• Tuberculosis and Respiratory Diseases
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• v.50 no.5
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• pp.540-548
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• 2001

Backgrounds : Because ventilator-induced lung injury is partly dependent on the intensity of vascular flow, we hypothesized that hypothermia may attenuate the degree of such an injury through a reduced cardiac output. Methods : Twenty-seven male Sprague-Dawley rats were randomly assigned to normothermia ($37{\pm}1^{\circ}C$)-injurious ventilation (NT-V) group (n=10), hypothermia ($27{\pm}1^{\circ}C$)-injurious ventilation (HT-V) group (n=10), or nonventilated control group (n=7). The two thermal groups were subjected to injurious mechanical ventilation for 20 min with peak airway pressure 30 cm $H_2O$ at zero positive end-expiratory pressure, which was translated to tidal volume $54{\pm}6\;ml$ in the NT-V group and $53{\pm}4\;ml$ in the HT-V group (p>0.05). Results : Pressure-volume (P-V) curve after the injurious ventilation was almost identical to the baseline P-V curve in the HT-V group, whereas it was shifted rightward in the NT-V group. On gross inspection, the lungs of the HT-V group appeared smaller in size, and showed less hemorrhage especially at the dependent regions, than the lungs of the NT-V group. [Wet lung weight (g)/body weight (kg)] ($1.6{\pm}0.1$ vs $2.4{\pm}1.2$ ; p=0.014) and [wet lung weight/dry lung weight] ($5.0{\pm}0.1$ vs $6.1{\pm}0.8$ ; p=0.046) of the HT-V group were both lower than those of the NT-V group, while not different from those of the control group($1.4{\pm}0.4$, $4.8{\pm}0.4$, respectively). Protein concentration of the BAL fluid of the HT-V group was lower than that of the NT-V group($1,374{\pm}726\;ug/ml$ vs $3,471{\pm}1,985\;ug/ml$;p=0.003). Lactic dehydrogenase level of the BAL fluid of the HT-V group was lower than that of the NT-V group ($0.18{\pm}0.10\;unit/ml$ vs $0.43{\pm}0.22\;unit/ml$;p=0.046). Conclusions : Hypothermia attenuated pulmonary hemorrhage, permeability pulmonary edema, and alveolar cellular injuries associated with injurious mechanical ventilation, and preserved normal P-V characteristics of the lung in rats.

• Tuberculosis and Respiratory Diseases
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• v.42 no.5
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• pp.752-759
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• 1995

Background: Bronchial asthma is characterized by noctunal dyspnea, cough and wheezing because of airway hyperresponsiveness to nonspecific stimuli. These symptoms and signs are also observed in patients with congestive heart failure. Therefore, this is so called "cardiac asthma". There are lots of experimental and clinical datas to suggest that airway dysfunctions occur in acute and chronic congestive heart failure. However, it is still controversial whether bronchial hyperresponsiveness is present in patients with congestive heart failure. To assess whether bronchial hyperresponsiveness is present in patients with congestive heart failure and to demonstrate the relationship between bronchial responsiveness and vascular pressure, we performed methacholine provocation test in 11 patients with mitral valvular heart disease. Methods: All patients were in the New York Heart Association functional class II and treated continuously with digoxin and/or dichlozid and/or angiotensin converting enzyme inhibitor except one patient. All patients were undergone right and left side heart catheterization for hemodynamic measurements. A 20 percent fall of peak expiratory flow rate were considered as positive response to methacholine provocation test. Results: 1) Only one patient who has normal pulmonary artery pressure, pulmonary capillary wedge pressure, cardiac index was positive in methacholine provocation test. 2) Their mean pulmonary artery pressure, pulmonary capillary wedge pressure were $21.72{\pm}9.70mmHg$, $15.45{\pm}8.69mmHg$ respectively which were significantly higher. Conclusion: It is speculated that in stable congestive heart failure patients, bronchial responsiveness as assessed by methacholine provocation test may not be increased.

• Tuberculosis and Respiratory Diseases
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• v.58 no.5
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• pp.498-506
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• 2005

Background : This study compared the bronchodilator efficacy and safety of tiotropium inhalation capsules ($18{\mu}g$ once daily) with a ipratropium metered dose inhaler (2 puffs of $20{\mu}g$ q.i.d.) in patients with chronic obstructive pulmonary disease (COPD). Method : After the initial screening assessment and a two-week run-in period, patients received either tiotropium $18{\mu}g$ once daily or ipratropium $40{\mu}g$ four times daily over a period of 4 weeks in a double blind, double dummy, parallel group study. The outcome measures were the lung function, the daily records of the peak expiratory flow rate (PEFR), the patients' questionnaire, and the use of concomitant salbutamol. The forced expiratory volume in one second ($FEV_1$) and the forced vital capacity (FVC) were measured 5 minutes before inhalation, and 0.5, 1, 2 and 3 hours after inhaling the study drug on days 0, 14 and 28. Result : In 16 centers, 134 patients with a mean (SD) age of 66 (7) years and a predicted $FEV_1$ of 42 (12)% were analyzed. The trough $FEV_1$ response was significantly higher in the tiotropium group than in the ipratropium group after a four-week treatment period. The weekly mean morning PEFR of the tiotropium group was consistently higher than that of the ipratropium group during the 4-week treatment period with differences ranging from 12.52 to 13.88 l/min, which were statistically significant. Tiotropium was well tolerated by the COPD patients during the 4-week treatment period and had a similar safety profile to ipratropium. Conclusion : This study shows that tiotropium administrated once daily has a superior bronchodilator effect with a similar safety profile in treating COPD patients compared with ipratropium, inhaled four times daily.