No abstract

Premenstrual tension was studied in 16 females, using both biochemical and psychological parameters during the pre- and postmenstrual phases. Uptake of serotonin (5-HT) and the levels of 5-HT in platelet-rich plasma and platelet-poor plasma were determined. Degrees of distress experienced pre- and postmenstrually were quantified via the Moos menstrual distress questionnaire. The mean V_max was significantly lower during the premenstrual (tension) phase (8.2 ± 0.9 pmol/min) as compared to the postmenstrual (normal) phase (14.4 ± 3.2 pmol/min). There was no significant difference in the K_m values. A highly significant (p < 0.001) reduction in the levels of 5-HT in platelet-rich plasma (–23.2%) and platelet-poor plasma (-19.1%) was found during the premenstrual phase. There were correlations between the kinetic parameters of 5-HT uptake and some of the Moos symptoms.

A series of experiments was performed to characterize the nature of local tissue reactions to cocaine. The time‐course of tissue injury was assessed over a 21‐day period by gross and microscopic examination of the skin of rats administered 0.1–2.0% cocaine hydrochloride by i.e. or s.c. injection. Pronounced blanching, progressively severe hemorrhage, delayed extravasation of Evans blue dye, and eventual scar formation were seen grossly at injection sites. Marked engorgement of blood vessels, small hemorrhagic foci, and hyalinization of scattered muscle bundles of the pannieulus carnosus were apparent microscopically at 15 min post‐injection. Subsequent changes during (he next 3 h included progressively severe hemorrhage and loss of muscle bundles, degeneration of hair follicles and necrosis of the vascular endothelium and epidermis. Healing of cocaine‐induced lesions, as monitored for 21 days, was relatively rapid and complete. A hyperplastic epidermis covered formerly ulcerated areas by 6 days. Destroyed cellular structures in the derm is were replaced by collagen. Since cocaine's local tissue toxicity has been ascribed to vasoconstriction, the toxic potential of cocaine was contrasted with that of a potent vasoconstrictor, epinephrine (EPI). Although 0.1% EPI produced greater vasoconstriction than did cocaine, s.c. injection of EPI did not result in skin damage. The slight acidity of cocaine hydrochloride solutions appeared to be of little consequence, since s.c. injection of pH 5 and 6 saline had little effect on tissues. Our results suggest that cocaine is directly cytotoxic, though ischemia resulting from vascular injury and vasoconstriction may contribute to the local tissue injury caused by the drug.