Mechanism of Thrombocytopenia Induced in Mice by Anti-Platelet Serum

Abstract

Although anti-platelet serum is frequently used to produce thrombocytopenia, the mechanism of how platelets are removed from the circulation is poorly understood. In vitro studies indicated that anti-platelet serum caused platelet aggregation, whereas normal rabbit serum did not. The aggregation was dose related; at the lower dose, aggregated platelets were shown to deaggregate and platelets released from the aggregates responded normally to ADP but not to collagen. In mice whose platelets were previously labeled with Na₂³⁵SO₄, anti-platelet serum caused an increase in the amount of ³⁵S mucopolysaccharides (MPS) recovered from the kidneys. No increase in radioactivity was found in the lungs, livers, or spleens of similarly treated mice. The data suggest that platelet specific anti-serum causes platelets to aggregate leading to ADP (and consequently ³⁵S-MPS) release; the accumulation of ³⁵S in kidneys may be due to removal of MPS and/or platelets from the circulation.

Effects of Hypoxia on Thrombocytopoiesis and Thrombopoietin Production of Mice

“…RAMPS was prepared and absorbed with mouse RBC as previously described (10,12) and injected ip (0.1 ml diluted with saline to 0.5 ml per mouse).…”

Increased interaction of vascular endothelium and leucocytes after administration of antiplatelet serum: role in the developing vascular defect.

“…The effect of APS can thus be explained by direct damage to endothelial cells (McDonald and Clift, 1976), which makes them sticky for white cells. (b)Recent evidence indicates that the primary changes may be located in or on the granulocytes themselves (Fehr and Jacob, 1977).…”

Heterotoxicity of Human Serum V.

“…The relationship between the develop ment of thrombocytopenia and leukopenia, and the presence of circulating red cell ghosts was also investigated (table II). A rapid intravenous infusion of RBC hemolysate in a volume of 0.8 ml, equivalent to ap proximately 40"/o of the total circulating red cell volume [15], was often lethal, but the clinical characteristic of dying animals dif fered markedly from the previous groups; animals died quietly within 5 min. More-1 * 3 over, these animals developed a somewhat more moderate thrombocytopenia ( p > 0.01), while the survivors were not significantly thrombocytopenic.…”

“…Then, 1.2 ml of this mix ture was injected per mouse. Controls in the latter case included human serum treated in the same fashion but without MRBC, and serum kept at 0-4 C. The volumes of hemolysate which con tained ruptured RBC equal to approximately 40% of the calculated total red cell volume [15], were injected as controls, to make these experiments comparable to experiments using FHS; the extent of intravascular hemolysis in vivo after serum in fusion was 16-19%. Statistical Analysis. Student's t tests for un paired observations were employed to compare parallel hematological data.…”