• Tuberculosis and Respiratory Diseases
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• 제53권6호
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• pp.595-611
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• 2002

Akt/PKB protein kinase B, ALI acute lung injury, ARDS acute respiratory distress syndrome, CREB C-AMP response element binding protein, ERK extracelluar signal-related kinase, fMLP fMet-Leu-Phe, G-CSF granulocyte colony-stimulating factor, IL interleukin, ILK integrin-linked kinase, JNK Jun N-terminal kinase, LPS lipopolysaccharide, MAP mitogen-activated protein, MEK MAP/ERK kinase, MIP-2 macrophage inflammatory protein-2, MMP matrix metalloproteinase, MPO myeloperoxidase, NADPH nicotinamide adenine dinucleotide phosphate, NE neutrophil elastase, NF-kB nuclear factor-kappa B, NOS nitric oxide synthase, p38 MAPK p38 mitogen activated protein kinase, PAF platelet activating factor, PAKs P21-activated kinases, PMN polymorphonuclear leukocytes, PI3-K phosphatidylinositol 3-kinase, PyK proline-rich tyrosine kinase, ROS reactive oxygen species, TNF-${\alpha}$ tumor necrosis factor-a.

• Tuberculosis and Respiratory Diseases
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• 제74권3호
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• pp.120-123
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• 2013

Inhalation of toxic gases can lead to pneumonitis. It has been known that methane gas intoxication causes loss of consciousness or asphyxia. There is, however, a paucity of information about acute pulmonary toxicity from methane gas inhalation. A 21-year-old man was presented with respiratory distress after an accidental exposure to methane gas for one minute. He came in with a drowsy mentality and hypoxemia. Mechanical ventilation was applied immediately. The patient's symptoms and chest radiographic findings were consistent with acute pneumonitis. He recovered spontaneously and was discharged after 5 days without other specific treatment. His pulmonary function test, 4 days after methane gas exposure, revealed a restrictive ventilatory defect. In conclusion, acute pulmonary injury can occur with a restrictive ventilator defect after a short exposure to methane gas. The lung injury was spontaneously resolved without any significant sequela.

• Tuberculosis and Respiratory Diseases
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• 제68권6호
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• pp.334-344
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• 2010

Background: Based on the known immunoregulatory functions of moxifloxacin on phagocytes, the therapeutic effect of moxifloxacin on oleic acid (OA)-induced acute lung injury (ALI) was investigated. Methods: Moxifloxacin (10 mg/kg) was given to male Sprague-Dawley rats that had been given oleic acid (OA, $30{\mu}L$) intravenously. Five hours after OA injection, parameters demonstrating ALI were assessed to measure the effects of moxifloxacin on acute lung injury. Results: The pathological findings of OA-induced ALI's was diminished by moxifloxacin. Through ultrastructural and $CeCl_3$ EM histochemistry, moxifloxacin was confirmed to be effective in decreasing oxidative stress in the lung as well. Indices of ALI, such as lung weight/body weight ratio, protein content in bronchoalveolar lavage fluid, and lung myeloperoxidase were decreased by moxifloxacin. In diaminobenzidine immunohistochemistry, fluorescent immunohistochemistry, and Western blotting of the lung, moxifloxacin had decreased the enhanced expression of secretory phospholipase $A_2$ ($sPLA_2$) by OA. Conclusion: We concluded that moxifloxacin was effective in lessening acute inflammatory pulmonary edema caused by OA, by inhibiting the neutrophilic respiratory burst, which was initiated by the activation of $sPLA_2$.

• The Korean Journal of Pain
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• 제4권2호
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• pp.200-204
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• 1991

Neurolytic splanchnic nerve block is a relatively safe and effective method for the relief of intractable pain caused by upper abdominal cancer. We have experienced a case of severe acute respiratory failure during splanchnic nerve block under control of X-ray fluoroscopy. We think that the most likely cause of the acute respiratory failure was an asthmatic attack due to anxiety and dyspnea from the injury or stimulation of the diaphragm and pleura in this case.

• Tuberculosis and Respiratory Diseases
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• 제51권6호
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• pp.503-516
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• 2001

연구배경 : 급성 출혈성 쇼크에서 발생하는 급성폐손상의 병인론을 호중구의 산소기 생성과 연관하여 규명하고자 본 연구를 시행하였다. 급성출혈성쇼크에서 폐장내 산소기 생성의 주된 원인이 호중구의 침윤에 의한 것이며 이 때 PLA2의 활성화가호중구의 respiratory burst의 직접적인 원인임올 밝히고지 하였다. 방 법 : 체중 300-350 g 정도의 흰쥐에서 체중/kg 당 20ml정도의 혈액을 5분 동안 뽑아내어 급성 출혈성 쇼크를 유발하고 이 출혈성 쇼크 상태를 1시간 동안 유지하였다. 그 후 급성 폐손상의 지표들을 측정하였다. 동시에 폐장의 미세구조의 변화 및 세포화학적인 검사를 통하여 폐장조직내의 산소기의 형성을 확인하였다. 또한 PLA2 억제제인 mepacrine을 출혈직전에 투여하여 PLA2의 억제에 따른 변화도 검사, 비교하였다. 결 과 : 급성 출혈성 쇼크에 의해 유도된 급성 폐손상에서 호중구의 폐장내 침윤이 확인되었고 이 때 폐부종 및 조직내 산소기 형성의 증가가 관찰되었으며, 폐장내 PLA2의 활성도도 증가하였다. 그러나 mepacrine을 이용하여 PLA2를 억제한 결과, 폐부종의 감소, 산소기 형성의 감소가 확인되었다. 결 론 : 급성 출혈성 쇼크에 의한 급성폐손상은 호중구에 의한 산화성스트레스가 그 원인으로 생각되고 이 때 호중구에 의한 산화성스트레스의 발생에는 PLA2가 주된 역할을 한다고 사료된다.

• 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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• 제68권2호
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• pp.55-61
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• 2010

Background: The underlying pathogenesis of fat embolism-induced acute lung injury (ALI) has not been elucidated. In the present study, the pathogenesis of fat embolism-induced ALI was probed in association with neutrophilic oxidative stress in oleic acid (OA)-induced ALI of S-D rats. Methods: OA was injected intravenously to provoke ALI in experimental rats. Five hours later, indices of ALI were measured to confirm the role of the neutrophilic respiratory burst. The effect of an inhibition of phospholipase A2 (PLA2) was also evaluated. Results: The accumulation of neutrophils in the lung due to OA caused increased neutrophilic oxidative stress in lung, which was ameliorated by mepacrine. What were the results from inhibition of PLA2. Conclusion: Excess neutrophilic oxidative stress contributes to OA-induced ALI, which is lessened by the inhibition of PLA2.

• 대한약리학회:학술대회논문집
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• 대한약리학회 2006년도 The 6th Congress of the Federation of Asian and Oceanian Physiological Societies
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• pp.73-73
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• 2006

• 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.

• Tuberculosis and Respiratory Diseases
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• 제42권5호
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• pp.781-786
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• 1995

간세포암에 이환된 61세 남자에서 lipiodol과 doxorubicin을 이용하여 간동맥 항암 화학 색전술을 시행하였고 3일 후 급성 호흡 부전증이 발병하였으며 임상 양상 및 방사선학적 소견상 급성 폐부종 및 폐렴에 의한 급성 폐손상에 합당하였다. 감염, 혈전 및 종괴에 의한 폐색전증, 울혈성 심부전에 의한 급성 호흡 부전증의 가능성을 배제하기 위하여 혈액, 객담 배양 검사를 시행하였으나 균주는 동정되지 않았고 복부 전산화 단층 촬영, 복부 핵자기 공명 영상, 심 초음파 등을 시행하였으나 심장이나 하대 정맥에서 종괴나 혈전을 발견할 수 없었으며 심기능은 정상이었다. 상기 소견으로 본 환자의 급성 호홉 부전증의 원인으로서 lipiodol에 의한 폐 지방전색증을 추정하게 되었다. 환자는 보전적 요법을 시행받고 증상 발현 4주 후 임상증상 및 흉부 단순 촬영상 호전을 보여 퇴원하였다. 저자 등은 lipiodol과 doxorubicin을 이용하여 간세포암의 화학색전술을 시행 후 lipiodol에 의한 폐지방 색전증이 원인인 급성 폐손상이 발생한 종례를 경험하였기에 문헌고찰과 함께 보고하는 바이다.