Adrenaline Bitartrate 5 mM

Description

Intended use and general information
The platelets adhere to the basal membrane, to the microfibrils associated with elastin (but not elastin itself) and, above all to the collagen fibres with a mechanism mediated by the formation of an enzyme-substrate complex between glucosyl transferases of platelet membranes and incomplete galactosyl-hydroxylysine groups  present in collagen. At the same time as these adhesion phenomena occur, first phase aggregation take place sustained by ADP released from the erythrocytes and from the endothelial cells.

Besides intervening in the initial phases of the haemostasis, the platelets contribute to the activation of numerous plasmatic factors involved in the enzymatic reaction which bring about the transformation of fibrinogen to fibrin, and to blood coagulation. After seeing the importance of the role of the platelets in haemostasis, it is natural to ascribe many haemorrhagic diatheses, constitutional or acquired, to some anomalies of the platelet functions.

Thanks to research carried out in the last ten years on the identification of enzymatic anomalies which are at the basis of platelet diseases, and to the refining of laboratory techniques, it is now possible, with simple and reproducible methods, to identify each specific platelet change leading to a defect in haemostasis even in those patients in which the conventional parameters of coagulation are normal. The diagnosis and the classification of these platelet abnormalities has been made possible by the study of their biochemistry and by the different responses they give to the aggregative agents.

Research in the last few years has further demonstrated that numerous drugs can intervene as aggregating, anti-aggregating agents 1, 2, 3, 4 (tab. 1). Of great importance have been the first results obtained with the use of some anti-aggregative drugs such as anti-thrombotic agents5: aspirin6, dipyridamole, sulphinpyrazone, reo-pro and clopidogrel (Plavix) have been used with success in cerebral ischaemia, myocardial infarction, glomerularnephritis, and microangiopathic disorders.

Hence the evaluation of the platelet aggregation phenomenon induced in vitro by aggregating agents can be of great assistance in finding possible hyperaggregative tendencies of platelets and in monitoring the anti-aggregating therapies and the pharmaceutical treatments which in some way may alter platelet behaviour.

Table 1