In this thesis, some of the causes and mechanisms of platelet aggregation have been discussed. Platelet/granulocyte aggregates occur in stored blood and have been implicated in the development of respiratory distress syndrome following massive blood transfusions.
Seme of the factors that may be responsible for platelet aggregation in CPD anticoagulated blood have been examined.
Catecholamine concentrations were measured in blood plasma.
During blood collection, the concentration of plasma noradrenaline increased, but there seemed to be no relationship between the final noradrenaline concentration and the onset or extent of platelet aggregation.
It was found that platelet aggregation measured by the screen filtration pressure technique, occurred very rapidly in blood stored at 1°C, more gradually at 4°C, and not at all at ambient room temperature.
The measurement of plasma catecholamines, 5-hydroxytryptamine and adenosine di-phosphate concentrations during blood storage did not demonstrate that any one of these factors was responsible for the onset of platelet aggregation. However, it is suggested that these, and other factors, might act individually or synergistically to extend platelet aggregation during blood storage. It was found that adenosine di-phosphate released from erythrocytes might accelerate platelet aggregation in blood stored at 1°C.
It has been shown that potential platelet aggregating agents are released from platelets in blood stored at room temperature. It is suggested that the apparent lack of platelet aggregation at this temperature was due to a rapidly reduced pH, and the rapid degradation of adenosine nucleotides to aggregate inhibitory products.
The evidence suggests that platelet aggregation in stored blood is triggered by the cold, and that it may involve an energy dependent mechanism, possibly independent of the platelet release reaction.
It is suggested that blood storage at roan temperature would reduce or prevent platelet aggregation.