| Japanese |
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| Title | 体外循環下開心術における凝固線溶系の変動 |
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| Subtitle | |
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| Authors | 田中國義*, 那須通寛*, 矢田公*, 湯浅浩*, 草川實*, 出口克己** |
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| Organization | *三重大学医学部胸部外科, **三重大学医学部第二内科 |
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| Journal | 循環制御 |
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| Volume | 9 |
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| Number | 1 |
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| Page | 103-109 |
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| Year/Month | 1988/ |
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| Article | 原著 |
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| Publisher | 日本循環制御医学会 |
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| Abstract | 体外循環下開心術における凝固線溶系の変動について検討した. 対象は成人開心術症例20例である. Antithrombin III（ATIII）は体外循環中, 有意の低下を示し, thrombin生成に対するheparin−ATIII complexの動員と消費が示唆された. またfibrinopeptide A（FPA）は体外循環中, 有意の増加を示した. この事は生成thrombinがheparin−ATIII complexによっても完全に中和されておらず, 残存thrombinによってfibrin形成がおこっている事を示すものと考えられた. 一方fibrinopeptide B β 15−42（FPBβ15−42）も体外循環中有意の上昇を示し, 線溶活性の発現が確認された. Kaolin活性化euglobulinによるfibrin平板溶解面積より求めた内因系線溶活性は, 体外循環開始直後に最も消費されていたが, 以後急速に前値へ回復した. Cl−inactivator添加euglobulinによるfibrin平板溶解面積より求めた外因系線溶活性（Cl−INA resistant fibrinolytic activity）は体外循環開始60分で前値の24倍にまで増加し, 以後急速に低下した. tissue plasminogen activator antigen（t−PA；Ag）もCl−INA resistant fibrinolytic activityと同様の変動を示した. 以上の結果より, 体外循環中はheparinの使用にもかかわらず凝固活性は発現しており, 微小循環におけるfibrin血栓の形成が推察された. 一方, 体外循環中の線溶活性の発現は, 主に血管内皮より放出されるt−PAによる外因系線溶が主体をなしており, その結果生じるplasminが血栓を溶解し, 微小循環の維持に役立っているものと考えられた. |
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| Practice | 基礎医学・関連科学 |
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| English |
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| Title | Alteration in Coagulation and Fibrinolysis Associated with Cardiopulmonary Bypass in Open Heart Surgery |
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| Authors | Kuniyoshi Tanaka, Michihiro Nasu, Isao Yada, Hiroshi Yuasa, Minoru Kusagawa, Katsumi Deguchi* |
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| Authors(kana) | |
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| Organization | Department of Thoracic Surgery, School of Medicine, Mie University, *2nd department of Internal Medicine, School of Medicine, Mie University |
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| Journal | Circulation Control |
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| Volume | 9 |
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| Number | 1 |
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| Page | 103-109 |
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| Year/Month | 1988/ |
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| Article | Original article |
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| Publisher | Japan Society of Circulation Control |
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| Abstract | The effect of heparin as an anticoagulant was examined and the nature of the fibrinolytic activity during CPB was clarified. Twenty patients undergoing valve replacement or aortocoronary bypass surgery were studied. FPA level were elevated gradually as the bypass proceeded, and ATIII decreased during CPB. This indicates that despite the use of heparin the coagulation system is activated, leading to fibrin formation in the microcirculation. On the other hand, FPB β 15−42 also increased to four times of the preoperative level at 2 hours of CPB. The intrinsic fibrinolytic activity determined by the activity of kaolin activated euglobulin was transiently activated only at the beginning of CPB. The Cl−inactivator resistant fibrinolytic activity and t−PA increased sharply during CPB and reached their maximum levels 1 hr after the start of CPB. This indicates that enhanced fibrimolytic activity during CPB is predominantly of extrinsic origin caused by t−PA released from vascular wall. |
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| Practice | Basic medicine |
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| Keywords | Cardiopulmonary bypass, fibrinopeptide A, Fibrinopeptide B β 15−42, Cl−INA resistant fibrinolytic activity, tissue plasminogen activator |
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