SummaryArtificial colloids based on gelatin are used as plasma expander to replace donor blood products. In laboratory experiments, gelatin reduced both the velocity and extend of platelet agglutination by ristocetin, and only the agglutination velocity by polybrene (p <0.05). Furthermore, gelatin delayed the in-vitro platelet plug formation under shear-stress in the absence of ADP (p <0.05), whereas gelatin induced no delay in the presence of ADP. Thus, after induction of vWF release from platelets by polybrene or ADP, platelet function was normal. These results indicate that gelatin affects in particular the functionality of plasma-vWF and partly inhibits platelet adhesion.These negative effects of gelatin on hemostasis were demonstrated in two clinical studies during cardiac surgery. In a randomized study of sixty patients undergoing cardiac surgery, gelatin as prime in the heart-lung machine appeared to result in diminished efficacy of aprotinin on hemostasis, whereas it did not affect hemostasis in non-aprotinin patients. An additional retrospective clinical study showed that only high dose of gelatin affected hemostasis. This suggests a limited role of plasma-vWF and a strong back-up mechanism of platelet-vWF in achieving hemostasis.

We conclude that, with human albumin the golden standard, 2.5% hydroxyethyl starch is a suitable colloid plasma substitute to be used as priming solution in an extracorporeal circuit as well as peri- and postoperative infusion fluid, reasonably well maintaining hemostasis.

A prospective consecutive study was undertaken to compare the hemodynamic effect of two cardioplegic solutions in CABG patients after bypass, and in relation to aorta occlusion time with the support of a automatic datalogging database. A total of 249 patients were randomized. One group received Bretschneider cardioplegic HTK solution (132 patients, group I) the other group received St. Thomas cardioplegic solution (117 patients, group II). The data was divided in four periods of aortic clamp time: less than or equal to 40 min (group I 26 patients, group II 32 patients); 41-60 min (group I 49 patients, group II 47 patients); 61-80 min (group I 30 patients, group II 29 patients); and greater than 80 minutes (group I 27 pts, group II 9 patients). Anesthesia regime and therapeutic drugs and infusions were given in both groups in similar dosages. Within both groups HR, CO, PAP, PCWP increased after bypass in relation to prebypass values. SVR decreased in both groups by 30%, MAP and PVR decreased only in group I. Between group I and II differences were found in the CI (3.0 vs. 3.3 l/min/m2), MAP (70 vs. 76 mmHg), PMAR (18 vs. 16 mHg), and SVR (827 vs. 954 dyn.sec.cm-5). In significantly more of the patients in group I, sinus rhythm started spontaneously after the release of the aorta clamp (39.5% vs. 20.4%, p less than 0.005). Patients in group I needed temporarily a pacemaker after bypass in 6.3% cases (in 1.1% of patients in group II,). There was no relation of the hemodynamic data in relation to aorta occlusion time within the groups.(ABSTRACT TRUNCATED AT 250 WORDS)

A variety of studies have been performed on the preservation of hemostasis by aprotinin during cardiopulmonary bypass (CPB). It appears that the mechanism of aprotinin to preserve hemostasis can be interpreted in different ways. Our previous studies suggested that preservation of platelet glycoprotein Ib (GpIb) antigen, and counteraction of heparin anticoagulation in the extrinsic clotting pathway might partly explain the preservative effect of aprotinin. A clinical study was therefore conducted to evaluate these effects during the use of low dose aprotinin. Improved agglutination by ristocetin (P < 0.05), and improved GpIb antigen expression (P < 0.05) during CPB showed better preserved platelet adhesive capacity in the aprotinin group than in the control group. Glycoprotein Ib antigen expression and the agglutination capacity with ristocetin during CPB were closely related (P < 0.05). Platelet GpIIb/IIIa antigen and adenosine diphosphate (ADP) aggregation were not significantly different between the aprotinin and control groups. Aprotinin had no effect on the extrinsic clotting pathway in the blood, since the thromboplastin clotting time was similar in both groups. These results indicate that the protection of platelet adhesive capacity during CPB is a main function of aprotinin, whereas no evidence was collected for enhanced extrinsic clotting by aprotinin during CPB.

To evaluate the biocompatibility and the efficacy of leukocyte removal filters, we performed a prospective study by using the cardiopulmonary bypass perfusate taken from the heart‐lung machine for 20 patients who underwent cardiac surgery and were randomly divided into four groups according to the filters used. A leukocyte removal filter was installed in the transfusion line while the perfusate was transfused to the patients. No increases of C3a, C5a, elastase, and thromboxane were found during leukocyte filtration by polyester filters (Optima, Sepacell R500, and Pall RC100). Activation of the complement cascade was observed during filtration by the cellulose acetate filter (Cellselect) although the efficacy of the Cellselect filter was evidently higher than that of the poly‐ester filter. These results imply that polyester leukocyte filters are superior to cellulose acetate filters in terms of biocompatibility but have a reduced efficacy. An optimal leukocyte filter providing both high efficacy and biocompatibility has yet to be developed.