Uterine rupture after prostaglandin analogues to induce midtrimester abortion.

Although prostaglandins are largely used and considered safe drugs to induce midtrimester abortion, the literature reports several cases of uterine rupture consequent to their administration. We report the second ever-described case of uterine rupture after administration of gemeprost and sulprostone for midtrimester abortion in a 45 years-old women with scarred uterus.She was admitted to our Unit for termination at 20 weeks' gestation because of trisomy 21 diagnosed by chromosomal analysis of amniotic liquid at 16 weeks' gestation. Five pessaries of gemeprost (one pessary, every 3 hours) were administered into the posterior vaginal fornix. Since the cervix remained closed and uneffaced, another cycle of 5 gemeprost administration was conducted. When the cervix changed in consistency and dilatation, we decided to administrate sulprostone. At the obstetric examination any visible fetus was evidenced. The abdominal ultrasonography showed an empty uterine cavity and the gestational sac with the dead fetus in abdomen. Emergency laparotomy was therefore undertaken. Primary suture of the ruptured uterus was initially attempted but in vain. Therefore, total abdominal hysterectomy was performed to control bleeding and eventual hypovolemic shock.Given the lack of strong evidence in literature and the fact that case reports are not an optimal method for assessing frequency of an event nor the overall risks of a procedure since they frequently report rare single events, other larger studies are needed to assess whether women with multiple risk factors (e.g. advanced age and previous uterine surgery), and administered with prostaglandins' association have a higher risk of uterine rupture.

Binge-like eating in mice.

OBJECTIVE: Given the lack of reliable murine model of binge-like eating, we tried to induce this pathological behavior in mice. METHOD: We used an experimental protocol mimicking the etiological factors involved in the development of binge eating in humans, that is, food restriction, refeeding (R-R) in presence of high palatable food, and stress (S). RESULTS: Mice subjected to at least three cycles of R-R plus S (forced swimming stress), showed a binge-like behavior evident as early as 4 h, persisting 24 h after stress application and not associated to depressive-like behavior. However, after the third R-R/S cycle, food intakes of mice returned to normal levels. DISCUSSION: (i) at least three cycles of R-R plus S are required to promote abnormal eating in mice, (ii) this is not associated to depressive-like behaviors, and (iii) the enhanced pathological behavior showed a transient nature not persisting after the third R-R/S cycle.

Behavioral effects of the beta3 adrenoceptor agonist SR58611A: is it the putative prototype of a new class of antidepressant/anxiolytic drugs?

A large body of evidence corroborates the notion that deficiencies of serotonergic system are likely involved in the pathogenesis of both depression and anxiety. Activation of beta(3) adrenoceptors has been shown to increase brain tryptophan content suggesting an elevation of brain serotonin (5HT) synthesis. SR58611A is a selective beta(3) adrenergic agent possessing a profile of antidepressant activity in routine rodents' experimental models of depression. The present study was undertaken to evaluate in rodents the antidepressant properties of SR58611A and to assess its putative anxiolytic value in experimental models of depression and anxiety. Compared to the control group, SR58611A (0.1, 1, 5 or 10 mg/kg) caused a dose-dependent reduction in immobility of Wistar male rats in the forced swim test. The maximum dose appeared to be equivalent to an effective dose of clomipramine (50 mg/kg). In addition, acute injection of SR58611A induced in rats a dose-dependent decrease in grooming response to a novel environment (novelty-induced grooming test). For any dose, the effect was lower than that of diazepam (1 mg/kg). Chronic treatment with SR58611A resulted also in an increased social interaction time in the social interaction test without affecting motor activity of rats. Furthermore, similarly to diazepam a chronic treatment with the highest doses of SR58611A was followed by increased exploratory behavior in Swiss male mice exposed to the elevated plus maze test. These effects are mediated by beta(3) adrenoceptors since i.p. pretreatment with the selective beta(3) adrenoceptor antagonist SR59230A (5 mg/kg) blocked the effects of SR58611A. Finally, also the 5HT antagonist methysergide (2 mg/kg) prevented the antidepressant and anxiolytic-like activity of SR58611A indicating that 5HT transmission is strictly involved in its action.

Stressors affect the response of male and female rats to clomipramine in a model of behavioral despair (forced swim test).

Aim of the present study was to evaluate the effects of physical stressors (electric foot-shocks) on effect of the antidepressant drug, clomipramine and plasma corticosterone levels in male and female rats tested in a model of behavioral despair (forced swim test,). Male and female rats of the Wistar strain were injected with clomipramine (50 mg/kg, i.p.) or saline. A group of animals also received electric shocks of different intensity and duration of 24, 5 and 1 h before being subjected to forced swim test. At the end of behavioral procedures, vaginal smears were assessed in all female animals and data on immobility time were plotted according to the ovarian cycle phase. After decapitation, corticosterone plasma levels were measured by radioimmunoassay in both male and female rats. Application of mild shocks (5 ms, 0.1 mA) significantly reduced immobility time in forced swim test of untreated male rats and augmented clomipramine effect on this parameter. Moderate shocks of higher intensity or duration (5 ms, 1.0 mA) also resulted in decreased immobility time of untreated male rats, but in reduced effect of clomipramine treatment. Furthermore, application of severe shocks (10 ms, 1.0 mA) increased the immobility time in untreated animals and totally abolished clomipramine effect in forced swim test. Untreated non-shocked female rats in proestrous and estrous phases exhibited a longer immobility time as compared to diestrous animals. Immobility time appeared to be generally higher when mild, moderate or severe shocks were applied prior to behavioral testing in proestrous and estrous animals, while the behavioral response of diestrous and metestrous animals did not differ from that of controls. Clomipramine effect on immobility time was generally reduced by application of shocks of every strengths. Stress-induced plasma corticosterone levels surge correlated with intensity and duration of shocks in both male and female rats, but clomipramine treatment generally blunted the hormonal response. However, severe shocks were followed by a surge of plasma corticosterone levels in both male and female clomipramine-treated rats. These results demonstrate that duration and intensity of stressful stimuli may deeply affect the behavioral response of rats in forced swim test and influence clomipramine effect in this behavioral model depending on gender-based variables, probably of the hormonal type. Plasma corticosterone levels correlate with the behavioral response to clomipramine treatment suggesting that reactivity of hypothalamus-pituitary-adrenal axis to stress may be involved in the antidepressant effect of this drug.