Mechanisms of or gan failures after Cardiopulmonary Bypass

• Published in: Jinko Zoki Vol. 20; no. 3; pp. 1276 - 1280
• Main Authors: HASHIMOTO Kazuhiro, SUZUKI Kazuhiko, KOYANAGI Katsuji, TAKAKURA Hiromitsu, MATSUI Michihiko, ARAI Tatsuta
• Format: Journal Article
• Language: Japanese
• Published: 一般社団法人 日本人工臓器学会 1991; JAPANESE SOCIETY FOR ARTIFICIAL ORGANS
• Subjects: arachidonic acid metabolite; cardiopulmonary bypass; elastase; endothelin; granulocyte
• ISSN: 0300-0818; 1883-6097
• DOI: 10.11392/jsao1972.20.1276

Summary; Mechanisms of organ failures following a cardiopulmonary bypass (CPB) were multi factorial although the hypoperfusion pressure was considered as a main cause. Plate-let aggregation initiated by the institution of CPB alternated eicosanoid metabolism, in which thromboxane A2 became dominant to prostaglandin I2. Reactive increase of endothelin excretion observed after the CPB also aggravated ischemic cellular damages due to induced vasoconstrictive status in the micro-vasculature. Further damages were accelerat-ed by elastase released from activated granulocytes. The damages were thought to be continued by both elastase and endothelin even after the CPB, however, thromboxane A2 related only during the CPB. The renal damage mainly concerned with endothelin and elastase, but not thromboxane A2. 体外循環下に生じる臓器障害のメカニズムは, 低灌流圧によるショック類似状態となることが主因と考えられるが,体外循環に特有な種々の生体反応がさらに障害を促進すると考えられた。人工心肺開始とともに始まる血小板凝集によって, eicosanoid metabol ismのバランスがthromboxane A2 優位となること, 又低灌流に刺激されてと考えられるendothehnの反応性増加により局所血管収縮が生じ, 各種臓器の虚血性障害が促進される。特にendothelinは心肺終了後においても増加傾向を示し, 活性型顆粒球より放出されるエラスターゼとともに, 心肺中・後においての細胞障害に関与していた。