• 제목/요약/키워드: Lung injury

검색결과 502건 처리시간 0.029초

기관지폐형성이상의 혈관적 측면 (Vascular Aspects of Bronchopulmonary Dysplasia)

  • 조수진
    • Neonatal Medicine
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    • 제18권2호
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    • pp.177-181
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    • 2011
  • Bronchopulmonary dysplasia (BPD) is characterized by arrest of vascular and alveolar development in premature infants. Recent advances in neonatology have increased the survival of immature babies. Consequently, the prevalence of BPD is increasing. Animal studies and autopsy findings of BPD have demonstrated interruption in vascular development and reversal of lung injury through promotion of vasculogenesis. Normal lung development is driven by temporal and spatial specific growth factors and cellto-cell signaling in vascular development. Lung injury through various pathways causes disruption in this complex interactive process and results in aberrant vascular development and subsequent BPD. By understanding the regulation of vascular growth of the lung, it would be possible to find new targets in the treatment and prevention of BPD in premature infants.

An Acute Pathophysiology of Environmental Strains of Cryptococcus neoformans Isolated from a Park in Busan

  • Choi, Seok-Cheol
    • 대한의생명과학회지
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    • 제16권3호
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    • pp.139-149
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    • 2010
  • The present study was carried out to elucidate whether an environmental strain of Cryptococcus neoformans (environmental C. neoformans) isolated from an environmental source in a park of Busan has an acute pathophysiological effect in rats. On the second day after peritoneal inoculation of environmental C. neoformans, adverse effects occurred from the viewpoint of hematology and biochemistry. Eosinophil damages and crystal formations were found in the blood. Disturbances in cytokines production were observed in the cerebral and pulmonary tissues. Fungal budding existed in the brain, lung, liver and kidney. Tissue injury findings such as inflammation, leukocyte infiltration, bleeding, or degeneration were found in the brain, lung, liver and kidney. The present data suggest that the environmental C. neoformans can cause systematically harmful effects even for short periods of infection (two days of cryptococcal infection) and the adverse effects are summarized as immune derangements and biochemical and/or histological dysfunction and injury on major organ such as the brain, lung, liver and kidney in the immunocompetent hosts. Further studies should be focused on comparing the differences between environmental and clinical strains of C. neoformans.

급성 폐손상에서 호중구 활성화의 분자학적 기전 (Molecular Mechanisms of Neutrophil Activation in Acute Lung Injury)

  • 염호기
    • 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.

흰쥐에서 내독소로 유도된 급성 폐손상에서 moxofloxacin의 개선효과 (Ameliorating Effects of Moxifloxacin on Endotoxin-Induced Acute Lung Injury in Rats)

  • 이영만;최휘건
    • 생명과학회지
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    • 제21권8호
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    • pp.1100-1108
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    • 2011
  • 흰쥐에서 내독소로 유도된 급성 폐손상에서 moxifloxacin의 효과를 형태학적으로 호중구의 폐장 내 침윤 및 세포질형 포스포리파아제(cytosolic phospholipase A2) 발현과 관련하여 알아보았다. 내독소는 잘 알려진대로 흰쥐에서 급성 폐손상을 유발하였고 이때 폐장 내의 호중구의 침윤 및 폐장 및 호중구에서의 세포질형 포스포리파아제의 발현이 증가하였고, 또한 염증성 사이토카인의 일종인 종양괴사성인자(tumor necrosis factor)의 발현도 증가하였다. 전자현미경을 이용한 산소기 생성의 검사에서도 내독소에 의하여 산소기의 생성이 폐장 내에 증가한 사실을 확인하였고, 산화성 스트레스에 유발되는 제2형 폐포세포에서의 층상체의 변화도 관찰하였다. 면역변환효과가 있다고 알려진 moxifloxacin은 이러한 변화들을 억제하고 형태학적으로 내독소에 의한 급성 폐손상을 현저히 감소시켰다.

CMIT/MIT 함유 가습기 살균제 제품의 제조 및 판매기업 형사판결 1심 재판 판결문에 대한 과학적 고찰 (II) - 동물실험, 폐 손상 판정기준, 개인 인과 (A Scientific Critique of a Korean Court's Acquittal for Involuntary Manslaughter Related to 5-chloro-2-methylisothiazol-3(2H)-one/2-methylisothiazol-3(2H)-one (CMIT/MIT), a Humidifier Disinfectant (HD) Part II: Animal experiments, criteria for HD lung injury, and causality on individual levels)

  • 박동욱;조경이;김지원;최상준;이소연;전형배;박태현
    • 한국환경보건학회지
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    • 제47권3호
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    • pp.193-204
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    • 2021
  • Objectives: In January 2021, the former heads of the manufacturer SK Chemical and the vendor Aekyung were acquitted for manufacturing and selling humidifier disinfectant (HD) containing 5-chloro-2-methylisothiazol-3(2H)-one/2-methylisothiazol-3(2H)-one (CMIT/MIT). In this article, we analyzed the rationale used in this judgement in the light of scientific consideration. Methods: The sentencing document for the judgements was obtained from the Korea Supreme Court Service. In particular, the judgements made by the court related to the toxicological and individual association with HD perspectives were discussed based on scientific evidence. Results: The ruling stated that the necessary conditions for causality between CMIT/MIT and such diseases were not met based on the fact that asthma and lung damage were not found in the inhalation exposure animal experiments. The judgment overlooked the inevitable limitations of using animal experiments for verifying health effects in humans, which are often inconsistent with the observations in animals. Among 11 governmentaffirmed lung injury cases with CMIT/MIT usage, three patients' humidifier disinfectant-associated lung injury (HDLI) pathology proved that CMIT/MIT could cause lung injury similar to that caused by PHMG and PGH. In addition, five children showed decreased lung function related to damage caused by humidifier disinfectant exposure. Conclusions: We conclude that there is sufficient evidence supporting the assertion that HDs containing CMIT/MIT cause lung injuries, including asthma, contrary to the court's decision.

Endotoxin Induces Late Increase in the Production of Pulmonary Proinflammatory Cytokines in Murine Lupus-Like Pristane-Primed Modelp

  • Chae Byeong-Suk;Park Jeong-Suk;Shin Tae-Yong
    • Archives of Pharmacal Research
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    • 제29권4호
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    • pp.302-309
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    • 2006
  • Lupus-like syndrome is characterized by multiple organ injuries including lungs and kidneys. Endotoxin induces a transiently intent systemic inflammatory response and indirectly transient acute lung injury in normal condition. However, whether endotoxin may trigger the persistent development of lung injury in chronic, inflammatory lupus-like syndrome compared with normal condition remains unclear. We examined the pulmonary vascular permeability and production of proinflammatory cytokines, such as TNF-${\alpha}$, IL-6, IL-10 and IFN-${\gamma}$, which play prominent roles in the pathogenesis of lupus-like tissue injury, 6 hand 72 h after i.p. lipopolysaccharide (LPS; endotoxin) injection in pristane-primed chronic inflammation ICR mice characterized by a lupus-like syndrome. These results demonstrated that levels of serum IL-6, IL-10 and IFN-${\gamma}$ and bronchoalveolar lavage (BAL) IL-6 and IFN-${\gamma}$ were remarkably increased 6 h in LPS-exposed pristane-primed mice compared with pristane-primed controls, while pulmonary vascular permeability and levels of serum and BAL TNF-${\alpha}$ were not. And levels of BAL TNF-${\alpha}$, IL-6 and IL-10 were significantly enhanced 72 h in LPS-exposed pristane-primed mice compared with pristane-primed controls. Also, LPS significantly induced the increased in vitro production of TNF-${\alpha}$, IL-6 and IL-10 by lung cells obtained from LPS-exposed pristane-primed mice compared with LPS-exposed normal mice. Our findings indicate that LPS may trigger persistent progression of lung injury through late overproduction of BAL TNF-${\alpha}$, IL-6, and IL-10 in lupuslike chronic inflammation syndrome compared with normal condition.

급성호산구성폐렴으로 발현된 전자담배 관련 폐 손상: 증례 보고 (Electronic Cigarette or Vaping-Associated Lung Injury Manifested as Acute Eosinophilic Pneumonia: A Case Report)

  • 곽정훈;김채리;황성호;용환석;오유환;강은영
    • 대한영상의학회지
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    • 제84권1호
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    • pp.298-303
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    • 2023
  • 전자담배 관련 폐 손상(electronic cigarette or vaping-associated lung injury)은 전자담배에 의해 발생하는 폐 손상으로, 주된 병리 소견은 기질화폐렴 혹은 미만성폐포손상이며 드물게 급성호산구폐렴을 보인다. 본 증례에서 대마 추출물이 없는 니코틴 액상 전자담배 흡연력의 34세 남자 환자가 급성 호흡기 증상, 흉부 CT에서 양측 폐하엽의 주변부의 다발성 경화와 간유리음영, 미만성의 소엽간격막 비후, 흉막삼출을 보였다. 기관지폐포세척액에서는 호산구증이 있었고 감염성 검사들은 모두 음성으로 보였기에 진단기준에 부합하는 급성호산구 폐렴으로 발현한 대마 추출물이 없는 니코틴 액상 전자담배 관련 폐 손상의 희귀한 증례를 보고한다.

황련으로 만든 한약 복용 후 발생한 급성 간손상을 동반한 간질성 폐렴 1예 (A Case of Interstitial Pneumonitis with Acute Live Injury Caused by Herbal Medicine Made from Golden Thread)

  • 전병우;김다민;박지현;정현애;송림화;한정호;정만표
    • Tuberculosis and Respiratory Diseases
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    • 제71권6호
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    • pp.470-475
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    • 2011
  • So far more than 350 drugs have been reported to be the cause for lung injury and the incidence tends to increase. Although infiltrative lung disease is the most common pattern of drug-induced lung injury, it can appear in the form of alveolar changes, vasculitis and other injury. Herbal medicine also has been known as a cause for interstitial pneumonitis, but it is difficult to identify the key herbal medicine because of the complex components of the contents. Till date, there is no report of pneumonitis caused by golden thread. Here we report a case of a 54-year-old male who developed interstitial pneumonitis with acute liver injury caused by herbal medicine made from golden thread.

Tetrafluoroethylene 흡입에 의한 급성폐손상 1예 (A Case of Acute Lung Injury Caused by Tetrafluoroethylene Inhalation)

  • 이수옥;최은정;김가영;김준철;박정철;정치영;김연재;이병기
    • Tuberculosis and Respiratory Diseases
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    • 제62권3호
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    • pp.223-226
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    • 2007
  • 저자들은 도색공장에서 작업 도중 우연히 누출된 tetrafluoroethylene 가스의 흡입으로 인하여 급성폐손상을 받았으나 보존적 치료로 별다른 합병증 없이 비교적 짧은 기간에 치유된 남자 환자 1예를 경험하였기에 문헌고찰과 함께 보고하는 바이다.

허혈 재관류 손상 실험의 쥐 생체 모델 작성 (Preparation of In Vivo Rat Lung Model for Ischemia-Reperfusion Injury)

  • 이원진;박희철;홍기우
    • Journal of Chest Surgery
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    • 제28권11호
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    • pp.963-966
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    • 1995
  • Ischemia reperfusion injury occurs in various diseases. The role of oxygen free radicals in IR injury of the lung has been spotlighted and many studies have been performed. In this study, we tried to prepare a stable rat lung model for IR injury, focusing on surrounding conditions as hilar stripped left lung, clamped left pulmonary artery and bronchus,and declamped after determined period was passed, and right main pulmonary aretery was clamped. Arterial blood gas analyes were performed at 1, 10, 20, 30, minutes after reperfusion. Before clamping, PaO2 was 95 to 120 mmHg in all animals. There were six groups; Group I : temperature 15o C, and 120 minutes clamping, Group II: 20 oC, and 120 minutes clamping, Group III : 25 oC, and 120 minutes clamping, Group IV : 15oC, 90 minutes clamping, Group V : 20 oC, 90 minutes clamping,Group VI: 20 oC, 75 minutes clamping. Each groups contained 10 Sprague Dayley rats. The humidity was maintained 100 % as circulation imerged isotonic Hartmann`s solution of the pleural cavity. In group IV, V, and VI, PaO2 decreased significantly in all animals immediately after reperfusion, but 43 % survived till 10 minutes after reperfusion, it was 74.0$\pm$5.7, 73.3$\pm$10.8,and 88.2$\pm$17.7 mmHg. Pulmonary edema was observed histologically in 2/10 animals in group IV, 6/10 in group V , 3/10 in group VI, 9/10 in group I, and the other lungs showed all edema. We established a stable model by setting ischemic time,and temperature, between 75 to 90 minutes,15 to 20o C, and isotemperature Hartmann`s solution immersion of the pleural cavity.

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