• Tuberculosis and Respiratory Diseases
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• 제82권3호
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• pp.251-260
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• 2019

Background: Beyond its current function as a rescue therapy in acute respiratory distress syndrome (ARDS), extracorporeal membrane oxygenation (ECMO) may be applied in ARDS patients with less severe hypoxemia to facilitate lung protective ventilation. The purpose of this study was to evaluate the efficacy of extended ECMO use in ARDS patients. Methods: This study reviewed 223 adult patients who had been admitted to the intensive care units of 11 hospitals in Korea and subsequently treated using ECMO. Among them, the 62 who required ECMO for ARDS were analyzed. The patients were divided into two groups according to pre-ECMO arterial blood gas: an extended group (n=14) and a conventional group (n=48). Results: Baseline characteristics were not different between the groups. The median arterial carbon dioxide tension/fraction of inspired oxygen ($FiO_2$) ratio was higher (97 vs. 61, p<0.001) while the median $FiO_2$ was lower (0.8 vs. 1.0, p<0.001) in the extended compared to the conventional group. The 60-day mortality was 21% in the extended group and 54% in the conventional group (p=0.03). Multivariate analysis indicated that the extended use of ECMO was independently associated with reduced 60-day mortality (odds ratio, 0.10; 95% confidence interval, 0.02-0.64; p=0.02). Lower median peak inspiratory pressure and median dynamic driving pressure were observed in the extended group 24 hours after ECMO support. Conclusion: Extended indications of ECMO implementation coupled with protective ventilator settings may improve the clinical outcome of patients with ARDS.

• Tuberculosis and Respiratory Diseases
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• 제41권5호
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• pp.452-461
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• 1994

연구배경: ARDS발생 기전에 있어 TNF-$\alpha$나 IL-$1{\beta}$의 역할은 이들이 폐혈관 내피세포에 작용하여 모세혈관의 투과성을 증가시키는 것으로 추정되나 ARDS환자 발생 예측 지표로서의 TNF-$\alpha$ 및 IL-$1{\beta}$의 임상적 유용성에 대한 지금까지의 연구결과는 부정적이다. 이는 기존연구들이 다양한 질환들을 대상으로 함으로써 ARDS 발생기전의 다양성이 ARDS환자 발생 예측지표로서의 TNF-$\alpha$의 유용성을 부정적으로 나타나게하였을 가능성을 배제할 수 없다. 이에 저자들은 ARDS 발생이 내독소와 cytokines등에 의한 작용인 것으로 알려지고 있는 패혈증 증후군 환자들을 대상으로 TNF-$\alpha$와 IL-$1{\beta}$의 ARDS 발생의 예측 표지자로서 임상적 효용성을 검토하고자 본 연구를 시행하였다. 방법: 패혈증 증후군환자들을 대상으로 ARDS발생군(이하 ARDS군, 16명)과 호흡부전 상태에서 ARDS로는 진행하지않은 급성호흡 부전군(Acute hypoxemic respiratory failure group, 이하 AHRF군, 20명)으로 분류하여 등록시, 24시간 및 72시간후에 채혈하여 ARDS군은 ARDS 발생시에, AHRF군은 동맥혈 산소분압에 대한 폐포 산소분압의 비가 가장 낮은 시점의 TNF-$\alpha$와 IL-$1{\beta}$의 농도를 비교하였다. 또한 ARDS 및 AHRF군에서 쇽 발생군과 비발생군으로 분류하고 쇽 발생시에 측정된 TNF-$\alpha$와 IL-$1{\beta}$를 비발생군의 TNF-$\alpha$ 및 IL-$1{\beta}$의 값과 비교하였다. 대조군은 건강 대조군으로서 1회만 채혈하였다. 결과: 1) 혈중 TNF-$\alpha$의 농도: 본 연구에 사용한 Predicta kit의 TNF-$\alpha$ 농도 측정의 민감도는 평균${\pm}2$표준편차의 하한값이 10pg/mL이며, 특이도는 100%로, ARDS군 16명중 8명이, AHRF군 20명중 12명이 10pg/mL 이상으로 측정되어 두 군사이에서 혈중 TNF-$\alpha$가 10pg/mL 이상 발현된 비율의 차이는 없었다. ARDS 및 AHRF군의 혈중 TNF-$\alpha$의 중앙값 농도는 각각 10.26pg/mL(<10-16.99pg/mL, 사분위수범위, interquartile range), 10.82pg/mL(<10-20.38pg/mL)로서 두 군 사이에는 유의한 차이가 없었으며 (Fig. 1), ARDS 발생 전후의 혈중 TNF-$\alpha$의 농도도 중앙값이 10pg/mL미만(<10-15.32)pg/mL 및 10pg/mL미만(<10-10.22)pg/mL로서 유의한 차이가 없었고 6명중 2명만이 ARDS 발생 전에 비하여 TNF-$\alpha$의 값이 증가되었다. ARDS 및 AHRF군에서 패혈성 쇽이 발생한 환자들(26명)의 TNF-$\alpha$의 농도는 12.53(<10-20.82)pg/mL로서 비발생군(10명) <10pg/mL에 비해 유의하게 높았으나(p<0.01)(Fig. 2), 전체 생존군(<10, <10-12.92pg/mL)과 사망군(11.80, <10-20.8pg/mL)사이에는 유의한 차이가 없었다(P=0.28). 2) 혈중 IL-$1{\beta}$의 농도: 본 연구에 사용한 Quantikine kit의 최저 측정치는 0.3ng/mL로서 건강 대조군 10명중 1명을 제외한 모두에서 IL-$1{\beta}$측정치가 0.3pg/mL이하였다. ARDS 및 AHRF군의 검체 중 0.3ng/mL 이하로 측정된 경우는 ARDS, AHRF군에서 각각 1예가 있었다 ARDS 및 AHRF군의 혈중 IL-$1{\beta}$의 농도는 각각 2.22(1.37-8.01)ng/mL, 2.13(0.83-5.29)ng/mL으로서 두 군사이에는 유의한 차이가 없었으며(Fig. 3), ARDS 발생전(2.53, 0.3-8.38ng/mL)과 발생후(5.35, 0.66-11.51ng/mL)에서도 차이가 없었다. 패혈성 쇽 발생군(2.51, 1.28-8.34ng/mL)과 비발생군(1.46, 0.15-2.13ng/mL)사이에서는 통계적인 유의한 차이는 없었으나 비발생군에서 낮은 경향을 보였다(각각 P=0.44, P=0.054)(Fig. 4). 생존군과 사망군의 비교에 있어서는 각각 1.37(0.4-2.36), 2.84(1.46-8.34)ng/mL로서 생존군에서 유의하게 낮았다(p<0.05). 결론: 혈중내 TNF-$\alpha$의 농도는 패혈증증후군 환자들에서 패혈성 쇽의 발생과는 연관성이 있으나 혈중내 TNF-$\alpha$ 및 IL-$1{\beta}$의 농도 측정이 ARDS 발생의 예측 지표로서는 임상적 효용성이 적은 것으로 사료 되었다.

• Tuberculosis and Respiratory Diseases
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• 제73권1호
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• pp.1-10
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• 2012

Care of patients with sepsis has improved over the last decade. However, in the recent two years, there was no significant progress in the development of a new drug for critically ill patients. In January 2011, it was announced that the worldwide phase 3 randomized trial of a novel anti-Toll-like receptor-4 compound, eritoran tetrasodium, had failed to demonstrate an improvement in the mortality of patients with severe sepsis. In October 2011, Xigris (drotrecogin alfa, a recombinant activated protein C) was withdrawn from the market following the failure of its worldwide trial that had attempted to demonstrate improved outcome. These announcements were disappointing. The recent failure of 2 promising drugs to further reduce mortality suggests that new approaches are needed. A study was published showing that sepsis can be associated to a state of immunosuppression and loss of immune function in human. However, the timing, incidence, and nature of the immunosuppression remain poorly characterized, especially in humans. This emphasizes the need for a better understanding of sepsis as well as new therapeutic strategies. Many clinical experiences of the extracorporeal membrane oxygenator (ECMO) treatment for adult acute respiratory distress syndrome (ARDS) patients, which is caused by the H1N1 influenza A virus, were reported. The use of ECMO in severe respiratory failure, particularly in the treatment of adult ARDS, is occurring more commonly.

• Journal of Trauma and Injury
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• 제28권1호
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• pp.34-38
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• 2015

The case of a patient with a transfusion-related acute lung injury (TRALI) to whom extracorporeal membrane oxygenation (ECMO) had been applied is reported. A 55-year-old male injured with liver laceration (grade 3) without chest injury after car accident. He received lots of blood transfusion and underwent damage control abdominal surgery. In the immediate postoperative period, he suffered from severe hypoxia and respiratory acidosis despite of vigorous management such as 100% oxygen with mechanical ventilation, high PEEP and muscle relaxant. Finally, ECMO was applied to the patients as a last resort. Aggressive treatment with ECMO improved the oxygenation and reduced the acidosis. Unfortunately, the patient died of liver failure and infection. TRALI is a part of acute respiratory distress syndrome (ARDS). The use of ECMO for TRALI induced severe hypoxemia might be a useful option for providing time to allow the injured lung to recover.

• The Korean Journal of Physiology and Pharmacology
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• 제1권1호
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• pp.65-70
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• 1997

In order to investigate the effect of ANP on surfactant secretion from alveolar type II cell(AT II cell) during circulatory derangement in adult respiratory distress syndrome (ARDS), the secretion of surfactant from AT II cells was evaluated in purely isolated AT II cultures from rat lungs. For the simulation of sympathetic stimulation during circulatory derangement, primary AT II cultures were incubatedwith isoproterenol and IBMX. In this isoproterenol stimulated AT II cells, ANP were added in the media for the investigation of effect of ANP on surfactant secretion from AT II cells. For the evaluation of surfactant secretion, $[^3H]-methylcholine$ was incorporated and the level of radiolabelled choline chloride secreted from the cells was determined. As previously reported, isoproterenol and IBMX stimulated surfactant secretion from AT II cells. Isoproterenol showed synergistic increase of surfactant secretion with IBMX in AT II cells. In isoproterenol stimulated AT II cells, physiological level of ANP inhibited the secretion of surfactant in primary cultures of AT II cells. On the basis of these experimental it is suggested that, in association with ciculatory change during ARDS, increased secretion of ANP by the pulmonary edema, hypoxia and congestive heart heart failure might aggravate the symptoms of ARDS by reduction of surfactant secretion from AT II cells.

• Tuberculosis and Respiratory Diseases
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• 제38권1호
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• pp.70-73
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• 1991

We have experienced a case of lung injury caused by accidental inhalation of ammonia gas in a 34 year-old-man. By the explosion of ammonia tank in a refrigerator boat he inhaled ammonia gas. Several minutes later, he suffered from severe dyspnea and visual loss. On arrival at emergency room, analysis of arterial blood gas revealed severe hypoxemia and his chest film showed bilateral pulmonary infiltrates. Under the impression of adult respiratory distress syndrome, mechanical ventilator was applied to the patient. After recovery from ARDS and tracheal edema, he complained of some hemoptysis and productive sputum during the admission. So we checked bronchoscopy and bronchograpy which showed tracheal bullae just above carina and tubular bronchiectatic change in the right lower lobe. We report a case of lung injuries-ARDS, tracheal bullae, and bronchiectasis-caused by inhalation of ammonia gas with the review of the relevant literatures.

• 대한핵의학회지
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• 제18권1호
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• pp.45-53
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• 1984

The purpose of this study is to observe the changes of pulmonary capillary permeability and various hemodynamic parameters before and after Positive End-Expiratory Pressure(PEEP) in Adult Respiratory Distress Syndrome (ARDS). Using a canine oleic acid induced ARDS model, we measured the pulmonary capillary permeability with a slope of lung: heart radioactivity ratio, hemodynamic parameters with Swan-Ganz catheter and blood gas tensions. 1) In normal and ARDS dogs, the PEEP didn't significantly influence the slope of lung: heart radioactivity ratio. But in ARDS group the slope index was increased compaired with that of control group (p<0.05). 2) Also in ARDS group, $PaO_2$ was significantly decreased, and $PaCO_2,\;PvCO_2$, MPAP, $AaDO_2$, Qs/Qt were significantly increased compared with those of control group (p<0.05). 3) In normal dogs, the PEEP didn't influence blood pH or gas tension, $AaDO_2$, Qs/Qt, or hemodynamics. 4) In ARDS dogs, however, the PEEP significantly increased $PaO_2$ and decreased $AaDO_2$, Qs/Qt (p<0.05).

• Tuberculosis and Respiratory Diseases
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• 제52권1호
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• pp.62-69
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• 2002

저자들은 호흡곤란을 주소로 내원한 환자에서 미만성 간질성 폐질환 의심하에 고용량의 부신 피질 호르몬제 투여도중 폐병변 악화로 흉강경을 이용한 폐생검을 실시하여 침습성 폐 아스페르길루스증을 동반한 급성 간질성 폐렴을 경험하였기에 문헌고찰과 함께 보고하는 바이다.

• The Korean Journal of Physiology and Pharmacology
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• 제2권4호
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• pp.479-491
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• 1998

In order to know the pathogenesis of adult respiratory distress syndrome (ARDS) in association with the oxidative stress by neutrophils, the role of platelet activating factor (1-0-alkyl-2-acetyl-snglycero-3-phosphocholine, PAF) was investigated during acute lung injury induced by interleukin- $1{\alpha}$ (IL-1) in rats. An insufflation of IL-1 into the rat's trachea increased the acetyltransferase activity in the lung and the increase of PAF content was followed. As evidences of acute lung injury by neutrophilic respiratory burst, lung leak index, myeloperoxidase activity, numbers of neutrophils in the bronchoalveolar lavage fluid, neutrophilic adhesions to endothelial cells and NBT positive neutrophils were increased after IL-1 treatment. In addition, a direct instillation of PAF into the trachea caused acute lung leak and the experimental results showed a similar pattern in comparison with IL-1 induced acute lung injury. For the confirmation of oxidative stress during acute lung leak by IL-1 and PAF, a histochemical electron microscopy was performed. In IL-1 and PAF treated lungs of rats, the deposits of cerrous perhydroxide were found. To elucidate the role of PAF, an intravenous injection of PAF receptor antagonist, WEB 2086 was given immediately after IL-1 or PAF treatment. WEB 2086 decreased the production of hydrogen peroxide and the acute lung leak. In ultrastructural study, WEB 2086 mitigated the pathological changes induced by IL-1 or PAF. The nuclear factor kappa B (NFkB) was activated by PAF and this activation was inhibited by WEB 2086 almost completely. Based on these experimental results, it is suggested that the PAF produced in response to IL-1 through the remodeling pathway has the major role for acute lung injury by neutrophilic respiratory burst. In an additional experiment, we can also come to conclude that the activation of the NFkB by PAF is thought to be the fundamental mechanism to initiate the oxidative stress by neutrophils causing release of proinflammatory cytokines and activation of phospholipase $A_2$.

• Tuberculosis and Respiratory Diseases
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• 제40권1호
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• pp.6-15
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• 1993

연구배경 : 성인성 호흡곤란증후군에서 호기말양압(PEEP)이 저산소혈증을 호전시키는 기전은 감소된 기능적잔기량의 증가에 따른 생리적단락의 감소이며 어느 수준 이상의 PEEP에서는 심박출량이 유의하게 감소해 산소운반은 오히려 감소하는 것으로 알려져 있다. 산소운반이 최대인 PEEP 수준을 결정하는 비관혈적 지표로 폐유순도(compliance)가 보고되었으나 이의 유용성에 대해서는 논란이 많다. 한편 급성 폐동맥색전증은 성인성 호흡곤란증후군과는 달리 기능성 잔기량의 감소가 유의하지 않은 질환이며 따라서 PEEP의 적용에 따른 환기 및 혈류역학의 변화도 다를 것으로 추측된다. 저자들은 성인성 호흡곤란증후군과 급성 폐동맥색전증에서 총정적유순도(total static compliance)가 산소운반을 최대로하는 PEEP 수준의 결정에 유용한 지표로 이용될 수 있는가를 검정해보고, 성인성 호흡곤란증후군과는 저산소증의 기전이 다른 급성 폐동맥색전증에서 PEEP 적용에 따른 환기 및 혈역학의 변화에 대한 기초자료를 제공하고자 본 연구를 시행 하였다. 방법 : 한국산 잡견 14마리중 7마리에는 oleic acid 0.07ml/kg를 정주해 성인성 호흡곤란증후군을 유발하고, 나머지 7마리에는 자가혈병을 이용해 급성 폐동맥색전증을 유발한 후 PEEP 수준을 0, 5, 8, 12, 15 cm$H_2O$로 증가시켜가며 환기 및 혈역학의 제지표를 측정하였다. 결과: 1) PEEP수준의 증가에 따른 환기 및 혈역학의 변화 ARDS군에서 PEEP수준의 상승에 따라 동맥혈 산소분압및 동맥혈 이산화탄소분압은 증가하였고, 생리적단락과 심박출량은 감소하였다 (p<0.05). 급성 폐동맥색전증군에서도 PEEP수준의 상승에 따라 생리적단락 및 심박출량은 감소하였고, 동맥혈 산소분압 및 동맥혈 이산화탄소분압은 증가하였다 (p<0.05). PEEP수준 1 cm$H_2O$ 상승에 따른 변화로 심박출량의 감소는 급성 폐동맥색전증군에서 ARDS 군에 비해 유의하게 컸고, 동맥혈 산소분압, 동맥혈 이산화탄소분압, 생리적단락 및 폐혈관저항의 변화는 두군간에 유의한 차이가 없었다. 2) 산소운반과 총정적유순도 ARDS군에서 총정적유순도와 산소운반은 PEEP 적용후 증가해 5 cm$H_2O$에서 가장 컸으며 (p<0.05), 급성 폐동맥색전증군에서는 PEEP 적용후 총정적유순도와 산소운반이 감소하였다(p<0.05). 양군 모두 산소운반이 최대인 PEEP 수준에서 총정적유순도도 최대치를 기록하였다. ARDS군에서 산소운반의 변화와 총정적유순도의 변화사이에는 유의한 상관관계가 있었고 (r=0.86, p<0.01), 급성 폐동맥색전증군에서도 산소운반의 변화와 총정적유순도의 변화사이에 약한 상관관계가 있었다(r=0.60, p<0.01). 결론 : 이상의 결과로 ARDS와 급성 폐동맥색전증에서 PEEP의 적용시 산소운반을 최대로 유지하기 위한 PEEP수준의 결정에 총정적유순도가 유용한 지표로 이용될 수 있을것으로 생각된다.