Biomedical subjects
Publications and source records attributed to G Nollert.
Right atrial thrombosis during chemotherapy is commonly treated conservatively. We describe a minimally invasive surgical procedure to remove a right atrial thrombus in a patient with a history of recurrent lung embolism. Surgery was performed through a mini-thoracotomy without cardiopulmonary bypass during occlusion of both caval veins. Recovery was uneventful.
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BACKGROUND: The purpose of the study was to analyze the long-term results of aortic valvotomy and the risk factors associated with reoperation and survival. METHODS: From 1960 to 1977, 116 patients with congenital valvular aortic stenosis underwent isolated aortic valvotomy at a mean age of 13.7 +/- 7.8 years with a mean aortic gradient of 78 +/- 33 mm Hg. Fifteen patients had additional aortic regurgitation, and leaflet calcification was present in another 15 patients. RESULTS: Postoperatively the mean aortic gradient decreased to 19.4 +/- 11.3 mm Hg (p < 0.0001). Early mortality was 2.6%. At a mean follow-up of 23.8 years, 26 late deaths (22.4%) occurred among the 113 early survivors. Actuarial 10-, 20-, 30-, and 37-year survival rates were 94.6%, 79.7%, 76.2%, and 72.5%, respectively. According to multivariate Cox regression analysis, survival was influenced by preoperative New York Heart Association class (p = 0.0418), leaflet calcification (p = 0.0339), date of operation (p = 0.0253), and postoperative endocarditis (p < 0.0001). At a mean interval of 18.3 years, 37 patients required reoperation (31.9%) mainly because of recurrent aortic stenosis. The reoperation rate increased significantly 15 years postoperatively from 0.73%/year to 2.31%/ year (p < 0.0001). In a multivariate risk model, reoperation was influenced by older patient age (p = 0.0032) and the presence of leaflet calcification (p = 0.0289). CONCLUSIONS: AORTIC valvotomy is a simple and effective procedure for congenital aortic stenosis with excellent long-term results. However, the rate of reoperation increases 15 years postoperatively, and clinical follow-up should be intensified. Our results suggest that early repair should be performed and that adequate patient selection is the most important determinant of the longterm results.
OBJECTIVES: Hemodilution has been applied conventionally during cardiopulmonary bypass (CPB) and deep hypothermic circulatory arrest (DHCA) to counteract the increase in viscosity and deleterious rheological effects caused by hypothermia. However, liver dysfunction after low-flow bypass and DHCA is common, and little is known about the effects of hematocrit (Hct). The purpose of the present study is to evaluate the impact of two hemodilution priming protocols used clinically on liver perfusion and metabolism. MATERIALS AND METHODS: Ten piglets were randomized into 2 groups. One group (n = 5) had a crystalloid prime resulting in an Hct of about 15 % (low hematocrit; group L), the other (n = 5) a total-blood prime (Hct = 25 %; high hematocrit; group H). All animals underwent 70 min cooling at full flow (150 ml/kg/min), 30 min of low flow (50 ml/kg/min) at 15 degrees C followed by 45 min of DHCA and 75 min of rewarming at full flow. Liver blood flow (LBF) was assessed at the beginning of CPB at 34 degrees C, at the end of cooling at 15 degrees C, at the end of low flow, 5 min after the start of warming, and at the end of rewarming at 34 degrees C by injections of radioactive microspheres. Liver function was evaluated at the same time using the MEGX test, which measures the metabolism of lidocaine. RESULTS: LBF was insignificantly reduced during cooling, decreased during low flow (p = 0.001), and increased again after DHCA with the highest flow at the end of rewarming. LBF tended to be lower at all times in group L (p = 0.096). The liver lidocaine metabolic rate did not significantly decrease during cooling and low flow, but was increased at the end of rewarming (p = 0.01); the metabolism was higher in group H (p = 0.025). Multiregression analysis revealed liver blood flow (p = 0.003) and hematocrit (p < 0.001) as independent determinants of the liver lidocaine metabolism; arterial blood pressure and temperature did not have significant influence in this model. CONCLUSION: Hemodilution results in a tendency towards reduced liver blood flow during CPB; much worse is the resulting impaired liver metabolism, independent of reduced blood flow and pressure. Avoidance of low hematocrit during CPB may be a useful adjunct to preserve liver function in patients undergoing cardiac surgery with long duration CPB and DHCA.
Cerebral injury after cardiac surgery is still a major cause of mortality and morbidity after cardiac surgery. In an aging patient population the incidence is likely to increase. Comparisons between cardiac and other major surgery suggested that cardiopulmonary bypass (CPB) causes the neurological sequelae. Strategies to avoid brain injury target the reduction of emboli floating in the cerebral circulation, adequacy of cerebral oxygenation, and minimization of the whole body inflammatory response to the bypass circuit. Experimental and clinical studies demonstrated that manipulation of CPB can reduce abundant cerebral blood flow and the embolic load to the brain. Hematocrit, temperature, blood pressure, and acid-base status during CPB are parameters that have impact on the neurological outcome and can be optimized. Other possibilities to avoid cerebral complications include improvements of surgical techniques and devices or the application of new therapeutic drugs. However, further experimental studies and, most importantly, prospective randomized clinical trials are warranted to prove new innovative concepts in clinical practice.
Near-infrared spectroscopy assessment of cytochrome oxygenation could be a valuable technique to monitor cerebral intraneuronal oxygen delivery during cardiopulmonary bypass. However, the validity of the cytochrome signal has been questioned as it could easily be overwhelmed by the Hb signal. Five- to six-week-old control piglets (n = 5) underwent cardiopulmonary bypass at 37 degrees C. Study animals (n = 10) received 100 mg/kg of sodium cyanide to uncouple cytochrome from HB: Hematocrit was then decreased in steps of 5% from 35 to 5% with crystalloid hemodilution. In study piglets, the initiation of cardiopulmonary bypass was associated with oxygenated Hb increasing from 0 to 62.9 +/- 25.6 microM times the differential path-length factor, and oxidized cytochrome a,a3 increasing to 1.9 +/- 1.8 microM times the differential path-length factor. Cyanide caused oxygenated Hb to increase further to 132.3 +/- 48.9 microM times the differential path-length factor, and oxidized cytochrome c decreased to -7.0 +/- 2.6 microM times the differential path-length factor as anticipated, confirming uncoupling of electron transport. However, hemodilution subsequently resulted in linear decreases in oxidized cytochrome a,a3 (F = 8.57, p < 0.001) suggesting important cross-talk between the Hb and cytochrome signals as cytochrome is only intracellular. In control piglets, tissue oxygenation index showed a positive correlation with pump flow (r = 0.986, p = 0.013). The cytochrome signal as presently measured by near-infrared spectroscopy is highly dependent on hematocrit.
BACKGROUND: The arterial switch operation (ASO) is the treatment of choice for transposition of the great arteries. METHODS: Anatomical risk factors on mortality and morbidity were analyzed retrospectively in 312 patients who underwent ASO between 1982 and 1997. RESULTS: Survival was 95%, 92%, and 92% after 30 days, 5, and 10 years, respectively. Operative survival improved after 1990 to 97% (p < 0.001). Risk factors for operative mortality were complex anatomy (p = 0.018), coronary anomalies (p = 0.008), and prolonged bypass time (p < 0.001). Determinants of late mortality were coronary distribution (p = 0.03), position of the great arteries (p = 0.0095), bypass time (p = 0.047), and aortic coarctation (p = 0.046). After a follow-up of 3.6 +/- 2.7 years (0.1 to 14.9 years), 98% had good left ventricle function, 94% were in sinus rhythm, 2.4% had moderate to severe pulmonary stenosis, 0.3% had significant aortic regurgitation, and 1% had coronary stenosis. Freedom from reoperation was 100%, 96%, and 94% after 1, 5, and 10 years, respectively. No preoperative anatomic parameter correlated with long-term morbidity. CONCLUSIONS: ASO can be performed with low operative mortality (< 5%) and long-term morbidity. Malformations associated with complex transposition of the great arteries influence early and late mortality.
BACKGROUND: Near-infrared spectroscopy (NIRS) is used to monitor cerebral oxygenation during cardiac surgery. However, interpretation of the signals is controversial. The aim of the study was to determine which NIRS variable best correlated with brain damage as assessed by animal behavior and neurohistologic score and to compare the accuracy of NIRS and magnetic resonance spectroscopy (MRS) in predicting brain injury. METHODS: Forty 5-week-old piglets underwent 60 minutes of deep hypothermic circulatory arrest (DHCA) at 15 degrees C. Changes in brain adenosine triphosphate (ATP), phosphocreatine (PCr), and intracellular pH (pHi) were determined by MRS and correlated to changes in oxygenated hemoglobin (HbO2), deoxygenated hemoglobin (Hb), and oxidized cytochrome a,a3 (CytOx) NIRS signals. Brains were fixed on day 4 and examined using a neurohistologic score. RESULTS: Reductions in CytOx and HbO2 values were correlated closely with decreases in ATP, PCr, and pHi. The changes in CytOx and PCr showed the strongest correlation (r = 0.623). Maximal CytOx reduction during DHCA of more than -25 microM * differential pathlength factor (DPF) predicted brain damage with a sensitivity of 100% and a specificity of 75%. The histologic score was also correlated with a decrease in ATP (r = -0.52 for CytOx; r = -0.32 for ATP); HbO2, PCr, and pHi showed no correlations. CONCLUSIONS: Reduction in CytOx correlates with decreased brain energy state and predicts histologic brain injury after DHCA with a high sensitivity. These data suggest that the level of CytOx could be a very important predictor of brain damage during DHCA.
OBJECTIVES: Near-infrared spectrophotometry (NIRS) is a promising method for non-invasive monitoring of cerebral oxygenation and hemodynamics. This paper reviews studies in which we aimed to validate NIRS in an experimental model of cardiopulmonary bypass (CPB) and deep hypothermic circulatory arrest (DHCA) (validation study), use the method in experimental settings to optimize cerebral oxygenation during CPB (oxygenation study), and test its utility during routine cardiac surgery (clinical study). METHODS: Validation study: Forty 8-10 kg piglets underwent 60 min of DHCA at 15 degrees C, were extubated on the first postoperative day, and sacrificed on the 4th postoperative day for histologic investigations. During CPB and DHCA, the animals were investigated by NIRS (monitoring of cerebral oxygenated hemoglobin (HbO2) and oxidized cytochrome aa3 (Cytox)) and magnetic resonance spectroscopy (MRS) (monitoring of cerebral adenosine triphosphate (ATP) and phosphocreatine (PCr). Oxygenation study: A normoxic (n = 5) and a hyperoxic group (n = 5) of piglets underwent 120 min of DHCA and 6 h of reperfusion with NIRS monitoring. Neuronal damage was evaluated by histology. Clinical study: Patients (n = 41) undergoing routine cardiac surgery were investigated by NIRS and neuropsychological testings. RESULTS: Validation study: Reductions of CytOx and HbO2 values were closely correlated with decreases in ATP, PCr, and pHi. The changes in CytOx and PCr showed the strongest correlation (r = 0.623). Maximal CytOx reduction during DHCA predicted brain damage. Oxygenation study: Histology revealed a significant increase in brain damage in the normoxic group. Cytox and HbO2 tended to be lower during DHCA (p = 0.16). Clinical study: During CPB, arterial PCO2, pH and temperature were closely related to CytOx and HbO2. Patients who suffered from neuropsychological deficits had a lower CytOx minimum compared to those without these. CONCLUSIONS: NIRS measurements, especially the CytOx signal, correlate well with high energy phosphates and have a high sensitivity to predict histologic brain damage. NIRS is an important and useful tool in studies investigating cerebral oxygenation during CPB. The CytOx signal predicted impaired neuropsychological outcome in patients. Therefore, the CytOx signal holds much interest for future studies.
OBJECTIVES: It is controversial whether immature cyanotic hearts are more susceptible to ischemic injury than normoxemic hearts. Acutely induced alveolar hypoxic stress before cardiopulmonary bypass has been used as a model of cyanosis and is reported to worsen recovery of immature hearts after subsequent ischemic insult by means of a free radical injury mechanism. Because of concerns about the relevance of acute alveolar repair to the chronic cyanosis encountered clinically, we assessed the effects of chronic cyanosis without alveolar hypoxia, acute alveolar hypoxia, and normoxemia on recovery of cardiac function after deep hypothermic circulatory arrest. METHODS: A chronic cyanosis model was created in 8 lambs by an anastomosis between the pulmonary artery and the left atrium (cyanosis group). Eight lambs underwent sham operation (control). One week later, the animals underwent cardiopulmonary bypass with 90 minutes of deep hypothermic circulatory arrest at 18 degrees C. Another 8 lambs underwent 45 minutes of hypoxic ventilation before bypass, with arterial oxygen tension being maintained at 30 mm Hg (acute hypoxia group). Cardiac index, preload recruitable stroke work, and tau were measured. Malondialdehyde and nitrate-nitrite, nitric oxide metabolites, were also measured in the coronary sinus. Myocardial antioxidant reserve capacity at 2 hours of reperfusion was assessed by measuring lipid peroxidation in left ventricular tissue samples incubated with t-butylhydroperoxide at 37 degrees C. RESULTS: Oxygen tension was 35 +/- 3 mm Hg in the acute hypoxia group versus 93 +/- 7 mm Hg in the control group. In the acute hypoxia group the recovery of cardiac index, preload recruitable stroke work, and tau were significantly worse than that found in both the control and cyanosis groups. Preload recruitable stroke work at 2 hours of reperfusion was slightly but significantly lower in the cyanosis group than in the control group. The postischemic level of nitric oxide metabolites was significantly lower in the acute hypoxia group than in the cyanosis and control groups. However, malondialdehyde levels in the coronary sinus and myocardial antioxidant reserve capacity were not significantly different among the groups. CONCLUSION: Recovery of left ventricular function after deep hypothermic circulatory arrest in neonatal lambs with chronic cyanosis was slightly worse than that found in acyanotic animals. Acute hypoxia before bypass was associated with significantly worse recovery of left ventricular function, and the mechanism of injury may be related to an impairment of nitric oxide production. Free radical injury does not appear to explain any differences among cyanotic, acyanotic, and acutely hypoxic animals in recovery of left ventricular function after ischemia.
BACKGROUND: Lung function is often impaired after cardiac surgery and cardiopulmonary bypass (CPB), particularly in chronically cyanotic patients. This study aimed to evaluate lung function in a surgically created chronic cyanotic neonatal lamb model after CPB and deep hypothermic circulatory arrest (DHCA) and to assess the role of nitric oxide (NO) in the pathogenesis of increased pulmonary vascular resistance. METHODS: A chronic cyanosis model was surgically created in 7 lambs (4.7+/-0.8 days old) by anastomosing the pulmonary artery (PA) to the left atrium (LA). Another 7 lambs underwent a sham operation (control). One week later, the animals underwent shunt takedown and CPB with 90 minutes of DHCA at 18 degrees C. Cardiac index (CI), pulmonary vascular resistance index (PVRI), lung dynamic compliance (Cdyn), alveolar-arterial oxygen difference (AaDO2), left atrial plasma nitrate/nitrite (NO metabolites) levels, and pulmonary cGMP production (concentration difference between LA and PA) were measured before CPB and at 1 and 2 hours after reperfusion. RESULTS: The cyanosis model consistently produced significantly lower arterial oxygen tension (34.8+/-2.3 vs 93.1+/-8.8 torr in control, p < 0.001) and Qp/Qs (0.6+/-0.1 vs 1.0+/-0.0 in control, p < 0.001) than controls. Postoperative PVRI was significantly lower in the cyanosis group than in controls, although CPB with DHCA significantly elevated PVR in both cyanotic and control animals. There were no significant differences in AaDO2 and Cdyn after CPB between groups. The level of NO metabolites did not change before or after CPB in either cyanotic or acyanotic animals. NO metabolite levels tended to be higher in the cyanotic animals (p = 0.08). There was no significant difference in pulmonary cGMP production between both groups. CONCLUSIONS: These findings suggest that CPB with DHCA, per se, does not affect NO production in cyanotic or acyanotic neonatal lambs but causes increased PVR in both groups. Chronic cyanosis does not result in reduced pulmonary function after CPB with DHCA, and is associated with lower PVR. The mechanism may involve an increased NO production in cyanotic animals.
BACKGROUND: The objective of this study was to evaluate long-term survival, valve-related complications as well as prognostic factors for early and late outcome after open and closed mitral commissurotomy covering a follow-up period of 35 years. METHODS: From 1955 to 1977, 183 patients with mitral stenosis underwent mitral commissurotomy at our institution. Closed valvotomy was performed on 143 patients (group A) and open valvotomy on 40 patients (group B). RESULTS: Survival rates after 10, 20, and 30 years were 89%, 67.8%, and 49.1% in group A and 91.7%, 66.7%, and 45.9% in group B (p = not significant). The risk of late death increased significantly with an advanced preoperative New York Heart Association functional class, atrial fibrillation, higher age at operation, pre- or postoperative mitral regurgitation, and leaflet calcification. Forty-four patients in group A and 5 patients in group B required reoperation (p < 0.05). Independent predictors for reoperation in a multivariate analysis were a remaining postoperative mitral stenosis or regurgitation. A total of 68 patients showed valve-related complications. The linearized rate of valve-related morbidity and mortality was 2.1% per patient-years in group A versus 1.1% per patient-years in B (p < 0.01). CONCLUSIONS: Long-term survival for open and closed commissurotomy are excellent, showing no difference between the groups. However, both the incidence of reoperation as well as valve-related morbidity and mortality were significantly lower after open commissurotomy. In well-selected patients with pure mitral stenosis and no leaflet calcification, open commissurotomy still remains a valid surgical option.
OBJECTIVE: Several techniques for symmetric reconstruction of the aortic root in congenital supravalvular aortic stenosis have been developed, but it remains unclear whether these prove superior to patch enlargement of the noncoronary sinus alone. We reviewed our experience with surgical treatment of supravalvular aortic stenosis and investigated the impact of the surgical technique on long-term results. METHODS AND RESULTS: Seventy-five patients underwent operations to treat congenital supravalvular aortic stenosis at our institution between 1957 and 1998. Surgical procedures included patch enlargement of the noncoronary sinus only (n = 34), inverted bifurcated patch plasty (n = 35), and 3-sinus reconstruction of the aortic root (n = 6). There were 7 early deaths. Among those who survived the operation, 100% were alive at 5 years, 96% were alive at 10 years, and 77% were alive at 20 years. According to time-related analysis diffuse stenosis of the ascending aorta proved a risk factor for both survival and reoperation (P <.01 for each). Patients with multiple-sinus reconstructions of the aortic root accounted for only 2 of the 14 reoperations and none of the late deaths (both P <.001). Residual gradients were lower after multiple-sinus reconstruction of the aortic root (median 10 mm Hg vs 20 mm Hg for patch enlargement of the noncoronary sinus only, P =. 008), as was the prevalence of moderate aortic regurgitation at follow-up (3% vs 22%, P =.05). CONCLUSIONS: Results of operations for supravalvular aortic stenosis improved greatly after the introduction of more symmetric reconstructions of the aortic root. Multiple-sinus reconstructions (inverted bifurcated patch plasty and 3-sinus reconstruction) resulted in superior hemodynamics and were associated with reductions in both mortality rate and need for reoperation.
OBJECTIVES: Recent studies suggest that myocardial reperfusion injury is exacerbated by free radicals when pure oxygen is used during cardiopulmonary bypass. Partial replacement of the oxygenator gas mixture with nitrogen, however, such as has already been adopted clinically in many centers, could increase the risk of gaseous nitrogen microembolus formation and therefore of brain damage because of the low solubility of nitrogen, particularly under conditions of hypothermia. METHODS: Ten 7- to 10-kg piglets were cooled for 30 minutes to 15 degrees C on cardiopulmonary bypass and then rewarmed for 40 minutes to 37 degrees C. In 5 piglets cardiopulmonary bypass was normoxic and in 5 it was hyperoxic. In each group 3 bubble oxygenators without arterial filters and 2 membrane oxygenators with filters were used. Cerebral microemboli were monitored continuously by carotid Doppler ultrasonography (8 MHz) and intermittently by fluorescence retinography. RESULTS: Embolus count was greater with lower rectal temperature (P <.001), use of a bubble oxygenator (P <.001), and lower oxygen concentration (P =.021) but was not affected by the temperature gradient between blood and body during cooling or rewarming. CONCLUSIONS: Gaseous microemboli are increased with normoxic perfusion, but this is only important if a bubble oxygenator without a filter is used.
OBJECTIVES: Laboratory studies suggest that myocardial reperfusion injury is exacerbated by free radicals when pure oxygen is used during cardiopulmonary bypass. In phase I of this study we demonstrated that normoxic perfusion during cardiopulmonary bypass does not increase the risk of microembolic brain injury so long as a membrane oxygenator with an arterial filter is used. In phase II of this study we studied the hypothesis that normoxic perfusion increases the risk of hypoxic brain injury after deep hypothermia with circulatory arrest. METHODS: With membrane oxygenators with arterial filters, 10 piglets (8-10 kg) underwent 120 minutes of deep hypothermia and circulatory arrest at 15 degrees C, were rewarmed to 37 degrees C, and were weaned from bypass. In 5 piglets normoxia (PaO2 64-181 mm Hg) was used during cardiopulmonary bypass and in 5 hyperoxia (PaO2 400-900 mm Hg) was used. After 6 hours of reperfusion the brain was fixed for histologic evaluation. Near-infrared spectroscopy was used to monitor cerebral oxyhemoglobin and oxidized cytochrome a,a3 concentrations. RESULTS: Histologic examination revealed a significant increase in brain damage in the normoxia group (score 12.4 versus 8.6, P =.01), especially in the neocortex and hippocampal regions. Cytochrome a,a 3 and oxyhemoglobin concentrations tended to be lower during deep hypothermia and circulatory arrest in the normoxia group (P =.16). CONCLUSIONS: In the setting of prolonged deep hypothermia and circulatory arrest with membrane oxygenators, normoxic cardiopulmonary bypass significantly increases histologically graded brain damage with respect to hyperoxic cardiopulmonary bypass. Near-infrared spectroscopy suggests that the mechanism is hypoxic injury, which presumably overwhelms any injury caused by increased oxygen free radicals.
BACKGROUND: The initial step in the inflammatory process, which can be initiated by cardiopulmonary bypass and by ischemia/reperfusion, is mediated by interactions between selectins on endothelial cells and on neutrophils. We studied the effects of selectin blockade using a novel Sialyl Lewis X analog (CY-1503) on recovery after deep hypothermic circulatory arrest in a piglet model. METHODS: Twelve Yorkshire piglets were subjected to cardiopulmonary bypass, 30 minutes of cooling, 100 minutes of circulatory arrest at 15 degrees C, and 40 minutes of rewarming. Five animals received a bolus of 60 mg/kg of CY-1503 and an infusion (3 mg/kg per hour) for 24 hours from reperfusion (group O), and 7 randomly selected control piglets received saline solution (group C). Body weight and total body water content were evaluated 3 hours and 24 hours after reperfusion by a bio-impedance technique. Neurologic recovery of animals was evaluated daily by neurologic deficit score (0 = normal, 500 = brain death) and overall performance categories (1 = normal, 5 = brain death). The brain was fixed in situ on the fourth postoperative day and examined by histologic score (0 = normal, 5+ = necrosis) in a blinded fashion. RESULTS: Two of 7 animals in group C died. The neurologic deficit score was significantly lower in group O than in group C (postoperative day 1, P <.001; postoperative day 2, P =.02). The overall performance category was significantly lower in group O than in group C on postoperative day 2 (P =.01). Percentage total body water after cardiopulmonary bypass was significantly higher in group C than in group O (P =.03). Histologic score tended to be higher in group C than in group O, but this difference did not reach statistical significance (group O = 0.5 +/- 0.7; group C = 1.3 +/- 1.off CONCLUSION: Blockade of selectin adhesion molecules by saturation with a Sialyl Lewisx analog accelerates recovery after 100 minutes of deep hypothermic circulatory arrest in a piglet survival model.
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.