• Journal of Chest Surgery
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• 제33권2호
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• pp.132-138
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• 2000

Background: Inhaled nitric oxide therapy causes selective pulmonary vasodilation in congenital heart diseases with pulmonary hypertension. However discontinuation of inhaled nitric oxide therapy may be complicated by abrupt life-threatening rebound pulmonary hypertension(RPH) The purpose of this study was to prevent by comparing group I(without RPH n=13) and group II(with RPH n=6) to determine the risk factors involved inthe development of the RPH. Material and Method: Between Januarty 6, 1998 and April 14, 1999. we studied 19 consecutive children who were treated with inhaled nitric oxide for clinically significant pulmonary hypertension after an open heart surgery for congenital heart disease. the ratio of males and females was 12:7 ranging in age from 10 days to 6040 days(16 years) To identify the effects of nitric oxide between two groups we measured heart rate mean and systolic pulmonary arterial pressure mean and systolic systemic arterial pressure central venous pressure pH paO2/FiO2 and O2 saturation before and after the initiation and just before the withdrawal of the inhaled nitric oxide. result: In 6 of 19 patients(32%) withdrawal of inhaled nitric oxide caused RPH. In the two groups inhaled nitrix oxide decreased in pulmonary arterial pressure(PAP) without decreasing the systemic arterial pressure(SAP) and increased PaO2/FiO2 Compared with patients who had no RPH(group I) patients who had RPH(group II) were older in age (1204$\pm$1688 versus 546$\pm$1654 days p<0.05) received less nitric oxide therapy(34$\pm$18 versus 67$\pm$46 hours p<0.05) has shorter weaning process(5$\pm$3 versus 15一13 hours p<0.05) and received lowerconcentration of initial nitric oxide supply(11$\pm$8 versus 17$\pm$8 ppm p>0.05) and lower concentration just before the withdrawal nitric oxide(4.2$\pm$2.6 versus 5.6$\pm$2.6 ppm, p>0.05) Conclusion : We speculate that older age shorter of nitric oxide therapy shorter weaning process are the risk factors of RPH.

• Neonatal Medicine
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• 제15권1호
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• pp.14-21
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• 2008

• Biomolecules & Therapeutics
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• 제18권4호
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• pp.351-362
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• 2010

Nitric oxide (NO), synthesized from L-arginine by three isoforms of NO synthase (NOS), is a gaseous signaling molecule with an astonishingly wide range of biological and pathophysiological activities, including vasorelaxation, angiogenesis, anti-inflammation, and anti-apoptosis in mammalian cells. Recent studies have shown that NO donors and inhaled NO convert to biologically active NO under biological conditions and act as a signaling molecule in pathophysiological conditions. This review will discuss the roles of NO and its potential therapeutic implication in various human diseases, such as tumor, vascular regeneration, hypertension, wound healing, and ischemia-reperfusion injury.

• Journal of Trauma and Injury
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• 제28권3호
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• pp.104-107
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• 2015

Purpose: Nitric oxide (NO) is a vasodilator and inhaled NO (iNO) is used in acute respiratory distress syndrome (ARDS) to improve alveolocapillary gas exchange. The mechanism to improve oxygenation is likely to redistribute blood flow from unventilated areas to ventilated areas. Though improvement of oxygenation, iNO therapy has not been shown to improve mortality and considered as only rescue therapy in severe hypoxemia. We conducted the study to investigate an efficacy of iNO in trauma patients with severe hypoxemia. Methods: We reviewed the trauma patients who underwent iNO therapy retrospectively from 2010 to 2014. Degree of hypoxemia was represented as $PaO_2/FiO_2$ ratio (PFR) and the severity of patient was represented with sequential organ failure assessment (SOFA) score. Patients were divided into the survivor group and non-survivor group according to the 28-day mortality. Results: A total of 20 patients were enrolled. The mortality of 28-day was 40%. There were no significant differences between survivor and non-survivor group in age, sex, severity of injury, PFR and SOFA score. There was significant difference in initiation time of iNO after injury (p=0.047). Maximum combinations of sensitivity and specificity for timing of iNO therapy were observed using cut-off of 3-day after injury with a sensitivity of 88% and specificity of 75%. Conclusion: Though iNO therapy does not influence the mortality, iNO therapy may decrease the mortality caused by respiratory failure in the early phase of trauma.

• Tuberculosis and Respiratory Diseases
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• 제87권3호
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• pp.329-337
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• 2024

Background: Fractional exhaled nitric oxide (FeNO) is known to useful biomarker for detecting eosinophilic airway inflammation. However, there is a lack of evidence regarding the role of FeNO in chronic obstructive pulmonary disease (COPD). We aimed to assess whether elevated FeNO and its impact on treatment change into an inhaled corticosteroid (ICS)-containing regimen and association with acute exacerbation (AE) in patients with COPD. Methods: We retrospectively analyzed 107 COPD patients without a history of asthma from March 2016 to December 2019. The patients whose FeNO value was more than 50 parts per billion (ppb) were defined into the high FeNO group. Multivariable analysis with logistic regression was used to identify factors associated with AE in COPD. Results: The median FeNO value was 32 ppb (interquartile range, 19 to 45) and 34 (20.0%) patients were classified as high FeNO group (median 74 ppb). In the high FeNO group, changes in inhaler treatment into an ICS-containing regimen occurred in 23 of 34 patients after the measurement of FeNO. In multivariate analysis, high FeNO was not a contributing factor for AE, but only the high blood eosinophil count (≥300 cells/µL) was associated with AE (adjusted odds ratio, 2.63; 95% confidence interval, 1.01 to 6.91; p=0.049). Conclusion: High FeNO value had a significant impact on the prescription of ICSs in COPD patients, but it did not show a significant association with AE either on its own or with changes in treatment.

• Clinical and Experimental Pediatrics
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• 제52권10호
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• pp.1175-1180
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• 2009

신생아 폐고혈압 지속증은 치료가 힘들고 사망률이 높은 질환이나, 산화질소 흡입 치료가 시행된 이후 사망률의 많은 감소를 가져왔다. 그러나, 신생아 집중 치료실이 있는 병원이라도 이러한 산화질소 흡입 치료가 가능하지 않는 곳이 많고, 산화질소 투여에도 호전되지 않는 경우도 있다. 흡입 iloprost는 최근 원발성 혹은 이차성 폐고혈압 환자에서 사용이 늘고있는 폐동맥 확장제로, 신생아 폐고혈압 지속증에 사용한 증례가 외국에 보고된 바 있다. 환아는 출생시 심한 태변 착색과 출산 질식, 진행되는 저산소증을 보였으며, 신생아 폐고혈압 지속증으로 진단되었다. 환아는 지속적인 저산소증을 보였으며, 통상적인 지지 치료에도 호전되지 않았다. 당시 저자들의 병원에는 산화질소 흡입 치료가 가능하지 않아, iloprost 흡입 치료를 시도하였다. Iloprost 흡입 치료 이후 수시간 내에 산소 포화도가 증가하였으며, 심초음파상에는 동맥관을 통한 우좌 단락이 좌우로 바뀌었고, 우심실 압력이 감소하였다. Iloprost 흡입 치료를 하는 동안 특별한 부작용은 관찰되지 않았다. 저자들은 산화질소 흡입치료가 가능하지 않은 상황에서 신생아 폐고혈압 지속증 신생아의 치료로 iloprost 흡입 치료를 시도한 경험을 보고하는 바이다.

• Clinical and Experimental Pediatrics
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• 제55권9호
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• pp.330-336
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• 2012

Purpose: Fractional exhaled nitric oxide (FeNO) and forced expiratory flow between 25% and 75% of vital capacity ($FEF_{25-75}$) are not included in routine monitoring of asthma control. We observed changes in FeNO level and $FEF_{25-75}$ after FeNO-based treatment with inhaled corticosteroid (ICS) in children with controlled asthma (CA). Methods: We recruited 148 children with asthma (age, 8 to 16 years) who had maintained asthma control and normal forced expiratory volume in the first second ($FEV_1$) without control medication for ${\geq}3$ months. Patients with FeNO levels >25 ppb were allocated to the ICS-treated (FeNO-based management) or untreated group (guideline-based management). Changes in spirometric values and FeNO levels from baseline were evaluated after 6 weeks. Results: Ninety-three patients had FeNO levels >25 ppb. These patients had lower $FEF_{25-75}$ % predicted values than those with FeNO levels ${\leq}25$ ppb (P<0.01). After 6 weeks, the geometric mean (GM) FeNO level in the ICS-treated group was 45% lower than the baseline value, and the mean percent increase in $FEF_{25-75}$ was 18.7% which was greater than that in other spirometric values. There was a negative correlation between percent changes in $FEF_{25-75}$ and FeNO (r=-0.368, P=0.001). In contrast, the GM FeNO and spirometric values were not significantly different from the baseline values in the untreated group. Conclusion: The anti-inflammatory treatment simultaneously improved the FeNO levels and $FEF_{25-75}$ in CA patients when their FeNO levels were >25 ppb.

• Tuberculosis and Respiratory Diseases
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• 제48권6호
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• pp.964-972
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• 2000

저자들은 타카야수동맥염에 의한 만성 폐고혈압 환자 3예를 대상으로 혈관확장제 (NO 및 molsidomine)가 이들의 폐고혈압을 완화시킬 수도 있음을 관찰하였으며, 이와 관련하여 보다 많은 연구가 이루어져야 하리라 생각된다.

• Toxicological Research
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• 제13권3호
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• pp.251-256
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• 1997

Toluene inhalation increases glutamate level and its receptor in various brain regions. In this study, nitric oxide synthase (NOS) activities were investigated in various rat brain regions using NADPH diaphorase staining method which examined histochemical changes of NOS in the neural cells. Also, in vitro LDH leakage assay and MTT test were performed to investigate the toxic influences of toluene in cultured granule cell of rat cerebellum which was significantly affected with toluene in vivo. Rats were exposed to toluene of 10000 ppm for 3 days. 7 days and 14 days by 20 min $\times$ 2 times a day. NADPH diaphorase staining was processed in the different brain regions after inhalation. NADPH diaphorase staining density was not significantly changed at 3 days inhalation group, but the density decreased in proportion to the duration of toluene inhalation. Over 30% of staining density was decreased at 14 days group which was maximum duration of inhalation in this study. The tendency of staining density decrease was significant in granule cell of cerebellum. Cell death by toluene exposure was observed in cultured cerebellar granule cell. $EC_{50}$ measured with LDH leakage assay and MTT test were 43 mM and 72 mM respectively.

• Neonatal Medicine
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• 제28권1호
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• pp.1-6
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• 2021

Persistent pulmonary hypertension of the newborn (PPHN) is a consequence of the failure of a decrease in the elevated pulmonary vascular resistance after birth. Pulmonary vasodilators, including inhaled nitric oxide (iNO), have been the mainstream of targeted therapy for PPHN, but no drugs have been proven to be effective in preterm infants with PPHN. The fetus remains hemodynamically stable despite lower arterial oxygen tension and pulmonary blood flow as compared to full-term newborns. This adaptation is due to the lower oxygen requirement and high oxygen-carrying capacity of fetal circulation. The immature lungs of preterm infants are more vulnerable to reactive oxygen species, and the response of pulmonary vascular dilatation to blood oxygen tension is blunted in preterm infants. Recently, iNO has been reported to be effective in a selected group of preterm infants, such as those with prolonged preterm rupture of membrane-oligohydramnios-pulmonary hypoplasia sequence. PPHN in preterm infants, along with maximum supportive treatment based on fetal physiology and meticulous assessment of cardiovascular function, is in dire need of new treatment guidelines, including optimal dosing strategies for pulmonary vasodilators.