Maria Carla Roncaglioni

Effects of trazodone on serotonin in the brain and platelets of the rat.

Abstract Trazodone. a novel antidepressant with a structure different from the tricyclic compounds. inhibits the release of brain 5-HT induced by fenfluramine and blocks the uptake of 5-HT by rat platelets. Two known metabolites of trazodone. oxatriazolepyridin propionic acid and trazodone-N-oxide. do not share the properties of trazodone. A suggested hut unproven metabolite of trazodone. m-chlorophenyl piperazine. is however more active than trazodone as an inhibitor of 5-HT uptake. Trazodone and its derivatives are devoid of activity as releasers of 5-HT from rat platelets.

Bleeding in renal failure: is von Willebrand factor implicated?

Normal or increased concentrations of factor VIII procoagulant activity (VIIIC), factor VIII-related antigen (VIIIRA), and factor VIII-von Willebrand activity (VIIIVWF) were found in the predialysis plasma of 10 out of 11 patients with chronic renal failure (CRF). All patients had a bleeding time longer than 15 minutes and platelet retention to glass beads lower than 40%. The only patient who had reduced concentrations of all three factor VIII complex components was subsequently shown to have von Willebrands disease. In four patients with CRF, very low platelet retention, and slightly prolonged bleeding time none of the three factor VIII COMPLEX COMPONENTS WERE SELECTIVely modified in predialysis samples. These findings suggest that the bleeding tendency common in CRF is not necessarily linked to defective plasma factor VIII-related activities.

In vitro effect of suloctidil on 14C-5-hydroxytryptamine uptake and liberation in rat platelets.

Summary Suloctidil, a new drug endowed with antispasmodic and platelet function suppressing activities, has been shown to interfere in in vitro systems with the transport and the storage of 14 C-5-HT in rat platelets. Suloctidil inhibited the uptake of 14 C-5-HT and induced 14 C-5-HT loss from platelets. The inhibition of 14 C-5-HT uptake appeared to be either non-competitive or un-competitive, according to the concentration of the drug used. The effect of suloctidil in inducing 14 C-5-HT loss from platelets increased by increasing the concentration of the drug, the time and the temperature of incubation with platelets. It was inhibited neither by an inhibitory of 5-HT uptake (chlorimipramine) nor by an inhibitor of the platelet release reaction (acetylsalicylic acid) nor by an excess of cold 5-HT in the incubation medium. Lactate dehydrogenase loss was slight from platelets incubated with suloctidil. The observed effects of suloctidil differed in several respects from those exhibited by imipramine, (+)-fenfluramine, (+)-amphetamine and 4-chloroamphetamine.

Plasmatic and vascular factors of the hemostatic system in rats receiving an estrogen-progestogen combination

Treatment of rats for 10 estral cycles with an estrogen-progestogen combination giving 100% infertility triggered a vascular response characterized by increased prostacyclin activity in arterial walls and increased systolic blood pressure. In contrast, plasma fibrinolytic activity and physiological coagulation inhibitors as well as vascular fibrinolytic activity were not changed by this treatment. The same rats tended to have shorter occlusion times of an aortic prosthesis, and could represent a useful model to study the blood-vessel-wall interplay during oral contraceptive treatment.