Nagaoka H, Innami R, Funakoshi N, Fujiwara A, Itoh J
Department of Cardiovascular and Thoracic Surgery, Tsuchiura Kyodo General Hospital, Ibaraki, Japan.
Nihon Kyobu Geka Gakkai Zasshi. 1991 Sep;39(9):1723-30.
Arachidonic acid metabolism was investigated in 30 open heart cases, utilizing nonpulsatile cardiopulmonary bypass (CPB), consisted of 15 untreated cases (Group I) and 15 cases treated with aprotinin mostly given into CPB circuit during CPB (Group II). In group I, arterial blood concentration of thromboxane B2 (TXB2, stable metabolite of thromboxane A2, pg/ml) significantly increased from 45.9 +/- 40.5 preoperatively to 560.2 +/- 381.5 (p less than 0.01) at 30 minutes of CPB (total bypass) and to 830.5 +/- 591.1 (p less than 0.005) at the end of CPB (partial bypass). TXB2 levels in pulmonary artery (PA) and left atrium (LA) did not significantly increase just before, 5 minutes of CPB as compared with preoperative value. At the end of CPB TXB2 levels in PA (625.0 +/- 186.3) and LA (817.0 +/- 320.0) were significantly higher than preoperative value. However there was no significant difference between PA and LA values. Contrarily in group II TXB2 levels were significantly suppressed as compared with the value at each corresponding time in group I. beta-thromboglobulin levels also changed almost parallel to TXB2 levels in both groups. In conclusion, arachidonic acid metabolic disorders could occur in CPB circuit rather than in pulmonary circulation during CPB. Aprotinin administration into CPB circuit suppressed to some extent the platelet activation.
对30例心脏直视手术病例的花生四烯酸代谢进行了研究,采用非搏动性体外循环(CPB),其中包括15例未治疗的病例(I组)和15例在CPB期间主要经CPB回路给予抑肽酶治疗的病例(II组)。在I组中,血栓素B2(TXB2,血栓素A2的稳定代谢产物,pg/ml)的动脉血浓度在CPB 30分钟(全旁路)时从术前的45.9±40.5显著升高至560.2±381.5(p<0.01),在CPB结束时(部分旁路)升高至830.5±591.1(p<0.005)。与术前值相比,在CPB前、CPB 5分钟时肺动脉(PA)和左心房(LA)中的TXB2水平没有显著升高。在CPB结束时,PA(625.0±186.3)和LA(817.0±320.0)中的TXB2水平显著高于术前值。然而,PA和LA的值之间没有显著差异。相反,与I组中每个相应时间的值相比,II组中的TXB2水平显著受到抑制。两组中的β-血小板球蛋白水平变化也几乎与TXB2水平平行。总之,花生四烯酸代谢紊乱可能发生在CPB回路中,而不是在CPB期间的肺循环中。在CPB回路中给予抑肽酶在一定程度上抑制了血小板活化。