• Clinical and Experimental Pediatrics
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• v.46 no.8
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• pp.777-783
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• 2003

Purpose : The aim of this study was to evaluate the effect of inhaled nitric oxide(iNO) on gas exchange, hemodynamics and pulmonary inflammation in newborn piglets with E. coli induced septic lung. Methods : Twenty three instrumented and ventilated piglets were randomized into three groups : CON(n=6), PCON(n=9), and PNO(n=8). In the piglets of the PCON and PNO groups, E. coli septic lung was induced by endotracheal instillation of E. coli. Ten ppm iNO was given continuously in the PNO group after endotracheal instillation of E. coli. All animals were mechanically ventilated for six hour with a peak inspiratory pressure of 30 $cmH_2O$, frequency of 25 breaths/min, $FiO_2$ 1.0 and a positive end-expiratory pressure of 4 $cmH_2O$. All measurements were made at one hour intervals during the experiment. At the end of the experiment, lung tissue was harvested for the analysis of myeloperoxidase activity, indicative of lung inflammation. Results : All piglets with pulmonary instillation of E. coli developed E. coli sepsis. Piglets in the PCON group developed progresseve pulmonry hypertension, hypoxemia and hypercarbia compared to the CON group due to increased pulmonary vascular resistance, intrapulmonary shunt fraction and physiologic dead space fraction. iNO did not reverse pulmonary hypertension in the PNO group. However iNO significantly improved oxygenation, which was attributed to marked improvement of venous admixture and partial attenuation of increase in dead space fraction. Increased myeloperoxidase activity in PCON compared to CON was significantly attenuated in PNO. Conclusion : iNO improves oxygenation and lung inflammation in newborn piglets with E. coli induced septic lung.

• Tuberculosis and Respiratory Diseases
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• v.46 no.5
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• pp.628-635
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• 1999

Background : Maximal expiratory flow rate is determined by the size of airway, elastic recoil pressure and the collapsibility of airway in the lung. The obstruction of expiratory flow is one of the major functional impairments of emphysema, which represents COPD. Nevertheless, expiratory narrowing of upper airway may be recruited as a mechanism for minimizing airway collapse, and maintaining lung volume and hyperinflation by an endogenous positive end-expiratory pressure in patients with airflow obstruction. We investigated the physiologic role of trachea in respiration in emphysema. Method : We included 20 patients diagnosed as emphysema by radiologic and physiologic criteria from January to August in 1997 at Seoul Municipal Boramae Hospital. Chest roentgenogram, high resolution computed tomography(HRCT), and pulmonary function tests including arterial blood gas analysis and body plethysmography were taken from each patient. Cross-sectional area of trachea was measured according to the respiratory cycle on the level of aortic arch by HRCT and calibrated with body surface area. We compared this corrected area with such parameters of pulmonary function tests as $PaCO_2$, $PaO_2$, airway resistance, lung compliance and so on. Results : Expiratory cross-sectional area of trachea had significant correlation with $PaCO_2$ (r=-0.61, p<0.05), $PaO_2$ (r=0.6, p<0.05), and minute ventilation (r=0.73, p<0.05), but inspiratory cross-sectional area did not (r=-0.22, p>0.05 with $PaCO_2$, r=0.26, p>0.05 with $PaO_2$, and r=0.44, p>0.05 with minute ventilation). Minute ventilation had significant correlation with tidal volume (r=0.45, p<0.05), but it had no significant correlation with respiratory frequency (r=-0.31, p>0.05). Cross-sectional area of trachea had no significant correlation with other parameters of pulmonary function including $FEV_1$, FVC, $FEV_1$/FVC, peak expiratory flow, residual volume, diffusing capacity, airway resistance, and lung compliance, whether the area was expiratory or inspiratory. Conclusion : Cross-sectional area of trachea narrowed during expiration in emphysema, and its expiratory area had significant correlation with $PaCO_2$, $PaO_2$, and minute ventilation.

• Tuberculosis and Respiratory Diseases
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• v.59 no.1
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• pp.5-13
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• 2005

Chronic obstructive pulmonary disease (COPD) is a chronic progressive disease, characterized by irreversible airflow limitation, with a partially reversible component. The pathological abnormalities of COPD are associated with lung inflammation, imbalances of proteinase and antiproteinase, and oxidative stress, which are induced by noxious particles and gases in susceptible individuals. The physiological changes of COPD are mucus hypersecretion, ciliary dysfunction, airflow limitation, pulmonary hyperinflation, gas exchange abnormalities, pulmonary hypertension, cor pulmonale and systemic effects. The airflow limitation principally results from an increase in the resistance of the small conducting airways and a decrease in pulmonary elastic recoil due to emphysematous lung destruction. This article provides a general overview of the pathophysiology of COPD.

• Journal of Nuclear Fuel Cycle and Waste Technology(JNFCWT)
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• v.4 no.4
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• pp.345-352
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• 2006

The cemented and paraffin wastes form which are incorporated the concentrated wastes, the cemented waste form which is incorporated the spent ion-exchange resins, and the miscellaneous waste(decontamination paper) were irradiated up to $10^{+8}$ rads at $5.43{\times}10^{+5}$ rads/hr with Co-60(72,023.9 Ci) as an external irradiation source. As a result, the radiolysis gases such as $H_2,\;CH_4,\;N_2,\;C_2H_6,\;O_2,\;CO\;and\;CO_2$, were measured in all the wastes. The major gas which was generated in all the wastes was hydrogen($H_2$). The volume of the generated gases showed a difference from $0.029{\sim}0.788\;cm^3.atm/1.1g$ according to the type of wastes, and more was generated in the cemented waste form incorporated a spent ion-exchange resin than in the other wastes. More hydrogen($H_2$) gas was generated in the decontamination paper waste than in the other wastes, and the G($H_2$) value was 0.12.

• Tuberculosis and Respiratory Diseases
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• v.52 no.1
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• pp.14-23
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• 2002

Background: The opitmal ventilator setting during partial liquid ventilation(PLV) is controversial. This study investigated the effects of various gas exchange parameters during PLV in normal rabbit lungs in order to aid in the development of an optimal ventilator setting during PLV. Methods: Seven New-Zealand white rabbits were ventilated in pressure-controlled mode with the following settings; tidal volume($V_T$) 8 mL/kg, positive end-expiratory pressure(PEEP) 4 $cmH_2O$, inspiratory-to-expiratory ratio(I:E ratio) 1:2, fraction of inspired oxygen($F_TO_2$) 1.0. The respiration rate(RR) was adjusted to keep $PaCO_2$ between 35~45 mmHg. The ventilator settings were changed every 30 min in the following sequence : (1) Baseline, as the basal ventilator setting, (2) Inverse ratio, I:E ratio 2:1, (3) high PEEP, adjust PEEP to achieve the same mean inspiratory pressure (MIP) as in the inverse ratio, (4) High $V_T$, $V_T$ 15 mL/kg, (5) high RR, the same minute ventilation (MV) as in the High $V_T$. Subsequently, the same protocol was repeated after instilling 18 mL/kg of perfluorodecalin for PLV. The parameters of gas exchange, lung mechanics, and hemodynamics were examined. Results: (1) The gas ventilation(GV) group showed no significant changes in the $PaO_2$ at all phases. The $PaCO_2$ was lower and the pH was higher at the high $V_T$ and high RR phases(p<0.05). No significant changes in the lung mechanics and hemodynamics parameters were observed. (2) The baseline $PaO_2$ for the PLV was $312{\pm}$ mmHg. This was significantly lower when decreased compared to the baseline $PaO_2$ for GV which was $504{\pm}81$ mmHg(p=0.001). During PLV, the $PaO_2$, was significantly higher at the high PEEP($452{\pm}38$ mmHg) and high $V_T$ ($461{\pm}53$ mmHg) phases compared with the baseline phase. However, it did not change significantly during the inverse I:E ratio or the high RR phases. (3) The $PaCO_2$ was significantly lower at high $V_T$ and RR phases for both the GV and PLV. During the PLV, $PaCO_2$ were significantly higher compared to the GV (p<0.05). (4) There were no important or significant changes in of baseline and high RR phases lung mechanics and hemodynamics parameters during the PLV. Conclusion: During PLV in the normal lung, adequate $V_T$ and PEEP are important for optimal oxygenation.

• Tuberculosis and Respiratory Diseases
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• v.49 no.4
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• pp.466-473
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• 2000

Background : Patients with locally advanced non-small cell lung cancer are often treated with radiation alone or in combination with chemotherapy. Both modalities have a potentially damaging effect on pulmonary function. In order to examine changes in the cardiopulmonary exercise function of patients with locally advanced non-small cell lung cancer before and after conventional radiotherapy, we conducted a prospective study involving patients with such cancer, that had received radiation therapy. Method : Resting pulmonary function test, thoracic radiographic finding and cardiopulmonary exercise test(CPET) were assessed prior to and 4 weeks following radiation therapy in 11 male patients with locally advanced non-small cell lung cancer. Patient with endobronchial mass were excluded. Results : The forces vital capacity (FVC), forced expiratory volume in 1 second ($FEV_1$ and maximal voluntary ventilation (MVV) did not decreased between before and 4 weeks after radiation but the diffusing capacity (DLCO) had decreased by 11% 4 weeks after radiation, which was not statistically significant. No changes in maximal oxygen consumption ($VO_2$max), carbon dioxide production ($VCO_2$), exercise time and work load were attributed to radiation therapy. Follow up cardiopulmonary exercise testing revealed unchanged cardiovascular function, ventilatory function and gas exchange. No difference in cardiopulmonary exercise test performance was observed between pre- and post-radiation. Conclusion : Cardiopulmonary exercise function did not decrease within the short-term after the radiation of patients with locally advanced non-small cell lung cancer.

• Tuberculosis and Respiratory Diseases
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• v.45 no.5
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• pp.1022-1030
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• 1998

Background : In volume-controlled ventilation, the use of inspiratory pause increases the inspiratory time and thus increases mean airway pressure and improves ventilation. But under the same I : E ratio, the effects of inspiratory pause on mean airway pressure and gas exchange are not certain. Moreover, the effects may be different according to the resistance of respiratory system. So we studied the effects of inspiratory pause on airway pressure and gas exchange under the same I : E ratio in volume-controlled ventilation. Methods: Airway pressure and arterial blood gases were evaluated in 12 patients under volume-controlled mechanical ventilation with and without inspiratory pause time 5%. The I : E ratio of 1 : 3, $FiO_2$, tidal volume, respiratory rate, and PEEP were kept constant. Results: $PaCO_2$ with inspiratory pause was lower than without inspiratory pause ($38.6{\pm}7.4$ mmHg vs. $41.0{\pm}7.7$ mmHg. p<0.01). P(A-a)$O_2$ was not different between ventilation with and without inspiratory pause $185.3{\pm}86.5$ mmHg vs. $184.9{\pm}84.9$ mmHg, p=0.766). Mean airway pressure with inspiratory pause was higher than without inspiratory pause ($9.7{\pm}4.0\;cmH_2O$ vs. $8.8{\pm}4.0\;cmH_2O$, p<0.01). The resistance of respiratory system inversely correlated with the pressure difference between plateau pressure with pause and peak inspiratory pressure without pause (r=-0.777, p<0.l), but positively correlated with the pressure difference between peak inspiratory pressure with pause and peak inspiratory pressure without pause (r=0.811, p<0.01). Thus the amount of increase in mean airway pressure with pause positively correlated with the resistance of respiratory system (r=0.681, p<0.05). However, the change of mean airway pressure did not correlated with the change of $PaCO_2$. Conclusion: In volume-controlled ventilation under the same I : E ratio of 1 : 3, inspiratory pause time of 5% increases mean airway pressure and improves ventilation. Although the higher resistance of respiratory system, the more increased mean airway pressure, the increase in mean airway pressure did not correlated with the change in $PaCO_2$.

• Journal of Chest Surgery
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• v.32 no.7
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• pp.637-647
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• 1999

Background: Ischemia-reperfusion injury is one of the major contributing causes of early graft failure in lung transplantation. It has been suggested that triiodothyronine (T3) may ameliorate ischemia-reperfusion injury to various organs in vivo and in vitro. Predicting its beneficial effect for ischemic lung injury, we set out to demonstrate it by administering T3 into the in situ canine ischemia-reperfusion model. Material and Method: Sixteen adult mongrel dogs were randomly allocated into group A and B. T3 $(3.6\mug/kg)$ was administered before the initiation of single lung ischemia in group B, whereas the same amount of saline was administered in group A. Ischemia was induced in the left lung by clamping the left hilum for 100 minutes. After reperfusion, various hemodynamic parameters and blood gases were analyzed for 4 hours while intermittently clamping the right hilum in order to allow observation of the injured left lung function. Result: Arterial oxygen partial pressure $(PaO_2)$ decreased 30 minutes after reperfusion and recovered gradually thereafter in both groups. In group B the decrease of $PaO_2$ was less marked than in group A. The recovery of $PaO_2$ was faster in group B than in group A. The differences between the two groups were statistically significant from 30 minutes after reperfusion $(125\pm34$ mmHg and $252\pm44$ mmHg, p<0.05) until the end of the experiment $(178\pm42$mmHg and $330\pm37$ mmHg, p<0.05). The differences in the arterial carbon dioxide pressure, airway pressure and lung compliance showed no statistical significance. The malondialdehyde (MDA) level, measured from the tissue obtained 240 minutes after reperfusion, was lower in group B $(0.40\pm0.04\mu$M) than in group A $(0.53\pm0.05\mu$M, p<0.05). The ATP level of group B $(0.69\pm0.07\mu$M/g) was significantly higher than that of group A $(0.48\pm0.07\mu$M/g, p<0.05). The microscopic exami nation revealed varying degrees of injury such as perivascular neutrophil infiltration, capillary hemorrhage and interstitial congestion. There were no differences in the microscopic findings between the two groups. CONCLUSION T3 has beneficial effects on the ischemic canine lung injury including preservation of oxygenation capacity, less production of lipid peroxidation products and a higher level of tissue ATP. These results suggest that T3 is effective in pulmonary allograft preservation.

• Tuberculosis and Respiratory Diseases
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• v.45 no.6
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• pp.1223-1235
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• 1998

Background and Objective : Although prone positioning has been reported to improve gas exchange, prone positioning alone does not seem to be sufficient to increase systemic oxygen transport in an acute lung injury. The objective of this study was to investigate whether the combined therapy of low dose nitric oxide (NO) inhalation and prone positioning has an additive effect on the oxygenation and hemodynamics in patients with severe ARDS. Patients and Methods : Twelve patients with ARDS were included. Prone positioning alone, later combined with nitric oxide inhalation (5~10 ppm) from the supine position (baseline) were performed with serial measurement of gas exchange, respiratory mechanics and hemodynamic at sequential time points. The patient was regarded as a responder to prone positioning if an increase in $PaO_2/FiO_2$ of more than 20 mm Hg at 30 min or 120 min intervals after prone positioning was observed compared to that of the baseline. The same criterion was applied during nitric oxide inhalation. Results : Eight patients (66.5%) responded to prone positioning and ten patients (83.3%) including the eight just mentioned responded to the addition of NO inhalation. The $AaDO_2$ level also decreased promptly with the combination of prone positioning and NO inhalation compared to that of prone positioning alone ($191{\pm}109$ mm Hg vs. $256{\pm}137$ mm Hg, P<0.05). Hemodynamic parameters and lung compliance did not change significantly during prone positioning only. Following the addition of NO inhalation to prone positioning, the mean pulmonary artery pressure and pulmonary artery occlusion pressure decreased and cardiac output, stroke volume and oxygen delivery increased (P < 0.05) compared to those of prone 120 min. Conclusion : These findings indicate that NO inhalation would provide additional improvement in oxygenation and oxygen transport to mechanically ventilated patients with ARDS who are in a prone position.

• Tuberculosis and Respiratory Diseases
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• v.51 no.2
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• pp.97-107
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• 2001

Background : Tuberculosis itself causes not only lung parenchymal destruction but also pulmonary vascular damage. Secondary emphysema also causes pulmonary vascular damage, which can develop as a late sequela of pulmonary tuberculosis. Therefore, pulmonary circulatory impairment tends to be more severe in post-tuberculosis emphysema than in primary emphysema. In post-tuberculosis emphysema, the right ventricular function may play an important role. However, little information regarding the right ventricular function is available. The purpose of this study was to evaluate and compare the right ventricular function between post-tuberculosis emphysema and primary emphysema. Method: Post-tuberculosis emphysema(PTE) or primary emphysema(PE) was diagnosed by history, HRCT finding and pulmonary function. Twenty patients with post-tuberculosis emphysema were matched with 20 patients with primary emphysema according to both $FEV-1$ and FVC. Arterial blood gas analysis and echocardiography were done at rest and immediately after symptom-limited exercise. The right ventricular function was evaluated with the right ventricular ejection fraction using a modification of Simpson's method. Results : There was no significant difference in the demographics and pulmonary function between the two groups. In post-tuberculosis emphysema, the $PaCO_2$ was higher ($42.9{\pm}4.7$ vs $38.8{\pm}3.1\;mmHg$ at rest; $47.9{\pm}7.0$ vs $41.1{\pm}5.9\;mmHg$ after exercise; p<0.01) and the right ventricular ejection fraction was lower ($57.6{\pm}6.5$ vs $61.4{\pm}4.7%$ at rest; $51.1{\pm}10.8$ vs $59.8{\pm}6.6%$ after exercise; p<0.01) both at rest and after exercise. The $PaCO_2$ after exercise was also lower ($65.7{\pm}12.6$ vs $80.2{\pm}14.4\;mmHg$, p<0.01), while the Pa02 at rest tended to be lower($82.9{\pm}12.0$ vs $87.8{\pm}7.5$, p>0.05). In both groups, right ventricular ejection fraction correlated with the $PaCO_2$ after exercise(PTE r=0.536, PE r=0.557), and the $PaCO_2$ at rest(PTE r=-0.576, PE r=-0.588) and after exercise(PTE r=-0.764, PE r=-0.619). Conclusion : Impairment of the right heart function and gas exchange were more serious in post-tuberculosis emphysema than in primary emphysema, and gas exchange may be influenced by the right ventricular function in post-tuberculosis emphysema.