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Y Koh

Publications and source records attributed to Y Koh.

At least 19 recordsLinked to original sources
PubMed2006

Comparison of two commercial interferon-gamma assays for diagnosing Mycobacterium tuberculosis infection.

The clinical usefulness of ex vivo interferon-gamma assays may largely depend on the assay format and epidemiological status of tuberculosis (TB) in the region studied. From July 2004 to June 2005 a prospective comparison study was undertaken at a tertiary referral hospital in South Korea. The results of tuberculin skin tests (TST) and the commercially available QuantiFERON-TB Gold (QFT-G) and T SPOT-TB (SPOT) assays were compared in an intermediate TB-burden country. Of the 224 participants studied, results from all three tests (TST, QFT-G, and SPOT) were available in 218; 87 with active TB and 131 at a low risk for TB. Using 10 mm as a cut-off for TST, SPOT sensitivity (96.6%) was significantly higher than that seen for TST (66.7%) and QFT-G (70.1%). QFT-G showed superior specificity over TST (91.6 versus 78.6%). Although the specificity of QFT-G was higher than that of SPOT (91.6 versus 84.7%), the difference was not statistically significant. Whilst some differences were found in the performance of the two commercialised interferon-gamma assays, they seemed to be superior in their detection of Mycobacterium tuberculosis infection compared with tuberculin skin tests. The most appropriate choice of interferon-gamma assay to use may depend on the clinical setting.

Adolescent↗
PubMed2005

[Modified Komeda-David operation for postinfarction ventricular septal perforation].

The infarct exclusion technique with a xeno-pericardial patch which Komeda and associates firstly reported in 1990 is one of the best procedure to close ventricular septal perforation. A large patch can protect the perforation and the surrounding weak tissue from the internal left ventricular pressure. However, suturing this large patch to the left ventricular wall through the small incision is not technically easy because of the patch design in the ventricle. We modified the design of the patch. This round shaped bovine pericardial patch was sutured continuously to the left ventricular wall. Then, excessive part of the patch was trimmed to make a corn shape. Finally, the corn shaped patch fit the left ventricular wall naturally.

Aged↗
PubMed2003

Hypothermia attenuates vascular manifestations of ventilator-induced lung injury in rats.

Alveolar hemorrhage and pulmonary edema induced by mechanical ventilation are partly dependent on cardiac output. Because cardiac output is low during hypothermia, we hypothesized that hypothermia may protect against these vascular manifestations of ventilator-induced lung injury. Twenty-seven Sprague-Dawley rats were assigned to either normothermia (37 +/- 1 degrees C)-injurious ventilation (NT; n = 10), hypothermia (27 +/- 1 degrees C)- injurious ventilation (HT; n = 10), or nonventilated control ( n = 7). The two ventilated groups were subjected to injurious ventilation of peak airway pressure 30 cm H(2)O with zero end-expiratory pressure for 20 min. Compared with the NT group, the hemorrhage/congestion score of the lung (11.2 +/- 1.5 vs. 4.7 +/- 1.6; p < 0.001) and the ratio of wet/dry lung weight (6.1 +/- 0.8 vs. 5.0 +/- 0.1; p = 0.046) of the HT group were lower. Compared with the NT group, protein concentration (3,471 +/- 1,985 micro g/ml vs. 1,374 +/- 726 micro g/ml; p = 0.003) and lactate dehydrogenase level (0.43 +/- 0.22 U/ml vs. 0.18 +/- 0.1 U/ml; p = 0.046) in bronchoalveolar lavage fluid of the HT group were lower. Whereas pressure-volume curve was shifted to the right in the NT group after injurious ventilation, it was not shifted in the HT group. In conclusion, hypothermia in rats attenuated the degrees of vascular manifestations and alveolar epithelial injuries induced by injurious ventilation, and preserved the mechanical properties of the lung.

Animals↗
PubMed2001

Genistein prevents nuclear factor-kappa B activation and acute lung injury induced by lipopolysaccharide.

Protein tyrosine kinase (PTK) inhibitors have been proposed to reduce lung injury and lethal toxicity. The mechanisms responsible for the effects of PTK inhibitors remain obscure. The purpose of the present study was to examine whether genistein, a specific inhibitor of PTK, inhibits nuclear factor-kappa B (NF-kappaB) activation during acute lung injury induced by lipopolysaccharide (LPS) and, if so, to enumerate the effects of inhibition of NF-kappaB activation on LPS-induced proinflammatory gene products, such as cytokine-inducible neutrophil chemoattractant (CINC) and matrix metalloproteinase-9 (MMP-9), as well as neutrophil influx into the lungs. Intratracheal treatment of rats with LPS (6 mg/kg) resulted in increases in total protein and lactate dehydrogenase activity in bronchoalveolar lavage fluid and activated DNA-binding activity of NF-kappaB in alveolar macrophages and lung tissue. A 2-h pretreatment with genistein (50 mg/kg, intraperitoneally) inhibited the LPS-induced changes in lung injury parameters and the induction of NF-kappaB activation. Furthermore, these inhibitory effects of genistein correlated with a depression of LPS-induced protein tyrosine phosphorylation (approximately molecular masses of 46, 48, and 54 kD) and phosphorylation of Jun N-terminal kinase (JNK) in lung tissue. Genistein also substantially reduced the LPS-induced CINC production and MMP-9 activity and suppressed neutrophil recruitment. These results suggest that genistein attenuates LPS-induced acute lung responses through inhibition of NF-kappaB activation. In addition, NF-kappaB activation appears to be an important mechanism mediating LPS-induced CINC production and MMP-9 activity and resulting neutrophil recruitment associated with acute lung inflammation and injury.

Animals↗
PubMed2001

Pathogenic role of endothelin 1 in hemodynamic dysfunction in experimental acute pulmonary thromboembolism.

The plasma endothelin-1 (ET-1) level is elevated in patients with acute pulmonary thromboembolism (APE). Whether ET-1 is a pathogenic mediator or a simple marker of APE is not known. We investigated the role of ET-1 in hemodynamic dysfunction in APE through evaluating the effects of ET(A) receptor antagonist in an experimental APE model. We also examined ET-1 expression in embolized lungs. In a canine autologous blood clot pulmonary embolism model, ET(A) receptor antagonist ZD2574 (10 mg/kg, intravenous; ZD2574 group; n = 6) or vehicle (control group; n = 5) was administered. Hemodynamic and gas exchange parameters and plasma levels of ET-1 were serially measured. Prepro-ET-1 mRNA expression and the distribution of ET-1 peptide in lung tissues were also examined. With ZD2574 pulmonary arterial pressure and pulmonary vascular resistance significantly decreased, and were lower compared with the control group. The decrease in cardiac output was also less in the ZD2574 group. Plasma ET-1 levels increased after embolization. Prepro-ET-1 mRNA expression increased in embolized lungs and ET-1 peptide expression also increased in embolized lungs, particularly in the muscular pulmonary arteries, compared with normal lungs. These findings suggest that ET-1 partially contributes to hemodynamic derangements of APE, and that ET(A) receptor antagonists might constitute a useful therapeutic tool for APE.

Acute Disease↗
PubMed2001

Oncoprotein 18 overexpression increases the sensitivity to vindesine in the human lung carcinoma cells.

BACKGROUND: Oncoprotein 18 (op18) was first isolated as a molecule overexpressed in several malignant cells, suggesting a function of op18 in malignant processes, such as differentiation in hematologic malignancies, op18 also was found to enhance microtubule deassembly in the cells. Antimitotic agents that bind to tubulin have been used for chemotherapy to treat solid tumors, such as lung carcinoma. Vinca alkaloids, such as vindesine and vincristine, have commonly been used for chemotherapy of nonsmall cell lung carcinoma. The authors examined the role of op18 in the sensitivity of human lung carcinoma cells to antimitotic agents. METHODS: Expression of op18 mRNA was detected in all 17 lung carcinoma cell lines tested by Northern blotting. Oncoprotein 18 cDNA was transfected to SBC-3 human lung carcinoma cells, and the stable transfectants, SBC-3/op1-3, were isolated. The sensitivity of these transfectants against antimitotic agents were examined by the MTT assay in vitro. Cell cycle distribution of the transfectants on DNA histogram was analyzed by flow cytometry. RESULTS: Oncoprotein 18-transfected cells showed higher sensitivity to vindesine and vincristine, but not to taxanes. Vindesine-exposure increased the G2/M population of the cell cycle in the Mock transfectants, but not in SBC-3/op1, suggesting that the cell cycle dynamics were altered by op18 expression in SBC-3/op1. CONCLUSION: Oncoprotein 18 expression is associated with lung carcinoma cell sensitivity to vindesine and may be able to serve as a surrogate marker for the chemosensitivity to Vinca alkaloids in human lung carcinomas.

Antineoplastic Agents, Phytogenic↗
PubMed2001

Comparison of the response to the prone position between pulmonary and extrapulmonary acute respiratory distress syndrome.

OBJECTIVES: To determine whether the response to the prone position differs between acute respiratory distress syndrome (ARDS) resulting from a pulmonary cause (ARDSp) and that from an extrapulmonary cause (ARD-Sexp). DESIGN AND SETTING: Prospective observational study in a medical ICU of a university-affiliated hospital. SUBJECTS: A consecutive series of 31 patients with ARDSp and 16 with ARDSexp within 3 days of onset of ARDS. INTERVENTION: Prone position for at least 2 h. MEASUREMENTS AND RESULTS: In ARDSp, compared with the supine position (121 +/- 49 mmHg), PaO2/FIO2 was not increased after 0.5 h but was increased after 2 h in the prone position (158 +/- 60 mmHg). In ARDSexp, compared with the supine position (106 +/- 53 mmHg), PaO2/FIO2 was increased after 0.5 h (155 +/- 91 mmHg), but was not further changed after 2 h. Marked oxygenation response (increase in PaO2/FIO2 > 40% from baseline) after 0.5 h was 23% in ARDSp and 63% in ARDSexp, and that after 2 h was 29% and 63%, respectively. Static respiratory compliance decreased in the prone position in ARDSexp (30 +/- 11 ml/cmH2O at baseline, 27 +/- 11 after 0.5 h and 25 +/- 9 after 2 h) but not in ARDSp. Consolidation score as determined on the first chest radiography taken in the prone position decreased to a greater degree in ARDSexp (-2.4 +/- 4.1) than in ARDSp (0.3 +/- 4.1). CONCLUSION: Pulmonary ARDS and extrapulmonary ARDS in their early stages respond differently to the prone position with regard to the time course of oxygenation, respiratory mechanical behaviour, and radiographic change. These findings suggest that the early pathophysiology of ARDS differs according to the type of primary insult to the lung.

Aged↗
PubMed2001

Effect of ventilation mode on gas exchange during partial liquid ventilation at different perfluorocarbon doses in surfactant-depleted lung.

Although gas ventilation is an integral part of partial liquid ventilation (PLV), the role of ventilation mode during PLV is not established, especially at a varying perfluorocarbon dose. In 10 surfactant-depleted rabbits, PLV was performed at a low dose (10 ml/kg) and at a functional residual capacity (FRC) dose (30 ml/kg) of perfluorodecalin in pressure-control (PC) and volume-control (VC) modes in balanced sequence. In these four PLV trials, PC mode was adjusted to be identical to VC mode with regard to tidal volume and inspiratory-to-expiratory ratio. PaO2 during PLV in PC mode was higher than in VC mode at the Low dose (159 plus minus 93 mm Hg, 115 plus minus 75 mm Hg, respectively: p = 0.005) and at the FRC dose (228 +/- 114 mm Hg, 164 +/- 104 mm Hg, respectively: p = 0.002). PaCO2 during PLV in PC mode was lower than in VC mode at the Low dose (59 +/- 18 mm Hg, 72 +/- 20 mm Hg, respectively: p = 0.005), whereas PaCO2 at the FRC dose was not different between modes. Curves of inspiratory flow appeared least deformed with PLV in PC mode at the Low dose, whereas they were saw-tooth deformed with PLV in VC mode at both doses. Actual time for inspiratory gas flow during PLV was shorter in PC mode compared with VC mode at both doses. In conclusion, in surfactant-depleted rabbit, gas exchange during PLV was better with PC mode compared with VC mode, especially at a low perfluorocarbon dose. Given the same tidal volume, PC appeared to insufflate the perfluorocarbon-filled lung better than VC at both low and FRC doses of perfluorocarbon.

Animals↗
PubMed2001

Gene expression profiling of exposure to TZT-1027, a novel microtubule-interfering agent, in non-small cell lung cancer PC-14 cells and astrocytes.

Clinical use of TZT-1027, a microtubule-interfering agent that inhibits the polymerization of tubulin, is expected because of its potent effects on solid tumors. TZT-1027 is thought to act directly on cellular microtubules, and arrest cell mitosis, however, the molecular mechanisms of the microtubule damage by TZT-1027 have not been fully identified. To investigate the possible novel mechanisms of action of TZT-1027, we used the cDNA macroarray technique to examine its effect on the expression of hundreds of tightly transcriptionally controlled genes. We used two cell lines, one was human non-small cell lung carcinoma PC-14 cells as a model for cancer cells, and the other was human astrocytes as a model for normal neuronal cells, because the dose-limiting-factor of microtubule-interfering agents is mainly peripheral neurotoxicity. mRNAs prepared from the PC-14 and astrocyte cell lines treated with TZT-1027 were compared with 588 genes spotted onto the filter, and which gene groups TZT-1027 modulated between the two cell lines was investigated. TZT-1027 exposure modulated expression of a variety of genes including the genes encoding cell-cycle and growth regulators, receptors, angiogenesis and invasion regulators, rho family small GTPases and their regulators and growth factors and cytokines. However, the way of gene regulation by TZT-1027 exposure was different between PC-14 cells and astrocytes. Genes up-regulated in both PC-14 cells and astrocytes were those for RAR-epsilon, TNFR 1 and 2 and so on. Specifically altered genes in PC-14 cells, such as the genes coding for cytokeratin 8, XPG, fau and the genes regulated only in PC-14 cells may be involved in the antitumor activity of TZT-1027. On the other hand, growth factor receptor precursors was upregulated specifically in astrocytes by TZT-1027 and this gene regulation only in astrocytes may be candidates related with neurotoxicity.

Antineoplastic Agents↗
PubMed2001

Effects of heat pretreatment on histopathology, cytokine production, and surfactant in endotoxin-induced acute lung injury.

To determine the effect of heat stress on histopathology of acute lung injury (ALI) caused by administration of lipopolysaccharide (LPS), and to determine the roles of tumor necrosis factor (TNF)-alpha, interleukin (IL)-1beta, interferon (IFN)-gamma, IL-10 and surfactants in heat-induced tolerance to ALI, we administered either saline or LPS (3 mg/kg of body weight) intravenously to male Sprague-Dawley rats without and with heat pretreatment. Five hours after LPS or saline treatment (23 h after heat-pretreatment), samples were obtained. We found that the histopathologic features of LPS-induced ALI were attenuated by heat-pretreatment. Heat-pretreatment did not decrease the elevated plasma or BAL fluid levels of TNF-alpha, IL-1beta, and IFN-gamma by LPS. The plasma level of IL-10 in LPS-treated rats with heat-pretreatment, however, was increased compared to that of LPS-treated rats without heat-pretreatment (P = 0.001). There were no differences in the BAL fluid concentrations of light or heavy density pulmonary surfactant phospholipids depending on heat-pretreatment in LPS-treated rats. These observations suggest that IL-10 might play a role in decreasing LPS-induced acute lung injury after heat-pretreatment.

Acute Disease↗
PubMed2001

Residents' preparation for and ability to manage ethical conflicts in Korean residency programs.

The doctor-patient relationship in Korea has been deteriorating, and the numbers of malpractice suits and other medical disputes have been increasing annually for the past decade. Part of the problem may be physicians' lack of ethics education. The author and colleagues surveyed Korean residents from 14 university hospitals and found that most regularly experienced serious ethical dilemmas and had difficulty appropriately managing them. Few were familiar with medical law, and many resolved ethical conflicts either on their own or by talking with colleagues. Many did not follow guidelines for obtaining informed consent. Few had ethics committees or consultants available to them, and most did not discuss ethical dilemmas with attending physicians. The author describes the kinds of dilemmas faced by Korean residents and how they manage them, and he offers recommendations for improving ethics education and the ethics environment for Korean medical students and residents.

Adaptation, Psychological↗
PubMed2001

Inhaled nitric oxide down-regulates intrapulmonary nitric oxide production in lipopolysaccharide-induced acute lung injury.

OBJECTIVE: To examine whether inhaled nitric oxide (NO) affected the intrapulmonary production of NO, reactive oxygen species, and nuclear factor-kappaB in a lipopolysaccharide (LPS)-induced model of acute lung injury. DESIGN: Prospective, randomized, laboratory study. SETTING: Experimental laboratory at a biomedical institute. SUBJECTS: Twenty male rabbits weighing 2.5-3.5 kg. INTERVENTIONS: Saline or LPS (5 mg/kg of body weight) was administered intravenously with or without NO inhalation (10 ppm) in each group of five rabbits. MEASUREMENTS AND MAIN RESULTS: LPS increased the lung leak index, the neutrophils and NO levels in bronchoalveolar lavage fluid, and NO levels produced by resting and stimulated alveolar macrophages. Inhaled NO decreased the lung leak index, the neutrophils and NO levels as measured by nitrite levels in the lavage fluid, and NO produced by the resting and stimulated alveolar macrophages. Inhaled NO also blocked the activities of reactive oxygen species and nuclear factor-kappaB binding to DNA in lavage cells and in alveolar macrophages. CONCLUSION: Inhaled NO attenuates LPS-induced acute lung injury, possibly by decreasing NO production in the lungs. The mechanism of reducing NO production resulting from inhaled NO may involve, in part, the activities of reactive oxygen species and/or nuclear factor-kappaB.

Acute Disease↗
PubMed2001

Mechanistic scheme and effect of "extended sigh" as a recruitment maneuver in patients with acute respiratory distress syndrome: a preliminary study.

OBJECTIVE: To devise a new form of sigh ("extended sigh") capable of providing a sufficient recruiting pressure x time, and to test it as a recruitment maneuver in patients with acute respiratory distress syndrome. DESIGN: Prospective uncontrolled clinical trial. SETTING: Medical intensive care unit of a university-affiliated hospital. PATIENTS: Twenty consecutive patients diagnosed with acute respiratory distress syndrome (18 men, 2 women, age 59 +/- 10 yrs). INTERVENTIONS: From baseline settings of tidal volume (Vt) 8 mL/kg and positive end-expiratory pressure (PEEP) 10 cm H2O on volume control mode with the high pressure limit at 40 cm H2O, the Vt-PEEP values were changed to 6-15, 4-20, and 2-25, each step being 30 secs (inflation phase). After Vt-PEEP 2-25, the mode was switched to continuous positive airway pressure of 30 cm H2O for a duration of 30 secs (pause), after which the baseline setting was resumed following the reverse sequence of inflation (deflation phase). This extended sigh was performed twice with 1 min of baseline ventilation between. MEASUREMENTS AND RESULTS: Airway pressures and hemodynamic parameters were traced at each step during the extended sigh. Arterial blood gases and physiologic parameters were determined before the extended sigh (pre-extended sigh), at 5 mins after two extended sighs (post-extended sigh), and then every 15 mins for 1 hr. In our average patient, the recruiting pressure x time of the inflation phase was estimated to be 32.8-35.4 cm H2O x 90 secs. Compared with the inflation phase, inspiratory pause pressure of the deflation phase was lower at Vt-PEEP 6-15 (28.9 +/- 2.7 cm H2O vs. 27.3 +/- 2.8 cm H2O) and 4-20 (31.8 +/- 2.9 cm H2O vs. 31.1 +/- 2.9 cm H2O; both p <.05). Compared with pre-extended sigh, Pao2 (81.5 +/- 15.3 mm Hg vs. 104.8 +/- 25.0 mm Hg; p <.001) and static respiratory compliance both increased post-extended sigh (27.9 +/- 7.9 mL/cm H2O vs. 30.2 +/- 9.7 mL/cm H2O; p =.009). Improvement in these parameters was sustained above pre-extended sigh for the duration of the study. Major hemodynamic or respiratory complications were not noted during the study. CONCLUSION: We present a new form of sigh (i.e., extended sigh) capable of achieving an augmented recruiting pressure x time through a prolonged inflation on a gradually increased end-expiratory pressure. In view of the sustained effect and absence of major complications in our patients, extended sigh could be a useful recruitment maneuver in acute respiratory distress syndrome.

Airway Resistance↗
PubMed2001

Reversal of cisplatin resistance by the 1,4-benzothiazepine derivative, JTV-519.

The 1,4-benzothiazepine derivative JTV-519 is a new type of calcium ion channel modulator. We examined the modulatory effect of JTV-519 on the antitumor activity of several platinum compounds (cisplatin, carboplatin, and nedaplatin) in a human cancer cell line resistant to cisplatin (PC-14 / CDDP) in vitro. PC-14 / CDDP cells showed 8-fold resistance to cisplatin compared with the parental PC-14 cells as determined by dye formation [3-(4,5-dimethylthiazol-2-yl)-2,5-diphenyltetrazolium bromide, MTT] assay. In PC-14 / CDDP, but not PC-14 cells, augmentation of cytotoxicity was observed when a nontoxic concentration (10 mM) of JTV-519 was combined with the platinum compounds. Increased intracellular cisplatin accumulation was observed in PC-14 / CDDP cells in the presence of JTV-519 as measured by atomic absorption assay. Therefore, increased cisplatin accumulation was considered to be a possible mechanism underlying the reversing effect of JTV-519 on cisplatin resistance. These results suggest that JTV-519 is a potent agent reversing cisplatin resistance.

Antineoplastic Agents↗
PubMed2001

Cigarette smoke extract induces endothelin-1 via protein kinase C in pulmonary artery endothelial cells.

We examined the mechanism of endothelin (ET)-1 regulation by cigarette smoke extract (CSE) and the effect of platelets on CSE-induced stimulation of ET-1 gene expression in human and bovine pulmonary artery endothelial cells (PAECs). Our data show that CSE (1%) induces ET-1 gene expression (after 1 h) and ET-1 peptide synthesis (after 4 h) in bovine PAECs. The induction of preproET-1 mRNA level was due to de novo transcription, and new protein synthesis was not required for this induction. The protein kinase C inhibitors staurosporine (10(-8) mol/l) and calphostin C (10(-7) mol/l) abolished the induction of ET-1 gene expression by CSE in bovine and human PAECs. Although a lower concentration of platelets (10(6) cells/ml in bovine PAECs; 10(7) cells/ml in human PAECs) did not significantly alter ET-1 gene expression in PAECs, incubation of platelets with CSE (1%) and PAECs produced a significant increase in preproET-1 mRNA and ET-1 peptide compared with the values in the presence of CSE (1%) alone. CSE (1%) induced platelet aggregation and increased the expression of platelet membrane glycoproteins ex vivo. Thus our data suggest that CSE stimulates ET-1 gene expression via PKC in PAECs. CSE and platelets showed a synergistic effect on ET-1 gene expression, possibly through the activation of platelets by CSE.

Animals↗
PubMed2001

Lung cancer in patients with idiopathic pulmonary fibrosis.

Idiopathic pulmonary fibrosis (IPF) was reported to be associated with increased risk of lung cancer as a result of the occurrence of atypical or dysplastic epithelial changes in fibrosis which progressed to invasive malignancy. In that situation, the cancer will develop in the area of major fibrosis. To investigate the direct relationship between fibrosis and cancer development, the real concordance rate of the two lesions in the chest computed tomography (CT) was analysed and compared to the histological types of lung cancer. The subjects included 63 patients with combined lung cancer and IPF (IPF-CA), 218 patients with lone IPF, and 2,660 patients with primary lung cancer. All patients were diagnosed at Asan Medical Center during the same period. The age, percentage of smokers, and the male sex were significantly higher in IPF-CA compared with lone IPF. The odds ratio of smoking was 2.71 compared to nonsmoking IPF controls. In IPF-CA, 56% of the cancer was located in the periphery of the lung and 52% in the upper lobe. The majority of the cancers (64%) were found in the nonfibrotic area at chest CT. The most frequent cell type was squamous cell carcinoma (35%), and there was no significant difference in the cancer cell type between IPF-CA and total lung cancer population. These findings suggest that in combined lung cancer and idiopathic pulmonary fibrosis patients, the features of the lung cancer are similar to the total lung cancer population.

Aged↗
PubMed2001

Nitric oxide and molsidomine in the management of pulmonary hypertension in Takayasu's arteritis.

We present three patients with pulmonary hypertension in Takayasu's arteritis who showed long-term favorable response, clinically and hemodynamically, to nitric oxide donor molsidomine. In these patients, nitric oxide inhalation was effective in reducing pulmonary artery pressure (PAP) and pulmonary vascular resistance (PVR). Molsidomine (single dose of 4 mg p.o.) was also effective in reducing PAP and PVR, but nifedipine was not. With molsidomine, 4 mg tid, dyspnea, exercise capacity, and hemodynamic parameters were improved. These favorable responses have lasted during the 3-month follow-up period in all patients.

Adult↗