• Tuberculosis and Respiratory Diseases
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• v.44 no.2
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• pp.379-390
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• 1997

Background : It has long been suggested that neutrophils and their products are implicated as the central mediators of the acute lung injuries. Contrary to the dominant role of neutrophils in ARDS, many cases of ARDS has occurred in the setting of severe neutropenia without pulmonary neutrophil infiltration. Therefore it is certain that effector cell(s) other than neutrophil play an important role in the pathogenesis of ARDS. This experiment was performed to define the mechanism of ARDS in the setting of neutropenia, 1) by comparing the severity of endotoxin-induced lung injury, 2) by measurement of hydrogen peroxide production and cytokine concentration in the bronchoalveolar lavage cells and fluids obtained from different rats with and without cyclophosphamide-pretreatment. Method : The male Sprague-Dawleys were divided into the normal control (NC)-, endotoxin (ETX)-, and cyclophosphamide (CPA)-group in which neutropenia was induced by injecting cyclophosphamide intraperitoneally. Acute lung injury was evoked by injecting lipopolysaccharide (LPS) into a tail vein. The bronchoalveolar lavage (BAL) was performed at 3 and 6 hour after administration of LPS to measure the change of cell counts and concentrations of protein and cytokines, tumor necrosis factor-alpha (TNF-alpha) and interleukin-6 (IL-6). Hydrogen peroxide (HPO) production from BAL cells was measured at 6 hour after LPS administration by phenol red microassay with and without zymosan stimulation. Results : The results were as follows. A change of leukocyte counts in the peripheral blood after treatment with CPA : More than 95% of total leukocytes and neutrophils were reduced after CPA administration, resulting in severe neutropenia. A change of BAL cells : In the ETX-group, the number of total cells (p < 0.01) and of macrophage and neutrophil (p < 0.05) were increased at 3 and 6 hour after LPS administration compared to those of NC-group. In the CPA-group, the number of total leukocyte and macrophage were not changed after LPS administration, but neutrophil counts were significantly reduced and it took part in less than 0.1% of total BAL cells (p < 0.01 vs NC-group). BAL cells in this group were almost all macrophages (99.7%). A change of protein concentration in the BALF : In the ETX-group, protein concentration was increased at 3 hour and was more increased at 6 hour after LPS administration (p < 0.05 and < 0.01 vs NC-group, respectively). In the CPA-group, it was also significantly elevated at 3 hour after LPS administration (p < 0.05 vs NC-group), but the value was statistically not different from that of ETX-group. The value measured at 6 hour after LPS administration in the CPA-group became lower than that of ETX-group (p < 0.05), but showed still a higher value compared to that of NC-group (p < 0.05). A change of cytokine concentration in the BALF : TNF -alpha and IL-6 were elevated in the ETX - and CPA-group compared to those of NC-group at both time intervals. There was no statistical difference in the values of both cytokines between the ETX- and CPA-groups. Measurement of hydrogen peroxide production from BAL cells : There was no intergroup difference of HPO production from resting cells. HPO production after incubation with opsonized zymosan was significantly elevated in all groups. The percent increment of HPO production was highest in the ETX-group (89.0%, p < 0.0008 vs NC-group), and was 42.85 in the CPA-group (p = 0.003 vs NC-group ). Conclusion : Acute lung injury in the setting of neutropenia might be caused by functional activation of resident alveolar macrophages.

• Tuberculosis and Respiratory Diseases
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• v.44 no.2
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• pp.391-400
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• 1997

Background : Bronchoscopy is an essential procedure for identifying the bleeding site and evaluating cause of hemoptysis. However, it is controversial regarding to the timing of bronchoscopy in patients with hemoptysis. Early bronchoscopy, which was performed during hemoptysis or with 48hour after cessation of bleeding, was better for identifying the site of bleeding compared with delayed bronchoscopy, which was performed 48 hours after cessation of bleeding. The diagnostic yield of identifying the bleeding site by bronchoscopy was variable in reported literature and the safety of early bronchoscopy was not mentioned in previous literature. Therefore, we evaluated the efficacy and safety of early bronchoscopy in patients with hemoptysis. Method : From October 1994 to August 1996 in Samsung Medical Center, bronchoscopy was performed in patients with hemoptysis. Early bronchoscopy was performed prospectively during hemoptysis or within 48 hours after cessation of bleeding from May 1995 to August 1996. Delayed bronchoscopy group included patients who did not received early bronchoscopy at the same period or in whom bronchoscopy was performed 48 hour after cessation of bleeding from October 1994 to May 1995. Results : Early bronchoscopy group was performed 73 times in 71 patients. Delayed bronchoscopy was performed in 57 times in 55 patients. There was no difference as to amount and underlying cause of hemoptysis between both groups. Indentification of bleeding site by visualizing active bleeding was significantly higher in early bronchoscopy (38.3%) than delayed bronchoscopy group (8.7%)(p < 0.05). Indentification of bleeding site by bleeding after clot removal was 8 in early and 10 in delayed bronchoscopy. Indentification of bleeding site by visualizing active bleeding and bleeding after clot removal was 36 in early and 15 patients in delayed bronchoscopy(p > 0.05). Causes of hemoptysis was found in 18 patients in early and 16 patients in delayed bronchoscopy group. patients who had early bronchoscopy underwent surgery. We diagnosed the site of bleeding in 4 patients preoperatively. In 3 patients we made a treatment plan promptly right after bronchoscopy. Among early bronchoscopy group, bleeding over 100cc during bronchoscopy occurred in 2 patients. In early bronchoscopy group there was no other major complication during bronchoscopy. Conclusion : In patients with hemoptysis, early bronchoscopy which performed within 48 hours after cessation of bleeding was more effective procedure for identifying the bleeding site than delayed bronchoscopy which was performed after 48 hour cessation of bleeding.

• Tuberculosis and Respiratory Diseases
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• v.47 no.3
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• pp.321-330
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• 1999

Background : Early diagnosis and proper antibiotic treatment are very important in the management of ventilator-associated pneumonia (VAP) because of its high mortality. Bronchoscopy with a protected specimen brush (PSB) has been considered the standard method to isolate the causative organisms of VAP. However, this method burdens consumer economically to purchase a PSB. Another useful method for the diagnosis of VAP is quantitative cultures of aspirated specimens through bronchoscopic bronchoalveolar lavage (BAL), for which the infusion of more than 120 m1 of saline has been recommended for adequate sampling of a pulmonary segment. However, occasionally it leads to deterioration of the patient's condition. We studied the diagnostic efficacy of minibronchoalveolar lavage (miniBAL), which retrieves only 25 ml of BAL fluid, in the isolation of causative organisms of VAP. Methods: We included 38 consecutive patients (41 cases) suspected of having VAP on the basis of clinical evidence, who had received antibiotics before the bronchoscopy. The two diagnostic techniques of PSB and miniBAL, which were performed one after another at the same pulmonary segment, 'were compared prospectively. The cut-off values for quantitative cultures to define causative bacteria of VAP were more than $10^3$ colony-forming units (cfu)/ml for PSB and more than $10^4$ cfu/ml for BAL. Results: The amount of instilled normal saline required to retrieve 25 ml of BAL fluid was $93{\pm}32 ml$ (mean${\pm}$SD). The detection rate of causative agents was 46.3% (19/41) with PSB and 43.9% (18/41) with miniBAL. The concordance rate of PSB and miniBAL in the bacterial culture was 85.4% (35/41). Although arterial blood oxygen saturation dropped significantly (p<0.05) during ($92{\pm}10%$) and 10 min after ($95{\pm}3%$) miniBAL compared with the baseline ($97{\pm}3%$), all except 3 cases were within normal ranges. The significantly elevated heart rate during ($l25{\pm}24$/min, p<0.05) miniBAL compared with the baseline ($1l1{\pm}22$/min) recovered again in 10 min after ($111{\pm}26$/min) miniBAL. Transient hypotension was developed during the procedure in two cases. The procedure was stopped in one case due to atrial flutter. Conclusion: MiniBAL is a safe and effective technique to detect the causative organisms of VAP.

• Tuberculosis and Respiratory Diseases
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• v.46 no.3
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• pp.350-362
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• 1999

Background: Acute Respiratory failure which is developed after extubation in the weaning process from mechanical ventilation is an important cause of weaning failure. Once it was developed, endotracheal reintubation has been done for respiratory support. Noninvasive Positive Pressure Ventilation (NIPPV) has been used in the management of acute or chronic respiratory failure, as an alternative to endotracheal intubation, using via nasal or facial mask. In this study, we evaluated the usefulness of NIPPV as an alternative method of reintubation in patients who developed acute respiratory failure after extubation. Method: We retrospectively analyzed thirty one patients(eighteen males and thirteen females, mean ages $63\pm13.2$ years) who were developed acute respiratory failure within forty eight hours after extubation, or were extubated unintentionally at medical intensive care unit(MICU) of Asan Medical Center. NIPPV was applied to the patients. Ventilatory mode of NIPPV, level of ventilatory support and inspiratory oxygen concentration were adjusted according to the patient condition and results of blood gas analysis by the attending doctors at MICU. NIPPV was completely weaned when the patients maintained stable clinical condition under 8 $cmH_2O$ of pressure support level. Weaning success was defined as maintenance of stable spontaneous breathing more than forty eight hours after discontinuation of NIPPV. Respiratory rate, heart rate, arterial blood gas analysis, level of pressure support, and level of PEEP were monitored just before extubation, at thirty minutes, six hours, twenty four hours after initiation of NIPPV. They were also measured at just before weaning from NIPPV in success group, and just before reintubation in failure group. Results: NIPPV was successfully applied to thirty-one patients of thirty-two trials and one patient could not tolerated NIPPV longer than thirty minutes. Endotracheal reintubation was successfully obviated in fourteen patients (45%) among them. There was no difference in age, sex, APACHE III score on admission at MICU, duration of intubation, interval from extubation to initiation of NIPPV, baseline heart rate, respiratory rate, arterial blood gas, and $PaO_2/FiO_2$ between the success and the failure group. Heart rate and respiration rate were significantly decreased with increase $SaO_2$ after thirty minutes of NIPPV in both groups(p<0.05). However, in the patients of failure group, heart rate and respiratory rate were increased again with decrease in $SaO_2$ leading to endotracheal reintubation. The success rate of NIPPV treatment was significantly higher in the patients with COPD compared to other diseases(62% vs 39%) (p=0.007). The causes of failure were deterioration of arterial blood gas without aggravation of underlying disease(n=9), aggravation of undelying disease(n=5), mask intolerance(n=2), and retained airway secretion(n=l). Conclusion: NIPPV would be a useful therapeutic alternative which can avoid reintubation in patient who developed acute respiratory failure after extubation.

• Tuberculosis and Respiratory Diseases
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• v.40 no.2
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• pp.135-146
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• 1993

Background: In acute pulmonary embolism it has been postulated that the constriction of bronchi and pulmonary artery secondary to neurohumoral response plays an important role in cardiopulmonary dysfunction in addition to the mechanical obstruction of pulmonary artery. Serotonin is considered as the most important mediator. Positive end expiratory pressure (PEEP) stimulates $PGI_2$ secretion from the vascular endothelium, but its role in acute pulmonary embolism is still in controversy. Methods: To study the cardiopulmonary effect and therapeutic role of Ketanserin, selective antagonist of 5-HT2 receptor, and PEEP in acute pulmonary embolism experimental acute pulmonary embolism was induced in dogs with autologous blood clot. The experimental animals were divided into 3 groups, that is control group, Ketanserin injection group and PEEP application group. Results: Thirty minutes after embolization, mean pulmonary arterial pressure and pulmonary vascular resistance increased and cardiac output decreased. $PaO_2,\;P\bar{v}O_2$ and oxygen transport decreased and physiological shunt and $PaCO_2$ increased. After injection of Ketanserin, comparing with control group, mean pulmonary arterial pressure, pulmonary vascular resistance and physiological shunt decreased, while cardiac output, $PaO_2$ and oxygen transport increased. All these changes sustained till 4 hours after embolization. After PEEP application pulmonary vascular resistance, $PaO_2$ and $PaCO_2$ increased, while physiological shunt, cardiac output and oxygen transport decreased. After discontinuation of PEEP, mean pulmonary arterial pressure and pulmonary vascular resistance decreased and were lower than control group, while $PaO_2$ and cardiac output increased and higher than control group. $PaCO_2$ decreased but showed no significant difference comparing with control group. Conclusion: It can be concluded that Ketanserin is effective for the treatment of acute pulmonary embolism. With PEEP hemodynamic status deteriorated, but improved better than control group after discontinuation of PEEP. Thus PEEP may be applied carefully for short period in acute pulmonary embolism if the hemodynamic status is tolerable.

• Tuberculosis and Respiratory Diseases
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• v.42 no.6
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• pp.871-877
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• 1995

Background: The index which could predict the prognosis of critically ill patients is needed to find out high risk patients and to individualize their treatment. The APACHE III scoring system was established in 1991, but there has been only a few studies concerning its prognostic value. We wanted to know whether the APACHE III scores have prognostic value in discriminating survivors from nonsurvivors in sepsis. Methods: In 48 patients meeting the Bones criteria for sepsis, we retrospectively surveyed the day 1(D1), day 2(D2) and day 3(D3) scores of patients who were admitted to intensive care unit. The scores of the sepsis survivors and nonsurvivors were compared in respect to the D1 score, and also in respect to the changes of the updated D2 and D3 scores. Results: 1) Of the 48 sepsis patients, 21(43.5%) survived and 27(56.5%) died. The nonsurvivors were older($62.7{\pm}12.6$ vs $51.1{\pm}18.1$ yrs), presented with lower mean arterial pressure($56.9{\pm}26.2$ vs $67.7{\pm}14.2\;mmHg$) and showed greater number of multisystem organ failure($1.2{\pm}0.8$ vs $0.2{\pm}0.4$) than the survivors(p<0.05, respectively). There were no significant differences in sex and initial body temperature between the two groups. 2) The D1 score was lower in the survivors (n=21) than in the nonsurvivors ($44.1{\pm}14.6$, $78.5{\pm}18.6$, p=0.0001). The D2 and D3 scores significantly decreased in the survivors (D1 vs D2, $44.1{\pm}14.6$ : $37.9{\pm}15.0$, p=0.035; D2 vs D3, $37.9{\pm}15.0$ : $30.1{\pm}9.3$, p=0.0001) but showed a tendency to increase in the nonsurvivors (D1 vs D2 (n=21), $78.5{\pm}18.6$ : $81.3{\pm}23.0$, p=0.1337; D2 vs D3 (n=11), $68.2{\pm}19.3$ : $75.3{\pm}18.8$, p=0.0078). 3) The D1 scores of 12 survivors and 6 nonsurvivors were in the same range of 42~67 (mean D1 score, $53.8{\pm}10.0$ in the survivors, $55.3{\pm}10.3$ in the nonsurvivors). The age, sex, initial body temperature, and mean arterial pressure were not different between the two groups. In this group, however, D2 and D3 was significantly decreased in the survivors(D1 vs D2, $53.3{\pm}10.0$ : $43.6{\pm}16.4$, p=0.0278; D2 vs D3, $43.6{\pm}16.4$ : $31.2{\pm}10.3$, p=0.0005), but showed a tendency to increase in the nonsurvivors(D1 vs D2 (n=6), $55.3{\pm}10.3:66.7{\pm}13.9$, p=0.1562; D2 vs D3 (n=4), $64.0{\pm}16.4:74.3{\pm}18.6$, p=0.1250). Among the individual items of the first day APACHE III score, only the score of respiratory rate was capable of discriminating the nonsurvivors from the survivors ($5.5{\pm}2.9$ vs $1.9{\pm}3.7$, p=0.046) in this group. Conclusion: In sepsis, nonsurvivors had higher first day APACHE III score and their updated scores on the following days failed to decline but showed a tendency to increase. Survivors, on the other hand, had lower first day score and showed decline in the updated APACHE scores. These results suggest that the first day and daily updated APACHE III scores are useful in predicting the outcome and assessing the response to management in patients with sepsis.

• Tuberculosis and Respiratory Diseases
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• v.42 no.5
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• pp.744-751
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• 1995

Background: Asthma is an inflammatory disease because there are many inflammatory changes in the asthmatic airways. Axon reflex mechanisms may be involved in the pathogenesis of asthma. Sensory neuropeptides are involved in this inflammation, which is defined as neurogenic inflammation. Substance p, neurokinin A, and neurokinin B may be main neuropeptides of neurogenic inflammation in airways. These tachykinins act on neurokinin receptors. Three types of neurokinin receptors, such as $NK_1$, $NK_2$, and $NK_3$, are currently recognized, at which substance p, neurokinin A, and neurokinin B may be the most relevant natural agonist of neurogenic inflammation in airways. The receptor subtypes present in several tissues have been characterized on the basis of differential sensitivity to substance p, neurokinin A, and neurokinin B. Plasma extravasation and vasodilation are induced by substance p more potently than by neurokinin A, indicating NK1 receptors on endothelial cells mediate the response. But airway contraction is induced by neurokinin A more potently than by substance P, indicating the $NK_2$ receptors in airway smooth muscles. These receptors are used to evaluate the pathogenesis of brochial asthma. FK224 was identified from the fermentation products of Streptomyces violaceoniger. FK224 is a dual antagonist of both $NK_1$ and $NK_2$ receptors. Purpose: For a study of pathogenesis of bronchial asthma, the effect of FK224 on plasma extravasation induced by vagal NANC electrical stimulation was evaluated in rat airway. Method: Male Sprague-Dawley rats weighing 180~450gm were anesthetized by i.p. injection of urethane. Plasma extravasation was induced by electrical stimulation of cervical vagus NANC nerves with 5Hz, 1mA, and 5V for 2 minutes(NANC2 group) and for sham operation without nerve stimulation(control group). To evaluate the effect of FK224 on plasma extravasation in neurogenic inflammation, FK224(1mg/kg, Fujisawa Pharmaceutical Co., dissolved in dimethylsulphoxide; DMSO, Sigma Co.) was injected 1 min before nerve stimulation(FK224 group). To assess plasma exudation, Evans blue dye(20mg/kg, dissolved in saline) was used as a plasma marker and was injected before nerve stimulation. After removal of intravascular dye, the evans blue dye in the tissue was extracted in formamide($37^{\circ}C$, 24h) and quantified spectrophotometrically by measuring dye absorbance at 629nm wavelength. Tissue dye content was expressed as ng of dye per mg of wet weight tissue. The amount of plasma extravasation was measured on the part of airways in each groups. Results: 1) Vagus nerve(NANC) stimulation significantly increased plasma leakage in trachea, main bronchus, and peripheral bronchus compared with control group, $14.1{\pm}1.6$ to $49.7{\pm}2.5$, $17.5{\pm}2.0$ to $38.7{\pm}2.8$, and $12.7{\pm}2.2$ to $19.1{\pm}1.6ng$ of dye per mg of tissue(mean ${\pm}$ SE), respectively(p<0.05). But there was not significantly changed in lung parenchyma(p>0.05) 2) FK224 had significant inhibitory effect upon vagal nerve stimulation-induced airway plasma leakage in any airway tissues of rat,such as trachea, main bronchus, and peripheral bronchus compared with vagus nerve stimulation group, 49%, 58%, and 70%, respectively(p<0.05). Inhibitory effect of FK224 on airway plasma leakage in neurogenic inflammation was revealed the more significant in peripheral bronchus, but no significant in lung parenchyma. Conclusion: These results suggest that FK224 is a selective NK receptor antagonist which effectively inhibits airway plasma leakage induced by the endogenous neurotransmitters relased by neurogenic inflammation in rat airway. Tachykinin receptor antagonists may be useful in the treatment of brochial asthma.

• Tuberculosis and Respiratory Diseases
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• v.42 no.6
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• pp.855-861
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• 1995

Background: Parathyroid hormone-related protein(PTHrp) was first identified as the cause of hypercalcemia in malignancy. Hypercalcemia can be found in malignancy, especially in the epidermoid carcinoma of the lung, even without extensive metastases to the bones. The application of sensitive assays for PTHrp may help in the early diagnosis of lung cancer, in the monitoring of treatment and in the detection of recurrence. Method: Serum PTHrp was measured by radioimmunoassay detecting the N-terminal 1~34 peptide of human PTHrp(PTHrp 1-34) in 63 histologically confirmed lung cancer patients and 22 healthy controls. Result: Serum PTHrp(mean$\pm$S.E.) was $312{\pm}68.9pg/ml$ in 63 lung cancer patients and $158{\pm}38.2pg/ml$ in 22 controls(p>0.05). PTHrp was $356{\pm}103.9pg/ml$ in 34 epidermoid carcinoma patients, $281{\pm}148.7pg/ml$ in 15 adenocarcinoma patients and $316{\pm}140.8pg/ml$ in 9 small cell carcinoma patients. In epidermoid carcinoma patients, PTHrp was $570{\pm}472.3pg/ml$ in stage II(n=3; p<0.05 vs controls), $166{\pm}22.4pg/ml$ in stage IIIa(n=9), $282{\pm}113.3pg/ml$ in stage IIIb(n=12) and $668{\pm}367.9pg/ml$ in stage IV(n=9; p<0.05 vs controls). PTHrp was significantly increased in 8 epidermoid carcinoma patients with bone metastases($1526{\pm}811.2\;pg/ml$; p<0.0005 vs controls). Hypercalcemia was observed in an epidermoid carcinoma patient whose PTHrp value was 244 pg/ml. Conclusion: The serum PTHrp was increased in advanced epidermoid carcinoma patients even without hypercalcemia. The measurement of PTHrp may be not helpful in the early diagnosis of lung cancer. But the lung cancer should be suspected in the marked elevation of PTHrp. It may be of value in detecting patients of advanced diseases with bone metastases or patients who might develop the malignancy associated hypercalcemia.

• Tuberculosis and Respiratory Diseases
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• v.44 no.6
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• pp.1343-1352
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• 1997

Background : Heat-treated cells are known to be protected from lysis by TNF, which is considered to play a central role in the pathogenesis of sepsis-induced acute lung injury. The objective of the study was to investigate the effect of heat shock response by heat-pretreatment on the acute lung injury of the rats induced by intratracheally administered TNF-$\alpha$, Methods : We intratracheally instilled either saline or TNF (R&D, 500ng) with and without heat pretreatment in Sprague-Dawley rats weighing 250~350 g. The heated rats were raised their rectal temperature to $41^{\circ}C$ and was maintained thereafter for 13 minutes at 18 h before intratracheal administration of saline or TNF. After 5 h of intratracheal treatment, lung leak, lung myeloperoxidase activity (MPO) and heat shock proteins were measured in rats. Lung leak index was defined as counts per minute of $I^{25}$ in the right lung divided by counts per minutes of $I^{25}$ in 1.0 ml of blood. All data are expressed as means ${\pm}$SE. Results : There is no difference in acute lung leak index ($0.099{\pm}0.024$ vs $0.123{\pm}0.005$) among the rats given saline intratracheally with and without heat pretreatment, but MPO activity showed a decreased tendency in heat-pretreated rats ($4.58{\pm}0.79\;U/g$) compared with heat-unpretreated rats ($7.32{\pm}0.97\;U/g$) (P=0.064). Rats administered TNF intratracheally with heat-pretreatment had decreased lung leak index ($0.137{\pm}0.012$) and lung MPO activity ($5.51{\pm}1.04\;U/g$) compared with those of heat-unpretreated and TNF-administered rats ($0.186{\pm}0.016$, $14.34{\pm}1.22\;U/g$) (P<0.05 in each). There were no significant difference of lung leak index and MPO activity between TNF-treated rats with heat-pretreatment and saline-treated rats with and without heat-pretreatment. Conclusion : The heat shock response attenuated neutrophil recruitment and acute lung leak induced by intratracheal instillation of TNF-in rats.

• Tuberculosis and Respiratory Diseases
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• v.44 no.6
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• pp.1296-1307
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• 1997

Background : Erdosteine is a thiol derivative developed for the treatement of chronic obstructive bronchitis, including acute infective exacerbation of chronic bronchitis. Erdosteine has mucomodulating and antioxidant properties and especially exhibits excellent gastrointestinal tolerability. Methods : The study was conducted as a prospective evaluation, with 2 comparative groups orally treated with erdosteine 300mg (bid.) or ambroxol 30mg (b.i.d.) for 7 days and the design of trial was double-blind. The treatments have been assigned randomly to patients (n=80) with acute or chronic bronchitis. The primary end-point used to determine efficacy in this study was subjective symptoms including expectorating frequence, expectoration volume, expectorating difficulty, expectoration viscosity, cough intensity and dyspnea. The secondary end-points of efficacy was the result of arterial blood gas analysis and pulmonary function test. Safety was evaluated with adverse drug reactions and laboratory tests monitoring. 61 patients was included in the efficacy analysis, due to the fact that 19 patients drop-out for different reasons. The obtained values have been analyzed with paired Hest., ANOVA test., multivariate $t^2$-test, repeated measures analysis of covariance, two sample t-test, loglinear-logit model analysis, Fisher's exact test. Results : 1) There was no significant difference on demographic data and vital signs between erdosteine and ambroxol treated groups. 2) The comparison between erdosteine and ambroxol treated groups showed no significant difference in improvement of each symptom in spite of the more favorable efficacy obtained with erdosteine. No difference on the contrary was observed for arterial blood gas analysis and pulmonary function test. 3) As safety is concerned, no clinical significant changes in laboratory test and symptom were induced in erdosteine and ambroxol treated group and two patients in ambroxol treated group drop-out for adverse reactions in symptom. 4) In the evaluation of final clinical efficacy, erdosteine improved more effectively patient's overall symptoms {very good effect (11/31), good effect (12/31), moderate effect (6/31), no effect (2/31), aggravation (0/31)} than ambroxol {very good effect (6/30), good effect (14/30), moderate effect (5/30), no effect (4/30), aggravation (2/30)}. And the probability of symptomatic improvement by erdosteine compared to ambroxol was 2.5 times. (p<0.05). Conclusion : This study showed that erdosteine was clinically effective and safe drug for treatment of acute and chronic bronchitis.