2001 Fiscal Year Final Research Report Summary
Research for protection of pulmonary function during cardiopulmonary bypass
Project/Area Number |
12671291
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Research Category |
Grant-in-Aid for Scientific Research (C)
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Allocation Type | Single-year Grants |
Section | 一般 |
Research Field |
Thoracic surgery
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Research Institution | Tohoku University |
Principal Investigator |
ENDO Masato Tohoku University Hospital, Lecturer., 医学部・附属病院, 講師 (90282128)
|
Project Period (FY) |
2000 – 2001
|
Keywords | Lung protection / Lung perfusion / Cardiopulmonary bypass / Leukocyte erastase / Leukocyte depletion |
Research Abstract |
Lung perfusion model was made using removed sheep lungs after the initiation of conventional cardiopulmonary bypass (CPB). The lungs were perfused with CPB blood (15 ml/kg/min) and ventilated (FiO2 1.0, 10xboby weight (kg)cc x 15/min). Hemodynamic parameters, respiratory parameters and chemical mediaters were measured at 0, 10, 30, 60 minutes after commencement of lung perfusion. Pulmonary artery pressure and resistance were consistently elevated during lung perfusion. Blood level of leukocyte erastase was also consistently elevated during lung perfusion. Histological examination revealed the persistent edema of alveolar wall and leukocyte accumulation in alveolar space. The area filled with accumulated leukocytes and fibrinoid substance were consistently enlarged during lung perfusion. Pulmonary dysfunction after CPB seemed to be closely related with accumulation of activated leukocytes with active release of cytokines in lung. Leukocyte depletion by leukocyte filter in the line of lung perfusion prevented the elevation of blood leukocyte elastase level. Therefore, leukocyte depletion, leukocyte degranulation inhibitor, leukocyte-endothelial adherence inhibitors are expected to be useful to reduce pulmonary dysfunction during CPB.
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