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Biomedical subjects

C C Edwards

Publications and source records attributed to C C Edwards.

At least 73 records · Page 4Linked to original sources
PubMed1979

Relationship between packed cell volume, platelets, and platelet survival in red blood cell-hypertransfused mice.

In this study we have measured platelet and megakaryocyte concentration, blood volume, and platelet survival of mice after RBC hypertransfusion to PCVs of 62% to 90%. The platelet concentration of mice with PCVs up to 75% was decreased by up to one half. At higher PCVs a more severe thrombocytopenia developed, with platelet concentrations decreased to less than 10% of baseline in approximately one half of the mice. Blood volumes of the hypertransfused mice were increased up to twofold. Megakaryocyte concentrations were normal or increased. Platelet survival in mice with PCVs less than 75% was normal but was sharply decreased for mice with higher PCVs. The decrease in platelet concentration at moderately elevated PCVs may be explained by hemodilution in the larger blood volume. However, hemodilution alone cannot explain the severe thrombocytopenia at higher PCVs. The presence of decreased platelet survival with normal or increased megakaryocyte concentrations in this latter group suggests that the severe thrombocytopenia is the result of more rapid platelet destruction. In summary, elevation of the PCV by RBC hypertransfusion produces thrombocytopenia. The severity of the thrombocytopenia and the mechanisms involved in producing it change abruptly when the PCV exceeds 75%. These findings should be considered in interpretations of the influence of RBC hypertransfusion on hematopoiesis and in clinical and experimental studies of thrombopoiesis in polycythemic subjects.

Animals↗
PubMed1977

Biphasic thrombopoietic response to severe hypobaric hypoxia.

Thrombopoiesis has been studied during and after an 11 d exposure to discontinuous hypobaric hypoxia. Exposure of rats to 0.4 atmospheres for 16--17 h daily initially caused an increase in platelet count which reached a peak of 1.5 times baseline on days 4 and 5. This thrombocytosis was followed by a decrease in platelets to a nadir of 50--60% of baseline on days 12 and 13. That thrombocytosis results from increased platelet production is supported by increased [35S]sulphate incorporation into platelets and increased megakaryocyte size and turnover. The thrombocytopenia with continued hypoxia seems to result from decreased platelet production since 51Cr-platelet survival was normal while megakaryocyte concentration was decreased to one-half that of untreated controls. These observations suggest that differentiation of precursors into megakaryocytes was decreased during the thrombocytopenic period, although the fewer remaining megakaryocytes appeared stimulated because of their larger size and increased [3H]thymidine labelling. Thus, hypobaric hypoxia had a biphasic effect on thrombopoiesis with increased platelet production in the first few days of exposure followed by subnormal production.

Animals↗
PubMed1977

Evidence that stimulation of megakaryocytopoiesis by low dose vincristine results from an effect on platelets.

Appropriate low dosages of vincristine stimulate megakaryocytopoiesis and produce thrombocytosis. In this study of the thrombocytotic action of vincristine, administration of a single dose of 0.1 mg/kg to rats produced an increase in megakaryocyte concentration, diameter and 24 h [3H]thymidine labelling index. Transfusion of one body equivalent of platelets from normal donors prevented stimulation of megakaryocytopoiesis by vincristine whereas platelets from vincristine-treated donors did not. These results suggest that vincristine stimulates megakaryocytopoiesis by altering the functional role of circulating platelets in the regulation of thrombopoiesis.

Animals↗
PubMed1977

In vitro inhibition of platelet function and coagulation by pentamidine isethionate.

Pentamidine isethionate is a trypanocidal drug used for the treatment of Pneumocystis carinii pneumonitis. Hematological complications have occasionally been reported and include anemia, leukopenia, and thrombocytopenia. We report here several qualitative abnormalities of in vitro platelet function and coagulation that have not been described previously. Platelets were exposed in vitro to concentrations of pentamidine isethionate ranging from 0.5 to 100 mug/ml of platelet-rich plasma. Clot retraction, platelet adhesiveness to glass beads, and platelet aggregation (adenosine 5'-diphosphate [ADP], thrombin, epinephrine, collagen, and ristocetin) were inhibited in a dose-dependent fashion. The addition of pentamidine isethionate after aggregation had been initiated with ADP reversed both primary and, to a lesser degree, secondary aggregation. Platelet factor 3 availability and serotonin uptake and release (using collagen as the releasing agent) were not inhibited. Serotonin release with 10(-4) M ADP was slightly inhibited. Pentamidine isethionate prolonged the thrombin time of plasma at concentrations of 5 mug/ml and greater. The prothrombin time was prolonged at concentrations greater than 10 mug/ml of plasma. The inhibition of aggregation was reversed by washing and resuspension in plasma or by the addition of calcium or magnesium ions.

Amidines↗
PubMed1976

Platelet production capacity at intervals after acute thrombocytopenia.

Platelet producing capacity was examined at intervals after acute platelet depletion by reinduction of acute thrombocytopenia and assessment of the subsequent platelet recovery rates of 35S-sulfate incorporation into platelets. Platelet producing capacity was increased on days 1 and 2, somewhat decreased on days 3 and 4 and had returned to baseline by day 5. These studies suggest that there is an initial increase followed by a decrease on days 3 and 4 in cells which can respond to thrombopoietic stimulating factor after induction of acute thrombocytopenia.

Acute Disease↗