Bulutcu Füsun S, Bayindir Osman, Polat Bülent, Yalcin Yalim, öZbek Uğur, Cakali Emine
Departments of Anesthesiology and Reanimation, Cardiothoracic and Vascular Surgery, and Pediatric Cardiology, Kadir Has University, Florence Nightingale Hospital, Istanbul, Turkey.
J Cardiothorac Vasc Anesth. 2002 Jun;16(3):330-3. doi: 10.1053/jcan.2002.124142.
To evaluate whether the deleterious effect of cardiopulmonary bypass (CPB) can be prevented by controlling PaO(2) in cyanotic children.
Prospective, randomized, clinical study.
Single university hospital.
Pediatric patients undergoing cardiac surgery for repair of congenital heart disease (n = 24).
Patients were randomly allocated into 3 groups. Patients in the acyanotic group (group I, n = 10) had CPB initiated at a fraction of inspired oxygen (F(I)O(2)) of 1.0 (PO(2), 300 to 350 mmHg). Cyanotic patients were subdivided as follows: Group II (n = 7) had CPB initiated at an F(I)O(2) of 1.0, and group III (n = 7) had CPB initiated at an F(I)O(2) of 0.21 (PO(2), 90 to 110 mmHg). A biopsy specimen of right atrial tissue was removed during venous cannulation, and another sample was removed after CPB before aortic cross-clamping. The tissue was incubated in 4 mmol/L of t-butylhydroperoxide, and the malondialdehyde (MDA) level was measured to determine the antioxidant reserve capacity. Blood samples for cytokine levels, tumor necrosis factor (TNF)-alpha, and interleukin (IL)-6 response to CPB were collected after induction of anesthesia and at the end of CPB before protamine administration.
After initiation of CPB, MDA level rose markedly in the cyanotic groups compared with the acyanotic group (210 +/- 118% v 52 +/- 34%, p < 0.05), which indicated the depletion of antioxidants. After initiation of CPB, TNF-alpha and IL-6 levels of the cyanotic groups were higher than for the acyanotic group (168 +/- 77 v 85 +/- 57, p < 0.001; 249 +/- 131 v 52 +/- 40; p < 0.001). When a comparison between the cyanotic groups was performed, group II (initiating CPB at an F(I)O(2) of 1.0) had significantly increased MDA production compared with group III (initiating CPB at an F(I)O(2) of 0.21) (302 +/- 134% v 133 +/- 74%, p < 0.05). Group II had higher TNF-alpha and IL-6 levels than group III (204 +/- 81 v 131 +/- 52, p < 0.001; 308 +/- 147 v 191 +/- 81, p < 0.01).
Conventional clinical methods of initiating CPB at a hyperoxemic PO(2) may increase the possibility of myocardial reoxygenation injury in cyanotic children. This deleterious effect of reoxygenation can be modified by initiating CPB at a lower level of oxygen concentration. Subsequent long-term studies are needed to determine the best method of decreasing the oxygen concentration of the CPB circuit.
评估通过控制紫绀型儿童的动脉血氧分压（PaO₂）是否可预防体外循环（CPB）的有害影响。
前瞻性、随机、临床研究。
单一大学医院。
接受先天性心脏病修复心脏手术的儿科患者（n = 24）。
将患者随机分为3组。非紫绀组（I组，n = 10）在吸入氧分数（F(I)O₂）为1.0（PaO₂，300至350 mmHg）时开始CPB。紫绀型患者再细分为：II组（n = 7）在F(I)O₂为1.0时开始CPB，III组（n = 7）在F(I)O₂为0.21（PaO₂，90至110 mmHg）时开始CPB。在静脉插管期间取右心房组织活检标本，CPB后且在主动脉交叉钳夹前再取另一个样本。将组织置于4 mmol/L叔丁基过氧化氢中孵育，测量丙二醛（MDA）水平以确定抗氧化储备能力。在麻醉诱导后以及CPB结束且在给予鱼精蛋白前采集血样检测细胞因子水平、肿瘤坏死因子（TNF） - α和白细胞介素（IL） - 6对CPB的反应。
CPB开始后，与非紫绀组相比，紫绀组的MDA水平显著升高（210 ± 118%对52 ± 34%，p < 0.05），这表明抗氧化剂耗竭。CPB开始后，紫绀组的TNF - α和IL - 6水平高于非紫绀组（168 ± 77对85 ± 57，p < 0.001；249 ± 131对52 ± 40；p < 0.001）。当对紫绀组进行比较时，II组（在F(I)O₂为1.0时开始CPB）与III组（在F(I)O₂为0.21时开始CPB）相比，MDA生成显著增加（302 ± 134%对133 ± 74%，p < 0.05）。II组的TNF - α和IL - 6水平高于III组（204 ± 81对131 ± 52，p < 0.001；308 ± 147对191 ± 81，p < 0.01）。
以高氧血症的PaO₂开始CPB的传统临床方法可能增加紫绀型儿童心肌再灌注损伤的可能性。通过在较低氧浓度下开始CPB可减轻这种再灌注的有害影响。后续需要长期研究以确定降低CPB回路氧浓度的最佳方法。
