Search

Surface treatment of a cardiopulmonary bypass circuit with heparin improves its haemocompatibility. However, potential side effects of this layer of heparin are impairment of O2 transfer and CO2 transfer in the oxygenator and heat transfer in the heat exchanger.Therefore we studied these side effects during extracorporeal circulation with moderate hypothermia in 30 patients who underwent elective coronary artery bypass grafting surgery. All patients were heparinized systemically. In 15 patients (Duraflo II-group) we used an extracorporeal circuit (including a Bentley Bos-CM50 membrane oxygenator) which was treated with heparin. The results of this group were compared with those obtained from another group of 15 patients (control-group), who were operated upon with an identical extracorporeal circuit but without heparin surface treatment.We found no significant differences between the two groups in O2 transfer, CO2 transfer or heat transfer during normothermia or hypothermia.We concluded that neither O2 transfer and CO2 transfer of the oxygenator nor heat transfer of the heat exchanger were impaired by Duraflo II heparin surface treatment during clinical cardiopulmonary bypass with moderate hypothermia. [ABSTRACT FROM PUBLISHER]

This clinical study was performed to evaluate the inhibiting effects of heparin- coated extracorporeal circuits on thrombin formation during cardiopulmonary bypass (CPB). Thirty patients undergoing coronary artery bypass grafting were randomly divided into two groups with (Duraflo II, n=15) orwithout (control, n=15) the use of heparin-coated circuits. Standard systemic heparinization was performed in all the patients before CPB. The results showed that thrombin formation during the first phase of CPB was inhibited by heparin-coating identified by the significantly lower concentrations of thrombin-antithrombin III (TAT) complex formed in plasma in the Duraflo II group than in the control group (p <0.05). Heparin concentrations were higher in the Duraflo II group than in the control group at the end of CPB (p <0.05). However, after release of the aortic crossclamp in the second phase of CPB, thrombin became strongly activated in both the Duraflo II and the control groups indicated by a sharp increase of TAT complex as well as fibrinopeptide A. Thus, Duraflo II heparin-coating reduces thrombin formation in the early phase of CPB, however, this beneficial effect was counteracted after aortic crossclamp release by material-independent stimuli. Therefore, adequate systemic heparinization is still required despite improved haemocompatibility of the circuits offered by heparin-coating. [ABSTRACT FROM PUBLISHER]

The contact of blood with the artificial extracorporeal circuit causes a systemic inflammatory response due to blood activation. In this study, we compared two different paediatric membrane oxygenators used for extracorporeal circulation: a hollow fibre membrane oxygenator (Dideco Masterflo D-701, n = 10), and a flat sheet silicone membrane oxygenator (Avecor Kolobow 800-2A, n = 10). Blood compatibility was indicated by measuring complement activation as well as leukocyte and platelet activation. In patients perfused with a flat sheet membrane oxygenator, concentrations of complement split products C3a were significantly increased 30 minutes after the start of bypass (p < 0.01), whereas only a mild increase of C3a was found in patients perfused with a hollow fibre membrane oxygenator. Leukocyte and platelet counts dropped uniformly in both groups after the start of bypass mainly due to hemodilution. Activation of leukocytes and platelets identified by both plasma beta-glucuronidase and beta-thromboglobulin was similar in both groups. Infants perfused with a flat sheet membrane oxygenator received significantly more donor blood than those perfused with a hollow fibre oxygenator (p < 0.05). These results indicate that when used during paediatric cardiopulmonary bypass, a flat sheet membrane oxygenator has a higher complement activity than a hollow fibre membrane oxygenator, which is probably due to the relatively larger blood-surface contacting area of the oxygenator.

Heparin coating of an extracorporeal circuit for cardiopulmonary bypass improves the hemocompatibility of the circuit and reduces the inflammatory response of the body. It has not been established, however, that heparin coating also improves postoperative hemostasis. We therefore performed a study in 30 patients who underwent a routine coronary artery bypass graft operation subjected to cardiopulmonary bypass with an uncoated (control) or a heparin-coated extracorporeal circuit (Duraflo II). We found significantly higher plasma levels of heparin in the Duraflo II group. However, we found no significant differences between the two groups with regard to other parameters of activation of the fibrinolytic and coagulation systems and to activation of platelets. Postoperative blood loss and donor blood transfusions were reduced in the Duraflo II group but not to a statistically significant extent. We conclude that heparin coating of an extracorporeal circuit improves anticoagulation but does not significantly reduce platelet activation, fibrinolysis, postoperative blood loss, and donor blood transfusions in routine coronary bypass operations.

Cardiopulmonary bypass generates a systemic inflammatory response including the activation of the complement cascade and leukocytes contributing to postoperative morbidity. To evaluate whether the use of heparin-coated extracorporeal circuits could reduce these activation processes, we performed a study on 30 patients undergoing coronary artery bypass grafting who were randomly perfused with a heparin-coated circuit (Duraflo II, n = 15) or with a similar noncoated circuit (control, n = 15). Standardized systemic heparinization was applied for every patient before cardiopulmonary bypass. The use of heparin-coated circuits resulted in a reduction of systemic leukocyte activation during cardiopulmonary bypass reflected by reduced elastase release (p < 0.05) and tumor necrosis factor generation (p < 0.05) manifest after release of the aortic cross-clamp. In addition, blood samples taken from both the right and left atria after reperfusion revealed that the elastase release from the pulmonary microcirculation was absent in the Duraflo II group in contrast to the control group (p < 0.05). The pattern of complement activation, likely initiating this inflammatory reaction, was modified by heparin coating in two different aspects. There was a significant reduction of C3a generation after protamine administration in patients perfused with heparin-coated circuits, and there was a decrease of complement hemolytic capacity in pooled human serum incubated with heparin-coated tubing. These observations suggest that heparin coating might bind some of the complement components from the classic pathway, thereby reducing the inflammatory response to cardiopulmonary bypass.