Abstract Retrograde cerebral perfusion (RCP) techniques have been adopted in aortic arch surgery for clinical use. The clear benefits of RCP are that it reduces embolic injury and prolongs the permissible period of hypothermic circulatory arrest (HCA). At the same time, however, there is a great deal of evidence according to which RCP may be associated with an increased risk of fluid sequestration and cerebral edema. In the current study intermittent RCP was compared with continuous RCP and HCA alone to clarify if periodical RCP decreases fluid sequestration (I). HCA is an effective method of cerebral protection, but is associated with long cardiopulmonary bypass times, and coagulation disturbances. We tested the hypothesis that deep hypothermic RCP could improve cerebral outcome during moderate HCA (II and III). Glutamate excitotoxicity plays an important role in the development of ischemic brain injury. The purpose of the present study was to determine the efficacy of lamotrigine, a Na+ channel blocker, to mitigate cerebral injury after HCA (IV). A chronic porcine model was used in the present series of studies. Hemodynamic, electrophysiologic, and metabolic monitoring were performed until four hours after the instigation of rewarming. S-100β was measured up to 20 hours. Daily behavioral assessment performed until death or elective sacrifice on the seventh postoperative day. After continuous RCP the median fluid sequestration volume was 145 (0–250) ml compared with -50 (-100 - 0) ml after intermittent RCP (p = 0.04). In comparison of 15°C RCP to HCA alone during moderate 25°C hypothermia, 5/6 animals in the RCP group survived seven days compared with 2/6 in the HCA group (p = 0.04). The total histopathologic scores in the RCP(15°C) group were lower than those for the RCP(25°C) group during moderate 25°C hypothermia (p = 0.04). EEG bursts were recovered better in the RCP(15°C) group at 3 hours after the start of rewarming compared to HCA group (p = 0.05). The rate of EEG burst recovery was higher in lamotrigine treated animals compared to placebo treated animals after 4 hours during the rewarming (p = 0.02). Among the animals that survived for 7 days, the median behavioral score was higher in the lamotrigine group (8) compared with controls (7) (p = 0.02). The results indicate that intermittent RCP decreases the rate of fluid sequestration after continuous RCP. The cold RCP at moderate systemic hypothermia seems to provide a better neurological outcome than that with moderate temperature RCP, a finding suggesting that enhanced cranial hypothermia is the major beneficial factor of RCP. The Na+ channel blocker lamotrigine improves neurological outcome after a prolonged period of HCA. In conclusion, two refinements in the RCP concept are to administer it at low temperatures and if longer periods of perfusion are necessary, RCP should be applied intermittently.

Abstract Cessation of the blood circulation for some time during surgery of the aortic arch and repair of congenital heart defects is normally required to allow a bloodless operation field. Hypothermia is the most important mechanism for end-organ protection, particularly the brain, during such operations. Cardiopulmonary bypass is used for core cooling before total hypothermic circulatory arrest (HCA) or selective cerebral perfusion (SCP) are initiated. During hypothermic cardiopulmonary bypass, pH can be managed according to either pH- or alpha-stat principles. In the present work, the optimal pH management strategy for operations requiring HCA or SCP was explored. An experimental porcine model was used. Firstly, outcome was evaluated in a HCA model using either the α- or pH-stat perfusion strategy (I). Secondly, we sought to determine which acid-base management is more effective in attenuating ischemic brain injury during combined HCA and embolization conditions (II). In the third study, the impact of propofol anesthesia and α-stat perfusion strategy on outcome was explored (III). Finally, the acute effects of perfusion strategies in a SCP porcine were compared (IV). Hemodynamics, temperature, EEG (I-III), brain microdialysis, intracranial pressure (I-III), brain tissue oxygen partial pressure (I-III), and intravital microscopy (IV) were monitored intraoperatively. In the chronic studies, survival, postoperative neurologic recovery and brain histopathologic examination were evaluated (I-III). pH-stat strategy was associated with superior outcome compared to the α-stat strategy during a 75-minute period of deep HCA (I). In addition, despite the pH-stat strategy-related cerebral vasodilatation, this method provided better neuroprotection in a setting of cerebral particle embolization prior to a 25-minute period of deep HCA (II). Propofol anesthesia combined with α-stat perfusion strategy was observed to deteriorate the brain injury during HCA evaluated by key brain microdialysis parameters (III). Finally, when employing moderately hypothermic SCP, the differences between pH- and α-stat strategies in cerebral metabolism and microcirculation were minimal. These findings are clinically relevant since α-stat perfusion strategy is still the most commonly used acid-base perfusion strategy during hypothermic cardiopulmonary bypass in adults, and propofol one of the most used anesthetics in clinical practice. It is also noteworthy that the pH-stat strategy is not currently used in adults because of the perceived increased risk of atherosclerotic embolization. However, the advantage of pH-stat strategy over α-stat strategy could not be observed when employing SCP.

Abstract In the repair of complex congenital heart defects or in surgery of the aortic arch, normal circulation may be temporarily halted to ensure a clean, bloodless operation field. The brain is the organ most vulnerable to ischemic injury during this no-flow period, and the mortality and morbidity of these procedures today consists mostly of neurological complications. Hypothermia decreases the need for oxygen and other metabolites, and cooling the patient with an extracorporeal heart-lung machine can provide enough time to perform the necessary surgical procedures during a circulatory standstill. This procedure is referred to as hypothermic circulatory arrest (HCA). Sometimes the cerebral circulation can be maintained even if the rest of the body undergoes circulatory arrest, and this strategy, involving separate catheterization of brain-destined vessels, is referred to as selective cerebral perfusion (SCP). In this work, four separate brain protection strategies were evaluated. Two studies were performed on a surviving porcine model (I, II) to evaluate neurological recovery as well as cerebral metabolism and histopathology, and two were acute in design (III, IV), employing the modern technology of intravital microscopy to examine cerebral microcirculation. The first study (I) showed that the administration of hypertonic saline dextran (HSD) led to a decrease in intracranial pressure, improved brain metabolism, better neurological recovery and less histopathological injury of the brain tissue in association with HCA. In the second study (II) a novel pharmacological molecule, levosimendan, reduced the intracranial pressure during the operation, but no improvement in terms of cerebral metabolism, neurological recovery or histopathological brain injury was observed after HCA. In the third study (III), real-time intravital microscopy showed that in association with HCA, a leukocyte depleting filter (LDF) attached to the cardiopulmonary bypass circuit reduces the number of activated leukocytes in cerebral microcirculation. In the fourth study (IV), cerebral metabolism and microcirculation were similar during SCP independent of the acid-base management strategy. The results of this work suggest that HSD could be assessed in human trials, that levosimendan needs further studies to optimize its potential, that the LDF functions as designed and that the differences between the α- and the pH-stat acid-base management strategies with SCP did not differ in moderate hypothermia.

No description available.

Abstract During surgery of the aortic arch and pediatric heart surgery, the blood flow to the brain has to be interrupted at times to allow a bloodless operation field and adequate conditions for surgical repair. During this no-flow period the brain is exposed to a high risk of ischaemic injury, as it will become irreversibly damaged after 5 minutes of circulatory arrest at 37°C. Additional time can be gained by cooling the patient with an extracorporeal heart-lung machine, as hypothermia reduces the cerebral metabolic rate and allows longer safe periods of circulatory standstill. This method of cerebral protection, called hypothermic circulatory arrest (HCA), is widely used in clinical practice. Thus the brain becomes susceptible to ischaemic injury after 30 minutes of HCA at 15°C. Lower temperatures than this are not practicable, however, as they require longer periods of cardiopulmonary bypass, which may further aggravate cerebral injury. To ensure a better outcome for patients undergoing these operations, additional ways of protecting the brain are required. The present work focuses on neuroprotective biochemical and fluid therapy methods for use during HCA, employing a surviving porcine model. Fructose-1,6-bisphosphate (FDP), a high-energy intermediate of glycolysis, was examined for potential neuroprotective properties in two cerebral injury settings associated with HCA. First, FDP was administered before and after a 75-minute period of HCA at a brain temperature of 18°C. This led to better survival, neurological recovery and brain histopathological findings and had supportive effects on brain metabolism (I). Second, a 25-minute period of HCA along with an iatrogenic embolic load produced by microsphere injection was used to generate a massive ischaemic injury to the brain. In this setting FDP did not affect the neurological outcome but had a clear supportive impact on cerebral metabolism (II). In addition, cerebral histopathological samples taken during the first study were analysed by electron microscopy, which revealed significant preservation of the ultrastructure in the FDP-treated animals (III). Hypertonic saline dextran (HSD) is a novel fluid therapy method which has been shown to enhance the outcome after hypovolaemic shock with or without head injury and is potentially very effective in reducing ischaemia-reperfusion injury. Its administration led to a decrease in intracranial pressure, improved brain metabolism, faster and better recovery and less histopathologically observable morphological damage (IV). The findings indicate that both FDP and HSD have significant neuroprotective properties and should be assessed in humans as well.

Abstract Interruption of cerebral blood flow during hypothermic circulatory arrest (HCA) predisposes neurons to glutamate excitotoxicity. Reperfusion is followed by leukocyte infiltration, which results in an inflammatory reaction in the brain tissue. In the first study, the presynaptic glutamate release inhibitor lamotrigine (L) and the leukocyte-depleting filter (LF) were studied to determine if their combination could mitigate brain injury after HCA (I). The aim of the second study was to evaluate the possible neuroprotective effect of a 14-hour period of mild (32°C) hypothermia after HCA (II). Recent experimental research has demonstrated the neuroprotective properties of erythropoietin (EPO) and fructose-1,6-bisphosphate (FDP), whose effects during and after HCA were evaluated in the third and the fourth studies (III, IV). A chronic porcine model was used. The animals were randomly assigned to the study groups as follows: 8 animals in the L+LF group, 8 in the L group, and 8 in the control group (I); 10 animals in the hypothermia group and 10 in the normothermia group (II); 10 animals in the EPO group and 10 in the control group (III), and 12 animals in the FDP group and 12 in the control group (IV). Monitoring of hemodynamics, metabolism, temperature, electroencephalogram (EEG), brain microdialysis, intracranial pressure (II-IV), and brain tissue oxygen (II-IV) was carried out. A daily behavioral assessment was performed until death or until elective sacrifice on the seventh postoperative day, after which the brain was prepared for a histopathologic examination. The results of these studies indicate that lamotrigine has a neuroprotective effect during HCA. This is observed in terms of EEG burst recovery, behavioral and histopathologic outcome, and brain microdialytic findings. The combined use of lamotrigine and leukocyte filtration may further improve survival. A 14-hour period of mild hypothermia after HCA is associated with a poor outcome. However, it may preserve its efficacy when used for no longer than 4 hours. Administration of EPO before HCA proved ineffective in reducing mortality or brain histopathologic injury. Findings from brain microdialysis, brain tissue oxygen tension, and neuronal apoptosis, however, suggest that the drug has neuroprotective properties. Administration of FDP before and after HCA is associated with better survival, behavioral outcome, and brain histopathologic scores. The metabolic and brain microdialytic findings also suggest that this drug has supportive effects on myocardial and brain metabolism.

Abstract Ischaemic cerebral injury follows a well attested sequence of events including three phases, i.e. depolarization, biochemical cascade and reperfusion injury. Glutamate excitotoxicity plays an important role in the development of ischaemic brain injury following prolonged hypothermic circulatory arrest (HCA), and leukocyte infiltration and a cytokine-mediated inflammatory reaction are known to play a pivotal role in the reperfusion phase. The aim of this series of experimental studies was to develop biochemical and reperfusion-related strategies to improve brain protection. We tested the hypotheses that the Na+ channel blocker lamotrigine (I) or the N-Methyl-D-Aspartate-receptor antagonist memantine (III) could improve the cerebral outcome after HCA and studied whether a leukocyte-depletion filter (L-DF; LeukoGuard LG6®, Pall Biomedical, Portsmouth, U.K) could mitigate brain injury (II). The aim of the fourth study was to find out whether lamotrigine combined with the leukocyte-depleting filter can potentiate cerebral protection (IV). A chronic porcine model was used, in which haemodynamic, electrophysiological, metabolic and temperature monitoring were performed for four hours after the instigation of rewarming and S-100β measured up to 20 hours. Cytokines were measured, microdialysis was performed, and daily behavioural assessments were made until death or elective sacrifice on the seventh postoperative day, upon which a histopathological analysis of the brain was carried out. The rate of EEG burst recovery was higher in the lamotrigine-treated animals, the median being 40% of the baseline compared with 17% in the placebo group at 4 hours after the start of rewarming (p = 0.02) and 80% compared with 20% at 4 hours (p = 0.01). Complete behavioural recovery was seen in 5/8 of cases (63%) after lamotrigine administration, compared with 1/8 (13%) in the placebo group (p = 0.02). The median behavioural score among the animals that survived for 7 days was higher in the lamotrigine group (8) than in the controls (7) (p = 0.02). Mortality was 2/10 in the L-DF group and 5/10 in the controls, the median behavioural score on day 7 being higher in the L-DF group (8.5 vs. 3.5 p = 0.04). The median of the total histopathological score was 6.5 in the L-DF group and 15.5 in the control group (p = 0.005). In the memantine group 5/10 animals survived seven days, as compared with 9/10 in the placebo group, and the median behavioural score on day 7 was 3.5 compared with 7.5 in the placebo group (p = 0.39). The median of the total histopathological score was 16 in the memantine group and 14 in the placebo group (p = 0.25). In the LD-F + lamotrigine group 7/8 animals survived for seven days, as compared with 4/8 in the lamotrigine only group and 3/8 among the controls. EEG burst recovery 7 hours after the start of rewarming was highest in the LDF + lamotrigine group, the median being 94% (p = 0.024 vs. controls), compared with 81% in the lamotrigine group and 64% in the control group. The median behavioural score on day 7 was 9 in the LD-F + lamotrigine group (p = 0.004 vs. controls), 4 in the lamotrigine group and 0 in the control group, while the median of total histopathological score was 14 (p = 0.046 vs controls), 14.5 (p = 0.062 vs. controls) and 21, respectively. The control group had the highest intracerebral lactate, glutamate and glycerol levels after HCA. In conclusion, the results indicate that the NA+ channel blocker lamotrigine improves the neurological outcome after a prolonged period of HCA but that the NMDA receptor antagonist memantine does not have this property in the present setting. The leukocyte-depleting filter mitigates brain injury after a prolonged period of HCA, and lamotrigine can potentiate this effect.

Abstract There is a lack of reliable methods of evaluation of brain ischemic injury in patients undergoing cardiac surgery. The present study was, therefore, planned to evaluate whether serum S100β protein (I), brain cortical microdialysis (II), intracranial pressure (III) and electroencephalography (EEG) (IV) are predictive of postoperative death and brain ischemic injury in an experimental surviving porcine model of hypothermic circulatory arrest (HCA). One hundred and twenty eight (128) female, juvenile (8 to 10 weeks of age) pigs of native stock, weighing 21.0 to 38.2 kg, underwent cardio-pulmonary bypass prior to, and following, a 75-minute period of HCA at a brain temperature of 18°C. During the operation, hemodynamic, electrocardiograph and temperature monitoring was performed continuously. Furthermore, metabolic parameters were monitored at baseline, end of cooling, at intervals of two, four and eight hours after HCA and before extubation. Electroencephalographic recording was performed in all animals, serum S100β protein measurement in 18 animals, cortical microdialysis in 109 animals, and intracranial pressure monitoring in 58 animals. After the operation, assessment of behavior was made on a daily basis until death or elective sacrifice on the seventh postoperative day. All four studies showed that these parameters were predictive of postoperative outcome. Animals with severe histopathological injury had higher serum S100β protein levels at every time interval after HCA. Analysis of cortical brain microdialysis showed that the lactate/glucose ratio was significantly lower and the brain glucose concentration significantly higher among survivors during the early postoperative hours. Intracranial pressure increased significantly after 75 minutes of HCA, and this was associated with a significantly increased risk of postoperative death and brain infarction. A slower recovery of EEG burst percentage after HCA was significantly associated with the development of severe cerebral cortex, brain stem and cerebellum ischemic injury. In conclusion, serum S100β protein proved to be a reliable marker of brain ischemic injury as assessed on histopathological examination. Cerebral microdialysis is a useful method of cerebral monitoring during experimental HCA. Low brain glucose concentrations and high brain lactate/ glucose ratios after HCA are strong predictors of postoperative death. Increased intracranial pressure severely affected the postoperative outcome and may be a potential target for treatment. EEG burst percentage as a sum effect of anesthetic agent and ischemic brain damage is a useful tool for early prediction of severe brain damage after HCA. Among these monitoring methods, brain cortical microdialysis seems to be the most powerful one in predicting brain injury after experimental hypothermic circulatory arrest.

Die vorliegende Arbeit setzt sich mit den funktionellen und strukturellen Veränderungen im Zentralnervensystem im Zusammenhang mit angeborenen Vitien und deren chirurgischer Behandlung mit Hilfe der extrakorporalen Zirkulation (EKZ) sowohl klinisch als auch tierexperimentell auseinander mit dem Ziel, neuroprotektive Strategien zu entwickeln. Wir haben mit den verfügbaren Methoden der Neuroüberwachung die charakteristischen Verläufe definiert und beschrieben. Zusätzlich wurden diese nicht-invasiven Methoden wie die Nahinfrarot-Spektroskopie sowohl klinisch als auch tierexperimentell validisiert. Es konnte jedoch gezeigt werden, dass diese Methoden eine zuverlässig signifikante globale Alteration in der Oxygenation und Perfusion anzeigen. Durch das Erarbeiten und die Charakterisierung des Verlaufs der Serumwerte des astroglialen Proteins S-100B wurde die klinische Wertigkeit genauer definiert. Es konnte klinisch und tierexperimentell gezeigt werden, dass die abnorm erhöhten Werte des S-100B im Serum von einem signifikanten diagnostischen Wert sind. Im Gegensatz dazu wurde die untergeordnete Rolle der Bestimmung von neuronalen Marker im Serum bestätigt. Durch die tierexperimentellen Arbeiten wurde gezeigt, dass die überwiegenden morphologischen Veränderungen nach EKZ im Gehirn in den Astrozyten und Gliazelen zu finden sind. Die neuronale Zelldegeneration war nach dem tiefhypothermen Kreislaufstillstand überwiegend in Form von hypoxischer Zellnekrose. Die apoptotische Zelldegeneration trat zellspezifisch im Gyrus Dentatus des Hippocampus auf. Vor allem konnte die bedeutende protektive Rolle der Hypothermie und der hypothermen Perfusion der EKZ demonstriert werden. Bei einer effektiven systemischen Kühlung an der EKZ könnte ein Kreislaufstillstand ohne signifikante neuronale Schädigungen überstanden werden. Die EKZ und der tiefhypotherme Kreislaufstillstand stellen an sich für das unreife Gehirn eine grobe nicht-physiologische Situation dar. Im Tiermodel könnte histologisch gezeigt werden, das die systemische Vorbehandlung mit Methylprednisolone keine protektive Wirkung hat. Obwohl eine signifikante Neuroprotektion durch Gabe von FK506 und Cyclosporin unter extremen Bedingungen der EKZ und tiefhypothermem Kreislaufstillstand erzielt wurde, bedarf es vor einer klinischen Anwendung weiterer tierexperimenteller und klinischer Überprüfungen. / The aim of our clinical and experimental studies was to evaluate functional and structural changes in the brain during corrective cardiac surgery using cardiopulmonary bypass (CPB) and deep hypothermic circulatory arrest (DHCA) in order to develop neuroprotective strategies. Using the available neurmonitoring methods such as the transcranial Doppler and near infrared spectroscopy (NIRS) characteristic changes in cerebral perfusion and oxygenation were defined and described according to the changes in hemodynamic parameters such perfusion pressure, temperature and flow rate. The diagnostic value of the astrocytic cell protein S100B was evaluated by measurement of the serum concentrations in infants and children with and without neurological complications. Additionally, the normal and abnormal release patterns were evaluated in experimental setting using an animal model of CPB and DHCA. According to the neuropathological assessment of the brain initial morphological changes were found predominantly in the astroglial cells. Systemic hypothermic perfusion on CPB before the induction of circulatory arrest period of 60 minutes was significantly protective. Ischemic neuronal injury in form of cell nekrosis was found in different brain region particularly after the prolongation of circulatory arrest time in deep hypothermia. The apoptotic cell death was found predominantly in the hippocampal region of the dentate gyrus. The routinely prophylactic systemic use steroid during cardiac surgery is not protective against ischemia and has been found to induce apoptosis in the hippocampus. In the same model the systemic pre-treatment with single high dose of Cyclosporin and FK506 decreased significantly the ischemic neuronal cell injury in different brain region. However, before clinical use further studies are necessary to optimise the dose and mode of application.

Hintergrund: Das akute Nierenversagen ist eine häufige Komplikation nach einer Herzoperation bei Neugeborenen, Säuglingen und Kleinkindern. Die Bedeutung der postoperativen Hämodynamik für eine Nierenschädigung ist gut bekannt, jedoch ist der Einfluß des kardiopulmonalen Bypasses und des tiefen hypothermen Kreislaufstillstandes weniger klar. Überdies gibt es Veränderungen der Blutviskosität während und nach der Herzoperation am kardiopulmonalen Bypass, welche die Nierenfunktion beeinflussen können. Aus diesem Grunde wurde der Einfluß der Blutviskosität am kardiopulmonalen Bypass und des tiefen hypothermen Kreislaufstillstandes auf die Nierenfunktion in dieser Patientengruppe untersucht. Methode: Untersucht wurden 44 Patienten mit einem Körpergewicht unter 10 kg, die am kardiopulmonalen Bypass operiert wurden. Von diesen erfolgte die Herzoperation bei 7 Patienten unter zusätzlicher Anwendung des tiefen hypothermen Kreislaufstillstandes. Bei allen Patienten wurden zu verschiedenen Zeitperioden Messungen zur Beschreibung der Nierenfunktion (Diurese, Kreatinin-Clearance und Gesamtprotein, Albumin, alpha-1-Mikroglobulin, Transferrin, IgG, N-Acetyl-beta-D-Glucosaminidase im Urin) und Bestimmungen der Blut- und Plasmaviskosität, der Erythrozytenaggregation und des kolloidosmotischen Druckes durchgeführt. Beide Gruppen wurden hinsichtlich des Einflusses des Kreislaufstillstandes auf die Nierenfunktion miteinander verglichen. Ergebnisse: Die während des kardiopulmonalen Bypasses im Zusammenhang mit einem erhöhten transglomerulären Filtrationsgradienten entstandene Polyurie und Proteinurie normalisierte sich innerhalb von 24 Stunden postoperativ. Die renale Ausscheidung von N-Acetyl-beta-D-Glucosaminidase und die erhöhte Natriumausscheidung zeigten zusätzlich eine tubuläre Schädigung an. Bei Hypothermie hatte die Plasmaviskosität einen deutlichen Einfluß auf die Blutviskosität, die während hypothermer Perfusion mit den im Urin gemessenen Werten von Albumin und N-Acetyl-beta-D-Glucosaminidase korrelierte. Die Patienten in der Kreislaufstillstandsgruppe hatten eine längere Bypasszeit und eine niedrigere minimale Körpertemperatur im Vergleich zu den Patienten ohne Kreislaufstillstand (p < 0,05). Diurese und Kreatinin-Clearance zeigten keine Differenzen zwischen beiden Gruppen. Während der Reperfusion wurde in der Kreislaufstillstandsgruppe signifikant mehr Albumin renal ausgeschieden als in der Vergleichsgruppe, ebenso Albumin und N-Acetyl-beta-D-Glucosaminidase nach dem kardiopulmonalen Bypass (p < 0,01). Schlußfolgerung: Die kardiopulmonale Bypassperfusion könnte eine Proteinurie und einen milden tubulären Schaden verursachen. Die Blutviskosität scheint dafür ein mitbestimmender Faktor zu sein und ist möglicherweise während hypothermer Perfusion wesentlich von der Plasmaviskosität abhängig. Es ist notwendig und wünschenswert anhand einer prospektiven Interventionsstudie den Einfluß der Blut- und Plasmaviskosität auf die postoperative Nierenfunktion zu untersuchen. Der tiefe hypotherme Kreislaufstillstand kann die Empfindlichkeit der Niere für einen Ischämie-Reperfusions-Schaden steigern. Obgleich die Befunde mild sind und keinen schweren ischämischen Nierenschaden anzeigen, sollte der durch den Kreislaufstillstand verursachte potentielle Nierenschaden für die Planung des chirurgischen Eingriffs bei Patienten mit angeborenen Herzfehlern als zusätzliches Risiko für ein akutes Nierenversagen mit in Betracht gezogen werden. / Background: Acute renal failure is a common complication after cardiopulmonary bypass in infants. Whereas it is well known that postoperative hemodynamics inflict acute renal failure, the influence of extracoporeal circulation on the kidney is less clear. Moreover, changes in blood viscosity occur during and after surgery, which may influence renal dysfunction. For this reason, the impact of blood viscosity during cardiopulmonary bypass and circulatory arrest on renal function was investigated. Methods: 44 patients weighting less than 10 kg operated on cardiopulmonary bypass were investigated, inclusive of 7 patients who additionally underwent circulatory arrest. In all patients analyses of renal function (diuresis, creatinine clearance, urinary total protein, albumin, alpha-1-microglobulin, transferrin, IgG, and N-acetyl-beta-D-glucosaminidase), blood, and plasma viscosity measurements, erythrocyte aggregation and colloid osmotic pressure were performed. Both groups were compared with regard to the impact of circulatory arrest on renal function. Results: Polyuria and proteinuria that appeared during cardiopulmonary bypass indicated an elevated transglomerular filtration gradient, which recovered within 24 hours. The appearance of N-acetyl-beta-D-glucosaminidase in the urine and elevated sodium excretion were additionally indicative of mild tubular damage. With hypothermia, plasma viscosity could had a major impact on the blood viscosity, which, during hypothermic perfusion, seemed to be related to proteinuria and N-acetyl-beta-D-glucosaminidase values. The patients of the circulatory arrest group had a longer bypass time and a lower body temperature in compare to the patients without circulatory arrest (p < 0.05). Diuresis and creatinine clearance revealed no differences between both groups. During reperfusion in the circulatory arrest group significantly more albumin were excreted as in the comparison group, likewise albumin and N-acetyl-beta-D-glucosaminidase after cardiopulmonary bypass (p < 0.01). Conclusions: Cardiopulmonary bypass perfusion could cause proteinuria and mild tubular damage. Blood viscosity may be one possible contributing factor, which in hypothermia may depend mainly on plasma viscosity. It is necessary and desirable to investigate the impact of blood, and plasma viscosity on postoperative renal function based on a prospective intervention study. The deep hypothermic circulatory arrest can increase the sensitivity of the kidney to an ischemia-reperfusion injury. Although the findings are mild and do not indicate severe ischemic renal damage, potential renal damage by deep hypothermic circulatory arrest should be taken into account for planning surgical procedures for congenital heart disease patients with additional risks of acute renal failure.