The Experts below are selected from a list of 273 Experts worldwide ranked by ideXlab platform
Jose G. Venegas - One of the best experts on this subject based on the ideXlab platform.
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Lung [18f]fluorodeoxyglucose Uptake and Ventilation–Perfusion Mismatch in the Early Stage of Experimental Acute Smoke Inhalation
Anesthesiology, 2014Co-Authors: Guido Musch, Tilo Winkler, R. Scott Harris, Marcos F. Vidal Melo, Tyler J. Wellman, Nicolas De Prost, Richard L. Kradin, Jose G. VenegasAbstract:BACKGROUND Acute lung injury occurs in a third of patients with smoke inhalation injury. Its clinical manifestations usually do not appear until 48-72 h after inhalation. Identifying inflammatory changes that occur in pulmonary parenchyma earlier than that could provide insight into the pathogenesis of smoke-induced acute lung injury. Furthermore, noninvasive measurement of such changes might lead to earlier diagnosis and treatment. Because glucose is the main source of energy for pulmonary inflammatory cells, the authors hypothesized that its pulmonary metabolism is increased shortly after smoke inhalation, when classic manifestations of acute lung injury are not yet expected. METHODS In five sheep, the authors induced unilateral injury with 48 breaths of cotton smoke while the contralateral lung served as control. The authors used positron emission tomography with: (1) [F]fluorodeoxyglucose to measure metabolic activity of pulmonary inflammatory cells; and (2) [N]nitrogen in saline to measure shunt and Ventilation-Perfusion distributions separately in the smoke-exposed and control lungs. RESULTS The pulmonary [F]fluorodeoxyglucose uptake rate was increased at 4 h after smoke inhalation (mean ± SD: 0.0031 ± 0.0013 vs. 0.0026 ± 0.0010 min; P < 0.05) mainly as a result of increased glucose phosphorylation. At this stage, there was no worsening in lung aeration or shunt. However, there was a shift of Perfusion toward units with lower Ventilation-to-Perfusion ratio (mean ratio ± SD: 0.82 ± 0.10 vs. 1.12 ± 0.02; P < 0.05) and increased heterogeneity of the Ventilation-Perfusion distribution (mean ± SD: 0.21 ± 0.07 vs. 0.13 ± 0.01; P < 0 .05). CONCLUSION Using noninvasive imaging, the authors demonstrated that increased pulmonary [F]fluorodeoxyglucose uptake and Ventilation-Perfusion Mismatch occur early after smoke inhalation.
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lung 18f fluorodeoxyglucose uptake and Ventilation Perfusion Mismatch in the early stage of experimental acute smoke inhalation
Anesthesiology, 2014Co-Authors: Guido Musch, Tilo Winkler, Tyler J. Wellman, Nicolas De Prost, Richard L. Kradin, Scott R Harris, Marcos Vidal F Melo, Jose G. VenegasAbstract:BACKGROUND Acute lung injury occurs in a third of patients with smoke inhalation injury. Its clinical manifestations usually do not appear until 48-72 h after inhalation. Identifying inflammatory changes that occur in pulmonary parenchyma earlier than that could provide insight into the pathogenesis of smoke-induced acute lung injury. Furthermore, noninvasive measurement of such changes might lead to earlier diagnosis and treatment. Because glucose is the main source of energy for pulmonary inflammatory cells, the authors hypothesized that its pulmonary metabolism is increased shortly after smoke inhalation, when classic manifestations of acute lung injury are not yet expected. METHODS In five sheep, the authors induced unilateral injury with 48 breaths of cotton smoke while the contralateral lung served as control. The authors used positron emission tomography with: (1) [F]fluorodeoxyglucose to measure metabolic activity of pulmonary inflammatory cells; and (2) [N]nitrogen in saline to measure shunt and Ventilation-Perfusion distributions separately in the smoke-exposed and control lungs. RESULTS The pulmonary [F]fluorodeoxyglucose uptake rate was increased at 4 h after smoke inhalation (mean ± SD: 0.0031 ± 0.0013 vs. 0.0026 ± 0.0010 min; P < 0.05) mainly as a result of increased glucose phosphorylation. At this stage, there was no worsening in lung aeration or shunt. However, there was a shift of Perfusion toward units with lower Ventilation-to-Perfusion ratio (mean ratio ± SD: 0.82 ± 0.10 vs. 1.12 ± 0.02; P < 0.05) and increased heterogeneity of the Ventilation-Perfusion distribution (mean ± SD: 0.21 ± 0.07 vs. 0.13 ± 0.01; P < 0 .05). CONCLUSION Using noninvasive imaging, the authors demonstrated that increased pulmonary [F]fluorodeoxyglucose uptake and Ventilation-Perfusion Mismatch occur early after smoke inhalation.
G. Alexander Patterson - One of the best experts on this subject based on the ideXlab platform.
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Pulmonary Embolectomy After Single-Lung Transplantation
The Annals of thoracic surgery, 1997Co-Authors: Seiichi Noda, Thoralf M. Sundt, John P. Lynch, Elbert P. Trulock, Sudhir Sundaresan, G. Alexander PattersonAbstract:Single-lung transplantation for pulmonary hypertension results in a significant Ventilation/Perfusion Mismatch with dramatic shift of blood flow, but not Ventilation, to the replacement organ. This raises concern that the patient may be precariously dependent on the function of the transplanted lung. We report the successful management of a massive central pulmonary embolus to the transplanted lung in a 43-year-old woman 4 years after single-lung transplantation for primary pulmonary hypertension.
Keigo Endo - One of the best experts on this subject based on the ideXlab platform.
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Transient unilateral reverse Ventilation/Perfusion Mismatch in a patient with lung cancer.
Clinical nuclear medicine, 1992Co-Authors: Naoyuki Watanabe, Tomio Inoue, Noboru Oriuchi, Madoka Tateno, Tsuneo Hirano, Mitsuomi Matsumoto, Hiroshi Matsumoto, Yukio Nagamachi, Keigo EndoAbstract:The authors report a transient, unilateral reverse Ventilation/Perfusion (V/P) Mismatch in a patient with squamous cell lung cancer. The right lung was well perfused but not ventilated (unilateral reverse V/P Mismatch). However, lung imaging performed 3 days later demonstrated the absence of both Perfusion and Ventilation (V/P match). Reverse V/P Mismatch may be a transient process.
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pulmonary alveolar proteinosis with reverse Ventilation Perfusion Mismatch a case report
The Japanese journal of nuclear medicine, 1991Co-Authors: Naoyuki Watanabe, Tomio Inoue, Noboru Oriuchi, Madoka Tateno, Tsuneo Hirano, Katsumi Tomiyoshi, Keigo Endo, Y Sasaki, M Inagaki, H MichimataAbstract:Generally, non-ventilated segments are not perfused on lung scans (V/Q match). Now we report a very rare case with pulmonary alveolar proteinosis whose scintigraphy shows the decreased Ventilation, but well perfused (reverse V/Q Mismatch).
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Pulmonary alveolar proteinosis with reverse Ventilation/Perfusion Mismatch; a case report
Kaku igaku. The Japanese journal of nuclear medicine, 1991Co-Authors: Naoyuki Watanabe, Tomio Inoue, Noboru Oriuchi, Madoka Tateno, Tsuneo Hirano, Katsumi Tomiyoshi, Keigo Endo, Sasaki Y, Inagaki M, Michimata HAbstract:Generally, non-ventilated segments are not perfused on lung scans (V/Q match). Now we report a very rare case with pulmonary alveolar proteinosis whose scintigraphy shows the decreased Ventilation, but well perfused (reverse V/Q Mismatch).
Guido Musch - One of the best experts on this subject based on the ideXlab platform.
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Lung [18f]fluorodeoxyglucose Uptake and Ventilation–Perfusion Mismatch in the Early Stage of Experimental Acute Smoke Inhalation
Anesthesiology, 2014Co-Authors: Guido Musch, Tilo Winkler, R. Scott Harris, Marcos F. Vidal Melo, Tyler J. Wellman, Nicolas De Prost, Richard L. Kradin, Jose G. VenegasAbstract:BACKGROUND Acute lung injury occurs in a third of patients with smoke inhalation injury. Its clinical manifestations usually do not appear until 48-72 h after inhalation. Identifying inflammatory changes that occur in pulmonary parenchyma earlier than that could provide insight into the pathogenesis of smoke-induced acute lung injury. Furthermore, noninvasive measurement of such changes might lead to earlier diagnosis and treatment. Because glucose is the main source of energy for pulmonary inflammatory cells, the authors hypothesized that its pulmonary metabolism is increased shortly after smoke inhalation, when classic manifestations of acute lung injury are not yet expected. METHODS In five sheep, the authors induced unilateral injury with 48 breaths of cotton smoke while the contralateral lung served as control. The authors used positron emission tomography with: (1) [F]fluorodeoxyglucose to measure metabolic activity of pulmonary inflammatory cells; and (2) [N]nitrogen in saline to measure shunt and Ventilation-Perfusion distributions separately in the smoke-exposed and control lungs. RESULTS The pulmonary [F]fluorodeoxyglucose uptake rate was increased at 4 h after smoke inhalation (mean ± SD: 0.0031 ± 0.0013 vs. 0.0026 ± 0.0010 min; P < 0.05) mainly as a result of increased glucose phosphorylation. At this stage, there was no worsening in lung aeration or shunt. However, there was a shift of Perfusion toward units with lower Ventilation-to-Perfusion ratio (mean ratio ± SD: 0.82 ± 0.10 vs. 1.12 ± 0.02; P < 0.05) and increased heterogeneity of the Ventilation-Perfusion distribution (mean ± SD: 0.21 ± 0.07 vs. 0.13 ± 0.01; P < 0 .05). CONCLUSION Using noninvasive imaging, the authors demonstrated that increased pulmonary [F]fluorodeoxyglucose uptake and Ventilation-Perfusion Mismatch occur early after smoke inhalation.
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lung 18f fluorodeoxyglucose uptake and Ventilation Perfusion Mismatch in the early stage of experimental acute smoke inhalation
Anesthesiology, 2014Co-Authors: Guido Musch, Tilo Winkler, Tyler J. Wellman, Nicolas De Prost, Richard L. Kradin, Scott R Harris, Marcos Vidal F Melo, Jose G. VenegasAbstract:BACKGROUND Acute lung injury occurs in a third of patients with smoke inhalation injury. Its clinical manifestations usually do not appear until 48-72 h after inhalation. Identifying inflammatory changes that occur in pulmonary parenchyma earlier than that could provide insight into the pathogenesis of smoke-induced acute lung injury. Furthermore, noninvasive measurement of such changes might lead to earlier diagnosis and treatment. Because glucose is the main source of energy for pulmonary inflammatory cells, the authors hypothesized that its pulmonary metabolism is increased shortly after smoke inhalation, when classic manifestations of acute lung injury are not yet expected. METHODS In five sheep, the authors induced unilateral injury with 48 breaths of cotton smoke while the contralateral lung served as control. The authors used positron emission tomography with: (1) [F]fluorodeoxyglucose to measure metabolic activity of pulmonary inflammatory cells; and (2) [N]nitrogen in saline to measure shunt and Ventilation-Perfusion distributions separately in the smoke-exposed and control lungs. RESULTS The pulmonary [F]fluorodeoxyglucose uptake rate was increased at 4 h after smoke inhalation (mean ± SD: 0.0031 ± 0.0013 vs. 0.0026 ± 0.0010 min; P < 0.05) mainly as a result of increased glucose phosphorylation. At this stage, there was no worsening in lung aeration or shunt. However, there was a shift of Perfusion toward units with lower Ventilation-to-Perfusion ratio (mean ratio ± SD: 0.82 ± 0.10 vs. 1.12 ± 0.02; P < 0.05) and increased heterogeneity of the Ventilation-Perfusion distribution (mean ± SD: 0.21 ± 0.07 vs. 0.13 ± 0.01; P < 0 .05). CONCLUSION Using noninvasive imaging, the authors demonstrated that increased pulmonary [F]fluorodeoxyglucose uptake and Ventilation-Perfusion Mismatch occur early after smoke inhalation.
Seiichi Noda - One of the best experts on this subject based on the ideXlab platform.
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Pulmonary Embolectomy After Single-Lung Transplantation
The Annals of thoracic surgery, 1997Co-Authors: Seiichi Noda, Thoralf M. Sundt, John P. Lynch, Elbert P. Trulock, Sudhir Sundaresan, G. Alexander PattersonAbstract:Single-lung transplantation for pulmonary hypertension results in a significant Ventilation/Perfusion Mismatch with dramatic shift of blood flow, but not Ventilation, to the replacement organ. This raises concern that the patient may be precariously dependent on the function of the transplanted lung. We report the successful management of a massive central pulmonary embolus to the transplanted lung in a 43-year-old woman 4 years after single-lung transplantation for primary pulmonary hypertension.
