Adrenaline (A) and noradrenaline (NA) were both found to induce platelet aggregation in citrated platelet rich human plasma, adrenaline being about 8 times more effective than noradrenaline. No effect was obtained with isoproterenol. The aggregating effect of catecholamines was stereospecific, the l‐form of NA being 30 times as effective as the d‐form. Platelet aggregation induced by A and NA could be blocked by phentolamine, phenoxybenzamine and dibenamine in the concentrations 10‐6 M, 10‐4 M and 10 ‐4 M respectively, as well as with some β‐receptor blocking agents, pronethalol and propranolol, although only in a 10‐3 M concentration. Almost no effect was observed with MJ 1999. High concentrations (10‐3 M) of both α‐ and (β‐receptor blocking agents could block adenosine disphosphate induced aggregation indicating an unspecific effect of the blockers at this concentration. Uptake of 3H‐NA and 14C‐5‐HT in the platelets was inhibited by both α‐ and β‐receptor blocking agents in concentrations from about 10 ‐5 M. There was no obvious correlation between inhibition of uptake by α‐receptor blocking agents and their effect on catecholamine‐induced aggregation indicating that uptake of A or NA was not a necessary step in catecholamine mediated platelet aggregation.

SummaryThe adenosine diphosphate induced platelet adhesiveness to glass and the platelet spreading capacity on a siliconized glass surface have been studied in 8 hypovolemic subjects after infusion of 500 ml 6% solution of dextran 70 (Macrodex®) or 500 ml normal saline. Infusion of dextran caused a significant decrease in platelet adhesiveness compared with the controls while no effect was noted on the spreading capacity.It is proposed that the observed effect on platelet adhesiveness is due to dextran induced changes in the activity of plasma factors involved in the mechanisms leading to platelet adhesiveness.

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Summary. Repeated injections of nicotine tartrate in doses of 0.05–0.8 mg per kg in the cat cause a release of catechol amines in the adrenal venous blood, sometimes exceeding the loss in the gland compared with the control gland. The rapid resynthesis observed in some cases after nicotine injections was not observed when nicotine was infused over a period of 60–107 min in doses of 0.04–0.13 mg/kg/min. Increasing doses of nicotine within the dose range 0.1–0.4 mg/kg increased the release of adrenaline while doses of 0.8 mg/kg caused a rise also of noradrenaline. The release of catechol atmines during electrical stimulation uf the splanchnic nerve wts often considerably in excess of the loss in the stimulated gland. The maximal resynthesis of adrenaline corresponded to 325 μg per g gland and of noradrenalirie 745 μg per p gland.