Viscoelastic properties of blood studied through piezoresistance measurements.

Piezoresistance describes the change of electrical resistance in a material undergoing deformation. Heterogeneous materials having different resistivities of dispersed and continuous matrix phases, such as blood (comprised of red and white blood cells and platelets suspended in plasma), can exhibit the piezoresistance effect. For an initially isotropic material, two independent intrinsic material coefficients, λ1 and λ2, would uniquely describe the piezoresistance phenomenon. Materials undergoing deformation affect a material's resistivity in two ways: (a) by introducing anisotropy in the material, which is characterized by λ1 and (b) by changing the volume density of the inclusions, which is associated with (1/3 λ1+λ2). In this paper, the piezoresistance effect in bovine blood samples is studied under oscillatory shear flow with a planar sensor rosette. The first piezoresistance coefficient, λ1, was measured at various frequencies and shear rates in the blood flow and compared with cos δ (equal to G'/G*, where G' and G* are the storage and complex moduli, respectively), which reflects the degree of elasticity. The coefficient λ1 was found to have a trend similar to that of cos δ under all conditions tested. Thus λ1 might potentially be used to characterize the viscoelastic properties of blood and the deformability of red blood cells, thus clarifying pathophysiology and facilitating diagnosis.

Dose of prophylactic platelet transfusions and prevention of hemorrhage.

BACKGROUND: We conducted a trial of prophylactic platelet transfusions to evaluate the effect of platelet dose on bleeding in patients with hypoproliferative thrombocytopenia. METHODS: We randomly assigned hospitalized patients undergoing hematopoietic stem-cell transplantation or chemotherapy for hematologic cancers or solid tumors to receive prophylactic platelet transfusions at a low dose, a medium dose, or a high dose (1.1x10(11), 2.2x10(11), or 4.4x10(11) platelets per square meter of body-surface area, respectively), when morning platelet counts were 10,000 per cubic millimeter or lower. Clinical signs of bleeding were assessed daily. The primary end point was bleeding of grade 2 or higher (as defined on the basis of World Health Organization criteria). RESULTS: In the 1272 patients who received at least one platelet transfusion, the primary end point was observed in 71%, 69%, and 70% of the patients in the low-dose group, the medium-dose group, and the high-dose group, respectively (differences were not significant). The incidences of higher grades of bleeding, and other adverse events, were similar among the three groups. The median number of platelets transfused was significantly lower in the low-dose group (9.25x10(11)) than in the medium-dose group (11.25x10(11)) or the high-dose group (19.63x10(11)) (P=0.002 for low vs. medium, P<0.001 for high vs. low and high vs. medium), but the median number of platelet transfusions given was significantly higher in the low-dose group (five, vs. three in the medium-dose and three in the high-dose group; P<0.001 for low vs. medium and low vs. high). Bleeding occurred on 25% of the study days on which morning platelet counts were 5000 per cubic millimeter or lower, as compared with 17% of study days on which platelet counts were 6000 to 80,000 per cubic millimeter (P<0.001). CONCLUSIONS: Low doses of platelets administered as a prophylactic transfusion led to a decreased number of platelets transfused per patient but an increased number of transfusions given. At doses between 1.1x10(11) and 4.4x10(11) platelets per square meter, the number of platelets in the prophylactic transfusion had no effect on the incidence of bleeding. (ClinicalTrials.gov number, NCT00128713.)

Rituximab therapy for thrombotic thrombocytopenic purpura: a proposed study of the Transfusion Medicine/Hemostasis Clinical Trials Network with a systematic review of rituximab therapy for immune-mediated disorders.

The rationale for immunosuppressive therapy of thrombotic thrombocytopenic purpura (TTP) was established by observations that TTP may be caused by autoantibodies to ADAMTS13. Patients with high-titer autoantibodies to ADAMTS13 may have a higher mortality, and survivors may require prolonged plasma exchange therapy in spite of adjunctive glucocorticoid treatment. More intensive immunosuppressive therapy with rituximab may provide benefit for many of these patients. The Transfusion Medicine/Hemostasis Clinical Trials Network is developing a randomized, clinical trial to test the hypothesis that addition of rituximab to standard treatment of TTP with plasma exchange and glucocorticoids will decrease initial treatment failure rates as well as subsequent relapses over the following 3 years. To provide the background data for this clinical trial, a systematic review of all published reports on rituximab treatment of immune-mediated disorders was performed. Twelve articles have reported 27 patients treated with rituximab for TTP, with benefit described in 25 (93%) of the patients. Additional reports have described rituximab treatment of 37 other immune-mediated disorders, with clinical response in most patients. These observations from small uncontrolled case series provide the background and rationale for a randomized clinical trial to establish the role of rituximab in the management of patients with TTP.

Hemoglobinopathy case finding by pulse oximetry.

Pulse oximetry is a widely used, noninvasive instrument for monitoring oxygen saturation. Its use, however, is limited in the setting of dyshemoglobinemias. We report a case of hemoglobin Rothschild in an Asian patient diagnosed as a result of routine pulse oximetry. This case reiterates the limitations of pulse oximetry in patients with dyshemoglobinemias, while introducing its use as a case-finding tool for such conditions.

Low-O(2) affinity erythrocytes improve performance of ischemic myocardium.

O(2) transport and O(2) diffusion interact in providing O(2) to tissue, but the extent to which diffusion may be critical in the heart is unclear. If O(2) diffusion limits mitochondrial oxygenation, a change in blood O(2) affinity at constant total O(2) transport should alter cardiac O(2) consumption (VO(2)) and function. To test this hypothesis, we perfused isolated isovolumically working rabbit hearts with erythrocytes at physiological blood-gas values and P(50) (PO(2) required to half-saturate hemoglobin) values at pH of 7.4 of 17 +/- 1 Torr (2,3-bisphosphoglycerate depletion) and 33 +/- 5 Torr (inositol hexaphosphate incorporation). When perfused at 40 and 20% of normal coronary flow, mean VO(2) decreased from the control value by 37 and 46% (P < 0.001), and function, expressed as cardiac work, decreased by 38 and 52%, respectively (P < 0.001). Perfusion at higher P(50) during low-flow ischemia improved VO(2) by 20% (P < 0.001) and function by 36% (P < 0.02). There was also modest improvement at basal flow (P < 0.02 and P < 0.002, respectively). The improvement in VO(2) and function due to the P(50) increase demonstrates the importance of O(2) diffusion in this cardiac ischemia model.