• Tuberculosis and Respiratory Diseases
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• v.46 no.5
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• pp.662-673
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• 1999

Background : Pressure-controlled ventilation (PCV) is frequently used recently as the initial mode of mechanical ventilation in the patients with respiratory failure. Theoretically, because of its high initial inspiratory flow, pressure-controlled ventilation has lower peak inspiratory pressure and improved gas exchange than volume-controlled ventilation (VCV). But the data from previous studies showed controversial results about the gas exchange. Moreover, the comparison study between PCV and VCV with various inspiration : expiration time ratios (I : E ratios) is rare. So this study was performed to compare the respiratory mechanics and gas exchange between PCV and VCV with various I : E raitos. Methods : Nine patients receiving mechanical ventilation for respiratory failure were enrolled. They were ventilated by both PCV and VCV with various I : E ratios (1 : 2, 1 : 1.3 and 1.7 : 1). $FiO_2$, tidal volume, respiratory rate and external positive end-expiratory pressure (PEEP) were kept constant throughout the study. After 20 minutes of each ventilation mode, arterial blood gas, airway pressures, expired $CO_2$ were measured. Results : In both PCV and VCV, as the I : E ratio increased, the mean airway pressure was increased, and $PaCO_2$ and physiologic dead space fraction were decreased. But P(A-a)$O_2$ was not changed. In all three different I : E ratios, peak inspiratory pressure was lower during PCV, and mean airway pressure was higher during PCV. But $PaCO_2$ level, physiologic dead space fraction and P(A-a)$O_2$ were not different between PCV and VCV with three different I : E ratios. Conclusion : There was no difference in gas exchange between PCV and VCV under the same tidal volume, frequency and I : E ratio.

• Tuberculosis and Respiratory Diseases
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• v.53 no.6
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• pp.619-634
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• 2002

Background : Many inflammatory mediators and collagenases are involved in the pathogenesis of acute lung injury (ALI) and acute respiratory distress syndrome (ARDS). The increase of matrix metalloproteinase-9 (MMP-9, gelatinase-B) produced mainly by inflammatory cells was reported in many ALI models and connective tissue cells. In this study, the expression of MMP-9 in ventilator-induced lung injury (VILI) model and the effects of matrix metalloproteinase inhibitor (MMPI) on VILI were investigated. Methods : Eighteen Sprague-Dawley rats were divided into three groups: low tidal Volume (LVT, 7mL/Kg tidal volume, 3 $cmH_2O$ PEEP, 40/min), high tidal volume (HVT, 30mL/Kg tidal volume, no PEEP, 40/min) and high tidal volume with MMPI (HVT+MMPI) groups. Mechanical ventilation was performed in room air for 2 hours. The 20 mg/Kg of CMT-3 (chemically modified tetracycline-3, 6-demethyl 6-deoxy 4-dedimethylamino tetracycline) was gavaged as MMPI from three days before mechanical ventilation. The degree of lung injury was measured with wet-to-dry weight ratio and acute lung injury score. Expression of MMP-9 was studied by immunohistochemical stain with a mouse monoclonal anti-rat MMP-9 $IgG_1$. Results : In the LVT, HVT and HVT+MMPI groups, the wet-to-dry weight ratio was $4.70{\pm}0.14$, $6.82{\pm}1.28$ and $4.92{\pm}0.98$, respectively. In the HVT group, the ratio was significantly higher than other groups (p<0.05). Acute lung injury score measured by five-point scale was $3.25{\pm}1.17$, $12.83{\pm}1.17$ and $4.67{\pm}0.52$, respectively. The HVT group was significantly damaged by VILI and MMPI protects injuries by mechanical ventilation (p<0.05). Expression of MMP-9 measured by four-point scale was $3.33{\pm}2.07$, $12.17{\pm}2.79$ and $3.60{\pm}1.95$, respectively, which were significantly higher in the HVT group (p<0.05). Conclusion : VILI increases significantly the expression of MMP-9 and MMPI prevents lung injury induced by mechanical ventilation through the inhibition of MMP-9.