Sample diversion and bacterial culture are effective methods to reduce bacterial risk with WBP transfusion. Bacterial contamination of PSPs was assessed at 5.8-fold our current rate for apheresis PLTs utilizing comparable culture protocols.

The biophysical properties of small conductance Ca 2؉ -activated K ؉ (SK) channels are well suited to underlie afterhyperpolarizations (AHPs) shaping the firing patterns of a conspicuous number of central and peripheral neurons. We have identified a new scorpion toxin (tamapin) that binds to SK channels with high affinity and inhibits SK channel-mediated currents in pyramidal neurons of the hippocampus as well as in cell lines expressing distinct SK channel subunits. This toxin distinguished between the SK channels underlying the apamin-sensitive I AHP and the Ca 2؉ -activated K ؉ channels mediating the slow I AHP (sI AHP ) in hippocampal neurons. Compared with related scorpion toxins, tamapin displayed a unique, remarkable selectivity for SK2 versus SK1 (ϳ1750-fold) and SK3 (ϳ70-fold) channels and is the most potent SK2 channel blocker characterized so far (IC 50 for SK2 channels ‫؍‬ 24 pM). Tamapin will facilitate the characterization of the subunit composition of native SK channels and help determine their involvement in electrical and biochemical signaling.

The hypothesis that heparin-coated perfusion circuits reduce thrombin formation and activity; fibrinolysis; and platelet, complement, and neutrophil activation was tested in 20 consecutive, randomized adults who had cardiopulmonary bypass. Twenty identical perfusion systems were used; in 10, all blood-contacting surfaces were coated with partially degraded heparin (Carmeda process; Medtronic Cardiopulmonary, Anaheim, Calif.). All patients received a 300 U/kg dose of heparin. Activated clotting times were maintained longer than 400 seconds. Cardiopulmonary bypass lasted 36 to 244 minutes. Blood samples for platelet count, platelet response to adenosine diphosphate, plasma beta-thromboglobulin, inactivated complement 3b, neutrophil elastase, fibrinopeptide A, prothrombin fragment F1.2, thrombin-antithrombin complex, tissue plasminogen activator, plasminogen activator inhibitor-1, plasmin alpha 2-antiplasmin complex, and D-dimer were obtained at these times: after heparin was given, 5 and 30 minutes after cardiopulmonary bypass was started, within 5 minutes after bypass was stopped, and 15 minutes after protamine was given. After cardiopulmonary bypass, tubing segments were analyzed for surface-adsorbed anti-thrombin, fibrinogen, factor XII, and von Willebrand factor by radioimmunoassay. Heparin-coated circuits significantly (p < 0.001) reduced platelet adhesion and maintained platelet sensitivity to adenosine diphosphate (p = 0.015), but did not reduce release of beta-thromboglobulin. There were no significant differences between groups at any time for fibrinopeptide A, prothrombin fragment F1.2, or thrombin-antithrombin complex or in the markers for fibrinolysis: D-dimer, tissue plasminogen activator, plasminogen activator inhibitor-1, and alpha 2-antiplasmin complex. In both groups, concentrations of prothrombin fragment F1.2 and thrombin-antithrombin complex increased progressively and significantly during cardiopulmonary bypass and after protamine was given. Concentrations of D-dimer, alpha 2-antiplasmin complex, and plasminogen activator inhibitor-1 also increased significantly during bypass in both groups. Fibrinopeptide A levels did not increase during bypass but in both groups increased significantly after protamine was given. No significant differences were observed between groups for levels of inactivated complement 3b or neutrophil elastase. Radioimmunoassay showed a significant increase in surface-adsorbed antithrombin on coated circuits but no significant differences between groups for other proteins. We conclude that heparin-coated circuits used with standard doses of systemic heparin reduce platelet adhesion and improve platelet function but do not produce a meaningful anticoagulant effect during clinical cardiopulmonary bypass. The data do not support the practice of reducing systemic heparin doses during cardiac operations with heparin-coated extracorporeal perfusion circuitry.

No abstract

An in vitro continuous flow system with whole human blood was used to study blood-biomaterial interactions on a base polyurethane and three modified surfaces in the presence and absence of circulating Staphylococcus epidermidis. We hypothesized that the composition of the protein layer adsorbed on the surface of the biomaterial would influence the response of blood components and bacteria. We examined the test surfaces for adsorption of nine plasma proteins and adsorption profiles differed on the four surfaces. The positively charged surface, UC, adsorbed significantly higher amounts of fibronectin (P < .01), von Willebrand factor (P < .01), and fibrinogen (P < .05) than the other materials. As a consequence of increased adsorption of these adhesive proteins, the adhesion of platelets and bacteria was greater on UC than on any other surface. On the base polyurethane, BC, and the negatively charged surface, UA, protein adsorption was low, and these materials were largely free of adherent blood cells and bacteria. The heparinized surface, UH, adsorbed higher quantities (P < .01) of Hageman factor and high molecular weight kininogen relative to the other surfaces. Platelet adhesion, and surface coagulation were prominent on UC, and may have contributed to increased bacterial adhesion on this surface. In the presence of circulating bacteria, adsorption was generally lower than in the absence of bacteria. The pattern of protein adsorption was largely unaffected by the strain of circulating bacteria, but platelet responses (adhesion and activation) were greater in the presence of slime-producing S. epidermidis as compared to the non-slime-producing strain, suggesting that slime may have a direct activating effect on platelets.

Blood-contacting biomaterials may activate the complement cascade, thus promoting leukocyte adhesion to the biomaterial surface. We hypothesize that the extent of complement activation is modulated by biomaterial formulation and the presence of fluid shear stress. To investigate this hypothesis, we tested base poly(etherurethane ureas) formulated with or without Santowhitea antioxidant, a nucleophilic additive. We found that adherent leukocyte densities decreased with increasing shear stress. Moreover, leukocyte adhesion was decreased significantly further by Santowhitea additive under shear stress but not under static conditions. Monocytes showed a higher propensity for adhesion than did neutrophils under shear and static conditions. Under static conditions, adherent cells on the Santowhitea-containing polyurethane had a slightly more activated morphology than those on the base polyurethane. Cell adhesion under shear stress was significantly decreased when C3 or fibronectin was depleted from the suspension medium. Santowhitea additive increased Factor B adsorption to the test surface while shear stress increased Factor H adsorption. The combination of Santowhitea additive and shear stress increased the adsorption of both Factor B and Factor H and the serum protein Sterminal complement complex levels, but it did not further increase the state of activation of adherent cells. We conclude that leukocyte adhesion on poly(etherurethane urea) surfaces is sensitive to the levels of shear stress and that both C3 and fibronectin are required to maintain adhesion in the presence of shear stress. The low state of cellular activation and increased Factor H adsorption may explain the decreased adherent leukocyte density on the Santowhitea-containing polyurethane.

The practice of transfusing ABO-incompatible platelets, driven primarily by concerns about inventory management, has been considered generally safe because the accompanying plasma is usually diluted in the recipient's total blood volume. However, if the platelet product contains a large volume of plasma or a high concentration of incompatible isoagglutinin, there may be hemolysis of the recipient's red cells. Patients with a small blood volume, such as babies and children, are considered to be at particular risk for such a complication. We describe the case of a baby who suffered massive hemolysis of her group A red cells after transfusion of group O Apheresis Platelets containing a high-titered anti-A isoagglutinin. We also offer a review of the literature on this subject and recommendations to avoid acute hemolytic reactions as a result of platelet transfusion.

The molecular basis of many blood group antigens is known, and it provides a means for predicting the red blood cell phenotype. Molecular typing methods are useful when serologic typing cannot be performed, due to sample or reagent limitations. We discuss the implementation of a commercial molecular typing assay at our Transfusion Service, the indications for testing, and the advantages and drawbacks of the assay. We also present our algorithm for selecting candidates for testing.