Issue title: Microcirculation, Interstitium, Lymph, Pathophysiology and Disease. Proceedings of the International Symposium, Villa La Principessa, Lucca, Italy, June 19–20, 1981
Affiliations: Dept. of Pharmacology, King’s College, Strand, London WC2R 2 LS
Abstract: Circulating platelets show no tendency to adhere to the walls of normal blood vessels but do so rapidly and specifically where insides of vessels are damaged by injury or disease except, apparently, in capillaries. Adhesion is followed by aggregation of platelets except again in the smallest and also in the largest vessels, i.e. in the aorta. Such platelet aggregation is responsible for primary haemostasis and arterial, ego coronary thrombosis as well as for obstructive deposits in extracorporeal circulations. Measurements of the haemodynamic forces required to activate platelets, directly indicate that the flow abnormalities caused by atherosclerotic lesions in vivo cannot account for local activation of circulating platelets. On the other hand, there is considerable evidence for the indirect activation of platelets by the operation of haemodynamical forces on the red cells. High collision frequencies between red cells and platelets do not by themselves cause the latter to aggregate. It seems that the activation of platelets by erythrocytes depends on their providing a chemical agent, presumably ADP. Recent experimental and clinical evidence suggests that the activation of platelets by erythrocytes may be diminished by drugs. Chlorpromazine and similar drugs, in concentrations which stabilise the erythrocyte membrane against haemolysis but are too low to affect platelets directly, increase the “bleeding time” both experimentally and clinically under conditions in which this time is determined by the reactivity of platelets and in which the drug does not inhibit platelet aggregation directly.
Keywords: Platelet aggregation, bleeding time, platelet adhesion, ADP
