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Yoshihiro Minamiya - One of the best experts on this subject based on the ideXlab platform.

  • Polymorphonuclear leukocytes are activated during atelectasis before lung Reexpansion in rat.
    Shock (Augusta Ga.), 2008
    Co-Authors: Yoshihiro Minamiya, Hajime Saito, Naoko Takahashi, Hideki Kawai, Manabu Ito, Yukiko Hosono, Satoru Motoyama, Jun-ichi Ogawa
    Abstract:

    Although Reexpansion of a collapsed lung often causes pulmonary edema, the pathogenesis of the condition is not yet fully understood. To determine whether inflammatory changes occur in the pulmonary circulation during atelectasis and study the mechanism underlying the development of Reexpansion pulmonary edema, we used a rat model in which the left lung was collapsed by bronchial occlusion for 1 h and then reexpanded and ventilated for an additional 1 h. We evaluated the accumulation of polymorphonuclear leukocytes (PMNs) in the lung and the production of reactive oxygen species (ROS) in the pulmonary circulation using a fluorescent imaging technique. We also used confocal laser scanning microscopy and computerized image analysis to evaluate the membrane translocation of p47-phox, one of the nicotinamide adenine dinucleotide phosphate (reduced form) oxidase subunits, in PMNs sequestered in the lung. Polymorphonuclear leukocytes accumulated in the lung during atelectasis, and p47-phox was translocated to the plasma membrane, but no ROS production was observed. Marked PMN ROS production was observed after Reexpansion of the collapsed lung with air. Little ROS production was observed when the lung was reexpanded with nitrogen. During atelectasis, PMNs accumulate in the lung, where they are primed for respiratory bursting. After pulmonary Reexpansion, oxygen is supplied from the alveoli, and PMN respiratory bursting occurs.

  • pulmonary Reexpansion causes xanthine oxidase induced apoptosis in rat lung
    American Journal of Physiology-lung Cellular and Molecular Physiology, 2005
    Co-Authors: Satoshi Saito, Jun-ichi Ogawa, Yoshihiro Minamiya
    Abstract:

    The pathogenesis of Reexpansion pulmonary edema is not yet fully understood. We therefore studied its mechanism in a rat model in which the left lung was collapsed by bronchial occlusion for 1 h and then reexpanded and ventilated for an additional 3 h. We then evaluated the production of reactive oxygen species in the lungs using fluorescent imaging and cerium deposition electron microscopic techniques and the incidence of apoptosis using the TdT-mediated dUTP-digoxigenin nick end labeling (TUNEL) method. We found that pulmonary Reexpansion induced production of reactive oxygen species and then apoptosis, mainly in endothelial and alveolar type II epithelial cells. Endothelial cells and alveolar type I and II epithelial cells in the reexpanded lung were positive for TUNEL and cleaved caspase-3. DNA fragmentation was also observed in the reexpanded lung. In addition, wet-dry ratios obtained with reexpanded lungs were significantly higher than those obtained with control lungs, indicating increased fluid content. All of these effects were attenuated by pretreating rats with a specific xanthine oxidase inhibitor, sodium (-)-8-(3-methoxy-4-phenylsulfinylphenyl) pyrazolo[1,5-a]-1,3,5-triazine-4(1H)-one. It thus appears that pulmonary Reexpansion activates xanthine oxidase in both endothelial and alveolar type II epithelial cells and that the reactive oxygen species produced by the enzyme induce apoptosis among the endothelial and alveolar type I and II epithelial cells that make up the pulmonary water-air barrier, leading to Reexpansion pulmonary edema.

  • Pulmonary Reexpansion causes xanthine oxidase-induced apoptosis in rat lung.
    American journal of physiology. Lung cellular and molecular physiology, 2005
    Co-Authors: Satoshi Saito, Jun-ichi Ogawa, Yoshihiro Minamiya
    Abstract:

    The pathogenesis of Reexpansion pulmonary edema is not yet fully understood. We therefore studied its mechanism in a rat model in which the left lung was collapsed by bronchial occlusion for 1 h an...

Satoshi Saito - One of the best experts on this subject based on the ideXlab platform.

  • pulmonary Reexpansion causes xanthine oxidase induced apoptosis in rat lung
    American Journal of Physiology-lung Cellular and Molecular Physiology, 2005
    Co-Authors: Satoshi Saito, Jun-ichi Ogawa, Yoshihiro Minamiya
    Abstract:

    The pathogenesis of Reexpansion pulmonary edema is not yet fully understood. We therefore studied its mechanism in a rat model in which the left lung was collapsed by bronchial occlusion for 1 h and then reexpanded and ventilated for an additional 3 h. We then evaluated the production of reactive oxygen species in the lungs using fluorescent imaging and cerium deposition electron microscopic techniques and the incidence of apoptosis using the TdT-mediated dUTP-digoxigenin nick end labeling (TUNEL) method. We found that pulmonary Reexpansion induced production of reactive oxygen species and then apoptosis, mainly in endothelial and alveolar type II epithelial cells. Endothelial cells and alveolar type I and II epithelial cells in the reexpanded lung were positive for TUNEL and cleaved caspase-3. DNA fragmentation was also observed in the reexpanded lung. In addition, wet-dry ratios obtained with reexpanded lungs were significantly higher than those obtained with control lungs, indicating increased fluid content. All of these effects were attenuated by pretreating rats with a specific xanthine oxidase inhibitor, sodium (-)-8-(3-methoxy-4-phenylsulfinylphenyl) pyrazolo[1,5-a]-1,3,5-triazine-4(1H)-one. It thus appears that pulmonary Reexpansion activates xanthine oxidase in both endothelial and alveolar type II epithelial cells and that the reactive oxygen species produced by the enzyme induce apoptosis among the endothelial and alveolar type I and II epithelial cells that make up the pulmonary water-air barrier, leading to Reexpansion pulmonary edema.

  • Pulmonary Reexpansion causes xanthine oxidase-induced apoptosis in rat lung.
    American journal of physiology. Lung cellular and molecular physiology, 2005
    Co-Authors: Satoshi Saito, Jun-ichi Ogawa, Yoshihiro Minamiya
    Abstract:

    The pathogenesis of Reexpansion pulmonary edema is not yet fully understood. We therefore studied its mechanism in a rat model in which the left lung was collapsed by bronchial occlusion for 1 h an...

R Proietti - One of the best experts on this subject based on the ideXlab platform.

  • chestultrasounds to guide manual Reexpansion of a postoperative pulmonary atelectasis a case report
    Minerva Anestesiologica, 2011
    Co-Authors: Franco Cavaliere, Daniele G Biasucci, Roberta Costa, Paolo Maurizio Soave, Giada Addabbo, R Proietti
    Abstract:

    Reexpansion of a pulmonary atelectasis is often difficult, even after removing possible causes of bronchial obstruction. Chest ultrasounds, inexpensive and readily available at the patient bedside, may offer valuable support to guide recruitment maneuvers. We report the case of a 57-year-old woman that developed a complete collapse of the left lung seven days after undergoing an intestinal resection for perforation. A mucous plug occluding the main bronchus was removed with bronchoscopy, but persistent hypoxemia required mechanical ventilation; 24 hours later, an attempt to wean the patient from the ventilator failed. Chest X-rays revealed the persistence of a partial collapse of the left inferior lobe associated with a pleural effusion. A chest ultrasound confirmed the presence of a lung consolidation and of a modest pleural effusion. Manual Reexpansion was then attempted, and ventilatory pressures as well as the duration of forced inspirations were based on real-time ultrasound images. Complete Reexpansion was achieved within a few minutes and confirmed by chest X-ray. The patient was weaned from mechanical ventilation on the same day and discharged from ICU three days later.

  • Chest ultrasounds to guide manual Reexpansion of a postoperative pulmonary atelectasis: a case report.
    Minerva anestesiologica, 2011
    Co-Authors: Franco Cavaliere, Daniele G Biasucci, Roberta Costa, Giada Addabbo, M Soave, R Proietti
    Abstract:

    Reexpansion of a pulmonary atelectasis is often difficult, even after removing possible causes of bronchial obstruction. Chest ultrasounds, inexpensive and readily available at the patient bedside, may offer valuable support to guide recruitment maneuvers. We report the case of a 57-year-old woman that developed a complete collapse of the left lung seven days after undergoing an intestinal resection for perforation. A mucous plug occluding the main bronchus was removed with bronchoscopy, but persistent hypoxemia required mechanical ventilation; 24 hours later, an attempt to wean the patient from the ventilator failed. Chest X-rays revealed the persistence of a partial collapse of the left inferior lobe associated with a pleural effusion. A chest ultrasound confirmed the presence of a lung consolidation and of a modest pleural effusion. Manual Reexpansion was then attempted, and ventilatory pressures as well as the duration of forced inspirations were based on real-time ultrasound images. Complete Reexpansion was achieved within a few minutes and confirmed by chest X-ray. The patient was weaned from mechanical ventilation on the same day and discharged from ICU three days later.

Jun-ichi Ogawa - One of the best experts on this subject based on the ideXlab platform.

  • Polymorphonuclear leukocytes are activated during atelectasis before lung Reexpansion in rat.
    Shock (Augusta Ga.), 2008
    Co-Authors: Yoshihiro Minamiya, Hajime Saito, Naoko Takahashi, Hideki Kawai, Manabu Ito, Yukiko Hosono, Satoru Motoyama, Jun-ichi Ogawa
    Abstract:

    Although Reexpansion of a collapsed lung often causes pulmonary edema, the pathogenesis of the condition is not yet fully understood. To determine whether inflammatory changes occur in the pulmonary circulation during atelectasis and study the mechanism underlying the development of Reexpansion pulmonary edema, we used a rat model in which the left lung was collapsed by bronchial occlusion for 1 h and then reexpanded and ventilated for an additional 1 h. We evaluated the accumulation of polymorphonuclear leukocytes (PMNs) in the lung and the production of reactive oxygen species (ROS) in the pulmonary circulation using a fluorescent imaging technique. We also used confocal laser scanning microscopy and computerized image analysis to evaluate the membrane translocation of p47-phox, one of the nicotinamide adenine dinucleotide phosphate (reduced form) oxidase subunits, in PMNs sequestered in the lung. Polymorphonuclear leukocytes accumulated in the lung during atelectasis, and p47-phox was translocated to the plasma membrane, but no ROS production was observed. Marked PMN ROS production was observed after Reexpansion of the collapsed lung with air. Little ROS production was observed when the lung was reexpanded with nitrogen. During atelectasis, PMNs accumulate in the lung, where they are primed for respiratory bursting. After pulmonary Reexpansion, oxygen is supplied from the alveoli, and PMN respiratory bursting occurs.

  • pulmonary Reexpansion causes xanthine oxidase induced apoptosis in rat lung
    American Journal of Physiology-lung Cellular and Molecular Physiology, 2005
    Co-Authors: Satoshi Saito, Jun-ichi Ogawa, Yoshihiro Minamiya
    Abstract:

    The pathogenesis of Reexpansion pulmonary edema is not yet fully understood. We therefore studied its mechanism in a rat model in which the left lung was collapsed by bronchial occlusion for 1 h and then reexpanded and ventilated for an additional 3 h. We then evaluated the production of reactive oxygen species in the lungs using fluorescent imaging and cerium deposition electron microscopic techniques and the incidence of apoptosis using the TdT-mediated dUTP-digoxigenin nick end labeling (TUNEL) method. We found that pulmonary Reexpansion induced production of reactive oxygen species and then apoptosis, mainly in endothelial and alveolar type II epithelial cells. Endothelial cells and alveolar type I and II epithelial cells in the reexpanded lung were positive for TUNEL and cleaved caspase-3. DNA fragmentation was also observed in the reexpanded lung. In addition, wet-dry ratios obtained with reexpanded lungs were significantly higher than those obtained with control lungs, indicating increased fluid content. All of these effects were attenuated by pretreating rats with a specific xanthine oxidase inhibitor, sodium (-)-8-(3-methoxy-4-phenylsulfinylphenyl) pyrazolo[1,5-a]-1,3,5-triazine-4(1H)-one. It thus appears that pulmonary Reexpansion activates xanthine oxidase in both endothelial and alveolar type II epithelial cells and that the reactive oxygen species produced by the enzyme induce apoptosis among the endothelial and alveolar type I and II epithelial cells that make up the pulmonary water-air barrier, leading to Reexpansion pulmonary edema.

  • Pulmonary Reexpansion causes xanthine oxidase-induced apoptosis in rat lung.
    American journal of physiology. Lung cellular and molecular physiology, 2005
    Co-Authors: Satoshi Saito, Jun-ichi Ogawa, Yoshihiro Minamiya
    Abstract:

    The pathogenesis of Reexpansion pulmonary edema is not yet fully understood. We therefore studied its mechanism in a rat model in which the left lung was collapsed by bronchial occlusion for 1 h an...

Franco Cavaliere - One of the best experts on this subject based on the ideXlab platform.

  • chestultrasounds to guide manual Reexpansion of a postoperative pulmonary atelectasis a case report
    Minerva Anestesiologica, 2011
    Co-Authors: Franco Cavaliere, Daniele G Biasucci, Roberta Costa, Paolo Maurizio Soave, Giada Addabbo, R Proietti
    Abstract:

    Reexpansion of a pulmonary atelectasis is often difficult, even after removing possible causes of bronchial obstruction. Chest ultrasounds, inexpensive and readily available at the patient bedside, may offer valuable support to guide recruitment maneuvers. We report the case of a 57-year-old woman that developed a complete collapse of the left lung seven days after undergoing an intestinal resection for perforation. A mucous plug occluding the main bronchus was removed with bronchoscopy, but persistent hypoxemia required mechanical ventilation; 24 hours later, an attempt to wean the patient from the ventilator failed. Chest X-rays revealed the persistence of a partial collapse of the left inferior lobe associated with a pleural effusion. A chest ultrasound confirmed the presence of a lung consolidation and of a modest pleural effusion. Manual Reexpansion was then attempted, and ventilatory pressures as well as the duration of forced inspirations were based on real-time ultrasound images. Complete Reexpansion was achieved within a few minutes and confirmed by chest X-ray. The patient was weaned from mechanical ventilation on the same day and discharged from ICU three days later.

  • Chest ultrasounds to guide manual Reexpansion of a postoperative pulmonary atelectasis: a case report.
    Minerva anestesiologica, 2011
    Co-Authors: Franco Cavaliere, Daniele G Biasucci, Roberta Costa, Giada Addabbo, M Soave, R Proietti
    Abstract:

    Reexpansion of a pulmonary atelectasis is often difficult, even after removing possible causes of bronchial obstruction. Chest ultrasounds, inexpensive and readily available at the patient bedside, may offer valuable support to guide recruitment maneuvers. We report the case of a 57-year-old woman that developed a complete collapse of the left lung seven days after undergoing an intestinal resection for perforation. A mucous plug occluding the main bronchus was removed with bronchoscopy, but persistent hypoxemia required mechanical ventilation; 24 hours later, an attempt to wean the patient from the ventilator failed. Chest X-rays revealed the persistence of a partial collapse of the left inferior lobe associated with a pleural effusion. A chest ultrasound confirmed the presence of a lung consolidation and of a modest pleural effusion. Manual Reexpansion was then attempted, and ventilatory pressures as well as the duration of forced inspirations were based on real-time ultrasound images. Complete Reexpansion was achieved within a few minutes and confirmed by chest X-ray. The patient was weaned from mechanical ventilation on the same day and discharged from ICU three days later.