• Tuberculosis and Respiratory Diseases
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• v.53 no.4
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• pp.409-419
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• 2002

Background : The therapeutic effects of surfactant on acute lung injury derive not only from its recruiting action on collapsed alveoli but also from its anti-inflammatory effects. Pro-apoptotic action on alveolar neutrophils represents one of the important anti-inflammatory mechanisms of surfactant. In the present study, we evaluated the effects of sufactant on the apoptosis of human peripheral and rat alveolar neutrophils. Methods : In the (Ed- the article is not definitely needed but it helps to separate the two prepositions 'in') in vitro study, human neutrophils were collected from healthy volunteers. An equal number of neutrophils ($1{\times}10^6$) (Ed-confirm) was treated with LPS (10, 100, 1000ng/ml), surfactant (10, 100, $1000{\mu}g/ml$), or a combination of LPS (1000ng/ml) and surfactant (10, 100, $1000{\mu}g/ml$). After incubation for 24 hours, the apoptosis of neutrophils was evaluated by Annexin V method. In the in vivo study, induction of acute lung injury in SD rats by intra-tracheal instillation of LPS (5mg/kg) was followed by intra-tracheal administration of either surfactant (30mg/kg) or normal saline (5ml/kg). Tenty-four hours after LPS instillation, alveolar neutrophils were collected and the apoptotic rate was evaluated by Annexin V method. In addition, changes of the respiratory mechanics of rats (respiratory rate, tidal volume, and airway resistance) were evaluated with one chamber body plethysmography before, and 23 hours after, LPS instillation. Results : in the in vitro study, LPS treatment decreased the apoptosis of human peripheral blood neutrophils (control: $47.4{\pm}5.0%$, LPS 10ng/ml; $30.6{\pm}10.8%$, LPS 100ng/ml; $27.5{\pm}9.5%$, LPS 1000ng/ml; $24.4{\pm}7.7%$). The combination of low to moderate doses of surfactant with LPS promoted apoptosis (LPS 1000ng/ml + Surf $10{\mu}g/ml$; $36.6{\pm}11.3%$, LPS 1000ng/ml +Surf $100{\mu}g/ml$; $41.3{\pm}11.2%$). The high dose of surfactant ($1000{\mu}g/ml$) decreased apoptosis ($24.4{\pm}7.7%$) and augmented the anti-apoptotic effect of LPS (LPS 1000ng/ml + Surf $1000P{\mu}g/ml$; $19.8{\pm}5.4%$). In the in vivo study, the apoptotic rate of alveolar neutrophils of surfactant-treated rats was higher than that of normal saline-treated rats ($6.03{\pm}3.36%$ vs. $2.95{\pm}0.58%$). The airway resistance (represented by Penh) of surfactant-treated rats was lower than that of normal saline-treated rats at 23 hours after LPS injury ($2.64{\pm}0.69$ vs. $4.51{\pm}2.24$, p<0.05). Conclusion : Surfactant promotes the apoptosis of human peripheral blood and rat alveolar neutrophils. Pro-apoptotic action on neutrophils represents one of the important anti-inflammatory mechanisms of surfactant.

• Tuberculosis and Respiratory Diseases
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• v.47 no.5
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• pp.601-608
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• 1999

Background: Tuberculous pleural effusion responds well to the anti-tuberculosis agents in general, so no further aggressive therapeutic managements to drain the tuberculous effusion is necessary except in case of diagnostic thoracentesis. But in clinical practice, we often see some patients who later decortication need due to dyspnea caused by pleural thickening despite the completion of anti-tuberculosis therapy in the patients with tuberculous effusion. Especially, the patients with loculated tuberculous effusion might have increased chance of pleural thickening after treatment. The purpose of this study was that intrapleural urokinase instillation could reduce the pleural thickening in the treatment of loculated tuberculous pleural effusion. Methods: Thirty-seven patients initially diagnosed as having loculated tuberculous pleural effusion were randomly assigned to receive either the combined treatment of urokinase instillation and anti-tuberculosis agents(UK group) and anti-tuberculosis agents(Non-UK group) alone. The 16 patients in UK group received a single radiographically guided pig-tail catheter ranging in size from 10 to 12 French. 100,000 units of urokinase was dissolved in 150 ml of normal saline and instilled into the pleural cavity via pig-tail catheter every day, also this group was treated with anti-tuberculosis agents. While the 21 patients in Non-UK group were treated with anti-tuberculosis agents only except diagnostic thoracentesis. Then we evaluated the residual pleural thickening after treatment for their loculated tuberculous pleural effusion between the two groups. Also the duration of symptoms and the pleural fluid biochemistry like WBC counts, pH, lactic dehydrogenase(LDH), glucose, proteins, and adenosine deaminase(ADA) were compared. Results: 1) The residual pleural thickening(RPT)($5.08{\pm}6.77$ mm) of UK group was significantly lower than that($20.3222{\pm}26.37$ mm) of Non-UK group(P<0.05). 2) The duration of symptoms before anti-tuberculosis drug therapy of patients with RPT$\geq$10 mm($5.23{\pm}3.89$ wks) was significantly longer than the patients with RPT<10 mm($2.63{\pm}1.99$ wks)(P<0.05). 3) There were no significant differences in the pleural fluid findings like WBC count, glucose, LDH, proteins, pH, ADA between the patients with RPT$\geq$10 mm and the patients with RPT<10 mm. Conclusion : The treatment of loculated tuberculous pleural effusion with the urokinase instillation via percutaneous transthoraic catheter was effective to reduce the pleural thickening.

• Pediatric Gastroenterology, Hepatology & Nutrition
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• v.7 no.1
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• pp.40-47
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• 2004

Purpose: A new classification of gastrointestinal food allergy was published, but the changes of terminology between previously reported terms and the new ones were in a state of disorder. This has resulted in confusion between medical communication and diagnostic and therapeutic approaches. The clinical observations of infants presenting with gastrointestinal cow milk allergy (GI-CMA) were performed, and the changes in the terminology reviewed through the published Korean literature. Methods: Between March 2003 and July 2003, data from 37 consecutive infants with GI-CMA, aged 2 weeks to 15 months, were reviewed. The challenge and elimination test of cow milk, and the endoscopic and histologic findings, were used for the seven subdivisions of GI-CMA according to a new classification on the basis of patients' ages, clinical manifestations and location of gastrointestinal lesions. Results: The 37 patients had a mean age of $5.4{\pm}4.8$ months, with those observed in 26 (70.3%) of patients being below 6 months of age. The seven final diagnoses were; cow milk protein-induced enterocolitis (CMPIE) in 12 (32.4%), cow milk protein proctitis (PROC) in 12 (32.4%), IgE-mediated (IGE) in 6 (16.2%), gastroesophageal reflux-associated cow milk allergy (GERA) in 5 (13.5%) and eosinophilic gastroenterocolitis in 2 (5.4%). CMPIE was revealed as the typical type in 7 (18.9%) and the atypical type in 5 (13.5%), and all of typical CMPIE revealed cow milk protein-induced enteropathy. The mean age at symptom onset was $4.3{\pm}0.8$ months, and for those with typical and atypical CMPIE, and PROC and GERA were $3.8{\pm}4.6$, $10.4{\pm}3.8$, $3.4{\pm}3.9$ and $7.8{\pm}5.7$ months, respectively (p<0.05). The period from onset of symptom to diagnosis was $2.4{\pm}3.3$ (0.5~12) months, with those observed in atypical CMPIE and GERA being over 3months. Although the birth weights in all patients were within the 10~90 percentile range, the body weights on diagnoses were below the 3 percentile in 48.6%; IGE 16.7%, EOS 0%, typical CMPIE 85.7%, atypical CMPIE 60.0%, PROC 25.0% and GERA 100% (p<0.05). Through the review of the Korean literature, 8 case reports and 14 original articles for GI-CMA were found. Conclusion: GI-CMA is not a rare clinical disorder and is subdivided into seven categories on the basis of the patient's age, clinical manifestations and location of the gastrointestinal lesions. The terms for GI-CMA are changing with new classifications, and careful approaches are necessary for medical communications.

• Journal of Chest Surgery
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• v.40 no.4 s.273
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• pp.264-272
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• 2007

Background: Vascular endothelial growth factor (VEGF) plays an important role in angiogenesis, including stimulating the proliferation and migration of vascular smooth muscle cells (VSMCs). It has been known that diabetes is associated with accelerated cellular proliferation via VEGF, as compared to that under a normal glucose concentration. We investigated the effects of selective blockade of a VEGF receptor by using anti-Flt-1 peptide on the formation and hyperplasia of the neointima in balloon injured-carotid arteries of OLETF rats and also on the in vitro VSMCS' migration under high glucose conditions. Material and Method: The balloon-injury method was employed to induce neointima formation by VEGF. For f4 days beginning 2 days before the ballon injury, placebo or vascular endothelial growth factor receptor-1 (VEGFR-1) specific peptide (anti-Flt-1 peptide), was injected at a dose of 0.5mg/kg daily into the OLETF rats. At 14 days after balloon injury, the neointimal proliferation and vascular luminal stenosis were measured, and cellular proliferation was assessed by counting the proliferative cell nuclear antigen (PCNA) stained cells. To analyze the effect of VEGF and anti-Flt-1 peptide on the migration of VSMCs under a high glucose condition, transwell assay with a matrigel filter was performed. And finally, to determine the underlying mechanism of the effect of anti-Flt-1 peptide on the VEGF-induced VSMC migration in vitro, the expression of matrix metalloproteinase (MMP) was observed by performing reverse transcription-polymerase chain reaction (RT-PCR). Result: Both the neointimal area and luminal stenosis associated with neointimal proliferation were significantly decreased in the anti-Flt-1 peptide injected rats, ($0.15{\pm}0.04 mm^2$ and $ 36.03{\pm}3.78%$ compared to $0.24{\pm}0.03mm^2\;and\;61.85{\pm}5.11%$, respectively, in the placebo-injected rats (p<0.01, respectively). The ratio of PCNA(+) cells to the entire neointimal cells was also significantly decreased from $52.82{\pm}4.20%\;to\;38.11{\pm}6.89%$, by the injected anti-Flt-1 peptide (p<0.05). On the VSMC migration assay, anti-Flt-1 peptide significantly reduced the VEGF-induced VMSC migration by about 40% (p<0.01). Consistent with the effect of anti-Flt-1 peptide on VSMC migration, it also obviously attenuated the induction of the MMP-3 and MMP-9 mRNA expressions via VEGF in the VSMCS. Conclusion: Anti-Flt-1 peptide inhibits the formation and hyperplasia of the neointima in a balloon-injured carotid artery model of OLETF rats. Anti-Flt-1 peptide also inhibits the VSMCs' migration and the expressions of MMP-3 and MMP-9 mRNA induced by VEGF under a high glucose condition. Therefore, these results suggest that specific blockade of VEGFR-1 by anti-Flt-1 peptide may have therapeutic potential against the arterial stenosis of diabetes mellitus patients or that occurring under a high glucose condition.

• Tuberculosis and Respiratory Diseases
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• v.49 no.3
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• pp.332-342
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• 2000

Background : The importance of pro-inflammatory cytokines, especially tumor necrosis factor $\alpha$ (INF-$\alpha$) and interleukin-1$\beta$ (IL-1$\beta$), have been extensively documented in the generation of inflammatory lung disease. Lung epithelial cells are also actively involved in initiating and maintaining inflammation by producing pro-inflammatory mediators. Understanding the mechanism of pro-inflammatory cytokine expression in lung epithelial cells is crucial to the development of new therapeutic modalities for inflammatory lung disease. Transcription of most pro-inflammatory cytokines is dependent on the activation of NF-${\kappa}B$. However, the relationship between pro-inflammatory cytokine expression and NF-${\kappa}B/I{\kappa}B$ pathway in lung epithelial cells is not clear. Methods : BEAS-2B, A549, Na-H157, NCI-H719 cells were stimulated with IL-$1{\beta}$ or TNF-$\alpha$ at various times, and then IL-8 and TNF-$\alpha$mRNA expressions were assayed by Northern blot analysis. IL-$1{\beta}$ or TNF-$\alpha$-induced NF-${\kappa}B$ activation was assessed by the nuclear translocation of p65 NF-${\kappa}B$ subunit. The degradation of $I{\kappa}B{\alpha}$ and $I{\kappa}B{\beta}$ by IL-$1{\beta}$ or TNF-$\alpha$stimulation was assayed by Western blot analysis. The phosphorylation of $I{\kappa}B{\alpha}$ was evaluated by Western blot analysis after pre-treating cells with proteasome inhibitor followed by IL-$1{\beta}$ or TNF-$\alpha$ stimulation. The basal level of IKK $\alpha$ expression was evaluated by Western blot analysis. Results: $I{\kappa}B{\alpha}$ and $I{\kappa}B{\alpha}$ was rapidly degraded after 5 minutes of incubation with IL-$1{\beta}$ or TNF-$\alpha$ in BEAS-2B, A549, and NCI-H157 cells. The activation of NF-${\kappa}B{\alpha}$ and the induction of IL-8 and TNF-$\alpha$ mRNA expression were observed by IL-$1{\beta}$ or TNF-$\alpha$ stimulation in these cells. In contrast, neither the changes in NF-${\kappa}B/I{\kappa}B$ pathway nor IL-8 and TNF-$\alpha$mRNA expression was induced by IL-$1{\beta}$ or TNF-$\alpha$ stimulation in NCI-H719 cells. IL-$1{\beta}$ and TNF-$\alpha$-induced $I{\kappa}B$ phosphorylation was observed in BEAS-2B, A549, and NCI-H157 cells, but not in NCI-H719 cells. The basal level of IKK$\alpha$ expression was not different between cell. Conclusion : NF-${\kappa}B/I{\kappa}B$ pathway plays an important role in the expression of pro-inflammatory cytokine in most lung epithelial cells. The absence of the effect on NF-${\kappa}B/I{\kappa}B$ pathway in NCI-H719 cells sæms to be due to the defect in the intracellular signal transduction pathway upstream to IKK.

• Tuberculosis and Respiratory Diseases
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• v.49 no.3
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• pp.323-331
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• 2000

Purpose: Brain metastases are present in approximately 10-16% of small cell lung cancer patients at diagnosis. Brain metastasis is an important clinical problem associated with increasing the survival rate, with a cumulative incidence of up to 80% in patients surviving 2 years. Prophylactic cranial irradiation(PCI) reduces the incidence of brain matastasis and may prolong survival in patients with limited small-cell lung cancer who achieved complete remission. This study was performed to analyze the incidence of brain metastasis, survival and clinical aspects after PCI in patients with limited small-cell lung cancer who achieved complete remission. Methods : Between 1989 and 1999, forty-two patients with limited small-cell lung cancer who achived achieved complete remission after therapy were enrolled into this study retrospectively. All patients received etoposide and cisplatin(VPP) alternating with cytoxan, adriamycin, and vincristine(CAV) every 3 weeks for at least 6 cycles initially. All patients received thoracic radiotherapy: concurrent(38.1%) and sequential(61.9%). All patients received late PCI. Results : Most patients(88.1%) were men, and the median age was 58 years. The median follow-up duration was 18.1 months. During the follow-up period, 57.1% of the patients developed relapse. The most frequent site of relapse was chest(35.7%), followed by brain(14.3%), liver(11.9%), adrenal gland(44%), and bone(2.2%). With the Kaplan-Meier method, the average disease-free interval was 1,090 days(median 305 days). The average time to development of brain relapse after PCI and other sites relapse(except brain) were 2,548 days and 1,395 days(median 460 days), respectively. The average overall survival was 1,233 days(median 634 days, 21.1 months), and 2-year survival rates was 41.7%. The average overall survival in the relapse group was 642 days(median 489 days) and in the no relapse group was 2,622 days(p<0.001). The average overall survival in the brain relapse group was 928 days(median 822 days) and in the no brain relapse group was 1,308 days(median 634 days)(p=0.772). In most patients(85.7%), relapse(except brain) or systemic disease was the usual cause of death. Brain matastasis was the cause of death in 14.3% of the cases. Conclusions : We may conclude that PCI reduces and delays brain metastasis in patients with limited small cell lung cancer who achieved complete remission. We found decreased survival in relapse group but, no significant survival difference was noted according to brain matastasis. And relapse(except brain) or systemic disease was the usual cause of death. In order to increase survival, new treatment strategies for control methods for relapse and systemic disease are required.

• Radiation Oncology Journal
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• v.18 no.2
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• pp.133-137
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• 2000

Purpose :To investigate whether combined beta-carotene with X-Irradiation has more enhanced radition response than X-irradiation or not, we peformed a experiment about in vitro cytotoxlcity of beta-carotene and/or X-irradiation in the fibrosarcoma cells, tumor growth delay of combined beta-caroten with/or X-irradiation in the mouse fibrosarcoma. Materials and Methods : 2$\%$ emulsion of beta-carotene was serially diluted and used. X-Irradiation was given by 6 MeV linear accelerator. The cytotoxicity of beta-carotene in vitro was evaluated from clonogenic assay. To compare the cytotoxiclty between combined beta-carotene with X-irradiation and X-irradiation group, 2 mg/ml of beta-carotene was contacted to fibrosarcoma (FSall) cells for 1 hour before X-irradiation. For the tumor growth delay, single 20 Gy was given to FSall tumor hearing C3H/N mice whic was classified as beta-crotene with X-irradiation group (n=5) and X-irradiation alone group (n=5). 0.2 ml of 20 mg/kg of beta-carotene were i.p. injected to mice 30 minute before X-irradiation in the beta-crotene with X-irradiation group. The tumor growth delay defined as the time which reach to 1,000 mm$^{3}$ of tumor volume. Results : (1) Cytotoxicity in vitro: 1) survival fraction at beta-carotene concentration of 0.002,0.02,0.2 and 2 mg/ml were 0.69$\pm$0.07, 0.59$\pm$0.08, 0.08$\pm$0.008 and 0.02$\pm$0.006, respectively. 2) each survival fraction at 2, 4, 6 and 8 Gy in the 2 mg/ml of beta-carotene + X-irradiation group were 0.13$\pm$0.05, 0.03$\pm$0.005, 0.01 $\pm$0.002 and 0.009$\pm$0.0008, respectively. But each survival fraction at same irradiation dose in the X-irradiation group were 0.66$\pm$0.05, 0.40$\pm$0.04, 0.11$\pm$0.01 and 0.03$\pm$0.006, respectively(p<0.05). (2) The time which reach to 1,000 mm$^{3}$ of tumor volume of beta-carotene + X-irradiation group and X-irradiation alone group were 18, 19 days, respectively(p>0.05) Conclusion : The contact of beta-caroten to Fsall cells showed mild cytotoxicity which 띤as increased according to concentration. The cytotoxicity of combined beta-carotene with X-irradiation more increased than that of X-irradiation, additionally, And there was significant difference of cytotoxicity between two groups. But there were no significant difference of the growth delay of fibrosarcoma between two groups.

• Radiation Oncology Journal
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• v.19 no.1
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• pp.53-65
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• 2001

Purpose : To improve the local control of patients with nasopharyngeal cancer, we have implemented 3-D conformal radiotherapy and forward intensity modulated radiation therapy (IMRT) to used of compensating filters. Three dimension conformal radiotherapy with intensity modulation is a new modality for cancer treatments. We designed 3-D treatment planning with 3-D RTP (radiation treatment planning system) and evaluation dose distribution with tumor control probability (TCP) and normal tissue complication probability (NTCP). Material and Methods : We have developed a treatment plan consisting four intensity modulated photon fields that are delivered through the compensating tilters and block transmission for critical organs. We get a full size CT imaging including head and neck as 3 mm slices, and delineating PTV (planning target volume) and surrounding critical organs, and reconstructed 3D imaging on the computer windows. In the planning stage, the planner specifies the number of beams and their directions including non-coplanar, and the prescribed doses for the target volume and the permissible dose of normal organs and the overlap regions. We designed compensating filter according to tissue deficit and PTV volume shape also dose weighting for each field to obtain adequate dose distribution, and shielding blocks weighting for transmission. Therapeutic gains were evaluated by numerical equation of tumor control probability and normal tissue complication probability. The TCP and NTCP by DVH (dose volume histogram) were compared with the 3-D conformal radiotherapy and forward intensity modulated conformal radiotherapy by compensator and blocks weighting. Optimization for the weight distribution was peformed iteration with initial guess weight or the even weight distribution. The TCP and NTCP by DVH were compared with the 3-D conformal radiotherapy and intensitiy modulated conformal radiotherapy by compensator and blocks weighting. Results : Using a four field IMRT plan, we have customized dose distribution to conform and deliver sufficient dose to the PTV. In addition, in the overlap regions between the PTV and the normal organs (spinal cord, salivary grand, pituitary, optic nerves), the dose is kept within the tolerance of the respective organs. We evaluated to obtain sufficient TCP value and acceptable NTCP using compensating filters. Quality assurance checks show acceptable agreement between the planned and the implemented MLC(multi-leaf collimator). Conclusion : IMRT provides a powerful and efficient solution for complex planning problems where the surrounding normal tissues place severe constraints on the prescription dose. The intensity modulated fields can be efficaciously and accurately delivered using compensating filters.

• Tuberculosis and Respiratory Diseases
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• v.45 no.6
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• pp.1199-1213
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• 1998

Background : The number of immunocompromised hosts has been increasing steadily and a new pulmonary infiltrate in these patients is a potentially lethal condition which needs rapid diagnosis and treatment. In this study we sought to examine the clinical manifestations, radiologic findings, and therapeutic outcomes of pulmonary mycoses presenting as a new pulmonary infiltrate in immunocompromised hosts. Method : All cases presenting as a new pulmonary infiltrate in immunocompromised hosts and confirmed to be pulmonary mycoses by pathologic examination or by positive culture from a sterile site between October of 1996 and April of 1998 were included in the study and their chart and radiologic findings were retrospectively reviewed. Results : In all, 14 cases of pulmonary mycoses from 13 patients(male : female ratio = 8 : 5, median age 47 yr) were found. Twelve cases were diagnosed as aspergillosis while two were diagnosed as mucormycosis. Major risk factors for fungal infections were chemotherapy for hematologic malignancy(10 cases) and organ transplant recipients(4 cases). Three cases were receiving empirical amphotericin B at the time of appearance of new lung infiltrates. Cases in the hematologic malignancy group had more prominent symptoms : fever(9/10), cough(6/10), sputum(5/10), dyspnea(4/10), chest pain(5/10). Patients in the organ transplant group had minimal symptoms(p<0.05). On simple chest films, all of the cases presented as single or multiple nodules(6/14) or consolidations(8/14). High resolution computed tomograph showed peri-lesional ground glass opacities(14/14), pleural effusions(5/14), and cavitary changes(7/14). Definitive diagnostic methods were as follows : 10 cases underwent minithoracotomy, 2 underwent video-assisted thoracoscopic surgery, 1 underwent percutaneous needle aspiration and 1 case was diagnosed by culture of abscess fluid. All cases received treatment with amphotericin B with 1 case each being treated with liposomal amphotericin B and itraconazole due to renal toxicity. Lung lesion improved in 12 of 14 patient but 4 patients died before completing therapy. Conclusion : When a new lung infiltrate develops presenting either as a nodule or consolidation in a neutropenic patient with hematologic malignancy or in a transplant recipient, you should always consider pulmonary mycoses as one of the differential diagnosis. By performing aggressive work up and early treatment, we may improve prognosis of these patients.

• 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.