Studies to date have only investigated primary polydipsia in hospitalized psychiatric patient populations, where rates range from 3% to 25%. The objective of the present study was to determine the occurrence of primary polydipsia in a psychiatric outpatient population, and to determine the perceptions of outpatients with self-induced water intoxication regarding reasons for drinking excess fluids, health risks, and insight into their behavior. All 115 psychiatric outpatients from a Community Outreach Program in Kingston, Ontario, were invited to participate in this study. Of these, 89 (77.4%) were enrolled. Data collection included chart reviews, structured interviews, weight measurements, and urine collection. The incidence of primary polydipsia was found to be 15.7%. One-half of the polydipsic people presenting with medical complications suggestive for water intoxication had cigarette smoking as a strong correlate. There were interesting answers to the self-induced water intoxication questionnaire. These showed a lack of knowledge related to the normal quantity of fluids necessary daily and about healthy behaviors. Excessive drinking occurs in psychiatric patient populations outside of institutional/hospital settings. Patients have limited awareness of the severity and possible complications from their problem. Given the prevalence of polydipsia, more effort should be put into identifying and treating this problem.

Effects of dopamine and bromocriptine on TRH- or dibutyryladenosine 3’,5’-cyclic monophosphate (dbcAMP)-induced prolactin release from primary cultured rat pituitary cells were studied using a perifusion system. TRH (100 nmol/l) stimulated prolactin release from basal concentrations of 33.8 ± 0.5 to 151.2 ± 28.0 ng/ml (net increase) or 447% increase. Dopamine inhibited the basal release of prolactin throughout the experiment, but TRH (100 nmol/l) was still able to stimulate prolactin release under the influence of dopamine. The increment in prolactin release was inversely proportional to the dopamine concentration. When TRH (100 nmol/l) was introduced during a perifusion period with bromocriptine 1 nmol/l, the prolactin concentration was increased to 110.9% of basal levels. The stimulatory effect of TRH under the influence of bromocriptine (1 nmol/l) was significantly lower than that without bromocriptine (control), although the higher concentrations of bromocriptine (10 and 100 nmol/l) did not further reduce the peak concentration of TRH-induced prolactin release. During a perifusion period with a low concentration of dopamine (1 nmol/l plus 0.1 mmol/l ascorbic acid), introduction of dbcAMP (3 mmol/l) stimulated prolactin release to 48% of basal concentration. A higher concentration of dopamine further reduced the stimulatory effect of prolactin release. Bromocriptine impeded the stimulatory effect of dbcAMP (3 mmol/l) on prolactin release in a similar manner as dopamine. Since a higher concentration of bromocriptine (10 and 100 nmol/ 1) did not further inhibit the TRH-induced prolactin release whereas a higher concentration of dopamine did, it is concluded that dopamine acts through additional mechanism(s) other than the D₂ receptor transduction system.

The authors believe that a relationship exists between schizoid personality disorder and violent acts. The following case study is presented to contemplate such a possible relationship. There is a paucity of research on this topic. The authors suggest that further research closely examine the relationship between violent behavior and those character traits associated with schizoid personality disorder. If such a relationship is found, these character traits could be integrated with other risk factors known to predict violence.

A large number of studies have been performed concerning dopamine's inhibitory effect on prolactin release, but many of these studies have examined the effect of dopamine dissolved in a solution containing ascorbic acid. Ascorbic acid, routinely used to protect dopamine from oxidation, alone does not stimulate or inhibit prolactin release, but it can potentiate the inhibitory effect of dopamine in a static monolayer culture system by approximately 100 times. We have closely examined the inhibitory effect of dopamine on prolactin release in the absence of ascorbic acid using a perifusion system. Male rat adenohypophyses were dispersed with trypsin and cultured in a Petri dish to form cell clusters. Inhibition of prolactin release by dopamine (1 mumol/L) in the absence of ascorbic acid was sustained for only 63 min during the 2-h perifusion period. Following a 2-h period of incubation of dopamine in the same experimental solution, the dopamine concentration was reduced from 1 to 0.18 mumol/L, yet this "2-h-old dopamine" was still effective in inhibiting prolactin release (approximately 30 min). This result suggests that the lactotrophs may be desensitized by chronic exposure to a high concentration of dopamine in the absence of ascorbic acid. In contrast, when a low concentration of dopamine (3 nmol/L) containing ascorbic acid (0.1 mmol/L) was perifused, inhibition of prolactin release was sustained for the entire 2-h perifusion period. Although there may be a large number of explanations for dopamine's transient inhibitory effect on prolactin release, the present results suggest that dopamine may require supplementary agent(s) to effectively inhibit prolactin release and thus function as the prolactin release inhibitory factor (PIF).(ABSTRACT TRUNCATED AT 250 WORDS)