Nagashima M, Shin'oka T, Nollert G, Shum-Tim D, Rader C M, Mayer J E
Department of Cardiovascular Surgery, Children's Hospital, Boston, MA 02115, USA.
Circulation. 1998 Nov 10;98(19 Suppl):II378-84.
Cardiopulmonary bypass (CPB) induces an inflammatory reaction that activates neutrophils and releases free radicals in tissue. Ischemia-reperfusion further aggravates inflammation. Hemofiltration (HF) could potentially remove inflammatory mediators and reduce injury. This study assessed the effect of continuous high-volume HF during CPB on systemic edema formation and pulmonary function after deep hypothermic circulatory arrest (DHCA).
Anesthetized lambs (n = 16) underwent CPB with systemic cooling (40 minutes), DHCA (120 minutes at 18 degrees C), and rewarming (40 minutes). All animals were weaned from CPB and observed for 3 hours after reperfusion. Continuous HF was used in 8 lambs at a flow rate of 300 mL/kg per hour throughout CPB, simultaneously replacing hemofiltration volume with a balanced salt solution (HF group). In 8 control animals, no hemofiltration was performed. Hematocrit remained at 23% to 25% during the experiment in both groups. Pulmonary vascular resistance (PVR), lung dynamic compliance (Cdyn), alveolar-arterial oxygen difference (AaDO2), and total body water content (bioimpedance) were measured. Malondialdehyde (MDA), a product of lipid peroxidation, was assayed in lung tissue. Percent increase of body water content at 180 minutes of reperfusion was significantly lower in the HF group than in control (132 +/- 2% vs 152 +/- 5%, P < 0.005). There was less of a rise in PVR compared with baseline at 180 minutes of reperfusion in the HF group than in control (131 +/- 8% vs 238 +/- 26%, P < 0.005). In addition, percent recovery of Cdyn and AaDO2 in the HF group was preserved significantly (respectively, P < 0.05) 2 hours after reperfusion than in the control group. Lung tissue MDA in the HF group (46.2 +/- 12.6 vs 65.3 +/- 17.1 nmol/L per gram of tissue, P < 0.05) was significantly lower than in the control group.
High-volume, continuous hemofiltration during CPB attenuates systemic edema formation, pulmonary hypertension, the extent of lung dysfunction, and depression of cardiac output and reduces free radical-mediated tissue injury after CPB with DHCA. This technique may have a clinical application to reduce the morbidity rate of CPB.
体外循环(CPB)可引发炎症反应,激活中性粒细胞并在组织中释放自由基。缺血再灌注会进一步加重炎症。血液滤过(HF)有可能清除炎症介质并减轻损伤。本研究评估了CPB期间持续高容量HF对深低温停循环(DHCA)后全身水肿形成和肺功能的影响。
对16只麻醉的羔羊进行CPB,包括全身降温(40分钟)、DHCA(18℃下120分钟)和复温(40分钟)。所有动物脱离CPB后在再灌注后观察3小时。8只羔羊在整个CPB过程中以300 mL/kg每小时的流速进行持续HF,同时用平衡盐溶液补充滤过液量(HF组)。8只对照动物未进行血液滤过。两组实验期间血细胞比容均维持在23%至25%。测量肺血管阻力(PVR)、肺动态顺应性(Cdyn)、肺泡-动脉氧分压差(AaDO2)和全身含水量(生物电阻抗)。检测肺组织中脂质过氧化产物丙二醛(MDA)。再灌注180分钟时HF组全身含水量的增加百分比显著低于对照组(132±2%对152±5%,P<0.005)。再灌注180分钟时,HF组与基线相比PVR的升高幅度低于对照组(131±8%对238±26%,P<0.005)。此外,再灌注2小时后HF组Cdyn和AaDO2的恢复百分比显著高于对照组(分别为P<0.05)。HF组肺组织MDA(46.2±12.6对65.3±17.1 nmol/L每克组织,P<0.05)显著低于对照组。
CPB期间高容量持续血液滤过可减轻全身水肿形成、肺动脉高压、肺功能障碍程度及心输出量降低,并减少CPB联合DHCA后自由基介导的组织损伤。该技术可能在临床上用于降低CPB的发病率。