Abstract:
BACKGROUND: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). METHODS AND RESULTS: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. CONCLUSIONS: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.
journal_name
Circulationjournal_title
Circulationauthors
Nagashima M,Shin'oka T,Nollert G,Shum-Tim D,Rader CM,Mayer JE Jrsubject
Has Abstractpub_date
1998-11-10 00:00:00pages
II378-84issue
19 Suppleissn
0009-7322issn
1524-4539journal_volume
98pub_type
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