1990 Fiscal Year Final Research Report Summary
The Hematological Deterioration and its Influences to the Human Body During Cardiopulmonary Bypass
| Project/Area Number |
01480340
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| Research Category |
Grant-in-Aid for General Scientific Research (B)
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| Allocation Type | Single-year Grants |
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| Research Field |
Thoracic surgery
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| Research Institution | Niigata University |
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Principal Investigator |
EGUCHI Shoji Niigata University, School of Medicine, Professor, 医学部, 教授 (90018367)
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| Co-Investigator(Kenkyū-buntansha) |
OHZEKI Hajime Niigata University School of Medicine, Instructor, 医学部・付属病院, 助手 (70213717)
TSUCHIDA Shoichi Niigata University School of Medicine, Instructor, 医学部・付属病院, 助手 (20227383)
KANAZAWA Hiroshi Niigata University School of Medicine, Instructor, 医学部・付属病院, 助手 (10177496)
HAYASHI Junichi Niigata University School of Medicine, Instructor, 医学部, 助手 (30164940)
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| Project Period (FY) |
1989 – 1990
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| Keywords | Cardiopulmonary bypass / Artificial lung / Coagulation / Fibrinolysis / platelet / Neutrophil leucocyte / Complement |
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| Research Abstract |
The study is composed of the injury and reactions by each blood components such as leukocyte, platelet, coagulant factors, complement and other serum active proteins during cardiopulmonary bypass.
Following data was obtained form clinical cardiopulmonary bypass in our hospital and experimental mock circulation with artificial lung.
1. Accession of coagulation cascade and consumption of each coagulant factors were observed and finally thrombin-antithrombin III complex increased in circulating blood after clinical cardiopulmonary bypass. Activation of kininogen and prekalikrein followed by decreasing fibrinogen in mock circuits with normal temperature.
2. Fibrinolytic process with increased plasmin-d_2plasmin inhibitor complex was always observed in clinical cardiopulmonary bypass circulation, otherwise, mild fibrinolysis occurred in mock circulation.
3. The platelet counts decreased immediately after cardiopulmonary bypass in both clinical and experimental circulation and subsequent increasing possibly due to mobilization from pooled platelets in clinical circulation.
platelet aggregation activity was strongly suppressed in both circulation and need several days to get normal activity in clinical cases.
4. Polymorphonuclear leukocyte counts initially decreased during the hypothermic anoxic arrest and markedly increased after rewarming. Serum levels of neutrophil elastase significantly rose during CPB and superoxide anion was more generated after CPB.
5. Both complement factor 4 and 3 were activated during CPB under following circumstances ex. hypothermia or normothermia, in clinical or mock circuits.
Some drugs would be applied to diminish the hematological change and influence to the human body.
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