Abstract
Aprotinin does not influence the inflammatory reaction to cardiopulmonary bypass in humans
Highlights
Modified ultrafiltration (MUF) at the termination of cardiopulmonary bypass (CPB) has been considered to remove accumulated fluid and inflammatory mediators and thereby to improve cerebral metabolic rate in infants after cardiac surgery
We hold hemodilution to be an appropriate method for optimizing CPB procedures
Antiinflammatory reaction was significantly enhanced in these patients, which suggests that the physiological reaction of the organism to reduce deleterious effects to CPB is strengthened by using highdose aprotinin
Summary
Modified ultrafiltration (MUF) at the termination of cardiopulmonary bypass (CPB) has been considered to remove accumulated fluid and inflammatory mediators and thereby to improve cerebral metabolic rate in infants after cardiac surgery. The aim of this study was to investigate change in cerebral hemodynamics and oxygenation before and after MUF following corrective cardiac surgery of congenital heart defects. The aim of this study was to evaluate the serum kinetics of protein S-100 in relationship to possible free radicals mediated cerebral membrane injury in infants undergoing cardiac surgery by means of cardiopulmonary bypass (CPB). The aim of this study was to evaluate the patterns of changes in intravascular and intracellular oxygenation states in neonates with HLHS and infants with other congenital heart defects, undergoing corrective cardiac surgery using TCA in deep hypothermia. The purpose of our study was to evaluate the inflammatory response marker TNFα (tumor necrosis factor-α) and myocardial injury marker Troponin I during cardiopulmonary bypass (CPB) in cardiac lymph and to compare them with blood values taken from the coronary sinus (SC). The present study analyses the impact of heparin immobilisation in a model of simulated extracorporeal circulation SECC on leukocyte and platelet activation, expression of surface markers and adhesion receptors, as well as on leukocyte-platelet interaction
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