models were good. The area under the curve of (AUC) of LIS (0.622) was significantly less than those of APACHE II (0.743) and SAPS II (0.753). The AUC of GOCA (0.703) was not better than those of APACHE II and SAPS II. The AUCs of APACHE II and SAPS II tended to further increase when reinforced by LIS. In conclusion, GOCA was not superior to APACHE II or SAPS II. The performance of the APACHE II or SAPS II tended to improve when combining a general scoring system with a scoring system that focused on the severity of lung injury.

Abnormal peripheral blood T lymphocyte cell subsets in a subgroup of patients with chronic obstructive pulmonary disease

Smoking may induce changes in T lymphocyte cell subsets in peripheral blood. Abnormality of T lymphocyte cell subsets in peripheral blood and in bronchoalveolar-lavage fluid, and increased CD8+ T lymphocytes in the airways have been reported in patients with COPD. These findings suggest that T lymphocyte abnormalities might play a role in the pathogenesis of airflow limitation in smokers. To investigate this hypothesis this study was performed. Peripheral blood T lymphocyte cell subsets were measured by flow cytometry using specific monoclonal antibodies in 20 healthy nonsmokers, 20 healthy smokers, and 20 smokers with stable COPD. No significant differences in the peripheral blood T lymphocyte cell subsets were observed between the three groups. Because a previous study had shown peripheral blood T lymphocyte abnormalities in the subgroup of nonsmoking COPD subjects, we wanted to investigate what factors determine the subgroup of COPD with abnormal T lymphocyte cell subsets. We tried to measure the relationship between T lymphocyte cell subsets and physiologic indices of pulmonary function tests in smokers with COPD. The proportion of CD8+ T lymphocytes significantly correlated with DLco (p= 0.012) and DLco/VA (p=0.002), and CD4+/CD8+ ratio correlated with DLco/VA (p=0.01). Therefore, we attempted to divide the smokers with COPD into two subgroups on the basis of DLco/VA. Ten patients with low DLco/VA (DLco/VA<80 per cent predicted; COPD/low DLco/VA) and 10 patients with normal DLco/VA (DLco/VA/spl ges/80 per cent, COPD/normal DLco/VA) were subclassified. The COPD/normal DLco/VA subgroup had a significantly higher proportion of CD8+ T lymphocytes (p<0.5) and lower CD4+/CD8+ ratio (p<0.05) than the healthy smokers or COPD/low DLco/VA subgroup. Moreover,. FEV/sub 1//FVC significantly correlated with the CD4+/CD8+ ratio only in the COPD/normal DLco/VA subgroup (p=0.044). These findings suggest that T lymphocyte abnormalities might be involved in the pathogenesis of airflow limitation in a subgroup of COPE patients, presumably with small airways disease, but not in all COPD.