It was shown that in patients suffering from diffuse toxic goitre and in animals with experimental thyroxin toxicosis the platelet aggregation is decreased. Prostaglandin F2 alpha and cGMP restored platelet aggregating ability of patients and experimental animals while cAMP sharply lowered ADP-induced platelet aggregation in patients and animals with thyroxin toxicosis. Acetylsalicylic acid and indomethacin inhibited ADP-induced platelet aggregation approximately equally in patients and in healthy subjects. Thyroxin produced no effect on platelet aggregation in animals previously injected with indomethacin. It was concluded that disturbance of platelet aggregation in patients with diffuse toxic goitre proceeds like thrombopathy A.

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PubMedDate not supplied

[Inhibitory action of adrenaline on the antiaggregation activity of the arterial wall].

It has been shown in experiments on Wistar rats that adrenaline inhibits both in vitro and in vivo the capacity of the arterial wall for synthesizing an antiaggregating substance (prostacycline). It is suggested that adrenaline takes a direct part in body thrombogenesis during emotional stress and in conditions associated with the increased catecholamine output in the blood.

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PubMedDate not supplied

[Effect of acetylsalicyclic and nicotinic acids and complamin on the formation of a prostacyclin-like substance by the aortic wall].

Experiments on Wistar rats have shown that single oral administration of acetylsalicylic (300 mg/kg), nicotinic (3 mg/kg) acids and complamin (2 mg/kg) inhibits platelet aggregation. It has been established that acetylsalicylic acid inhibits, as an antiaggregation agent, platelet aggregation and synthesis of a prostacycline-like substance by the aortal wall, and decreases its antiaggregation activity. Nicotinic acid and complamin inhibit platelet aggregation but do not lower antiaggregation activity of the aortal wall. Therefore, these latter drugs compare very favorably with acetylsalicylic acid as antiaggregation agents.

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PubMedDate not supplied

[Role of vessel walls in the process of intravascular clot formation].

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Animals↗