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Biomedical subjects

R F Anton

Publications and source records attributed to R F Anton.

At least 73 records · Page 4Linked to original sources
PubMed1991

Increased severity of alcohol withdrawal in in-patient alcoholics with a co-existing anxiety diagnosis.

The purpose of this study was to determine whether alcoholics with a co-existing anxiety disorder (dual-diagnosed group) experienced different withdrawal symptomatology from alcoholics without an anxiety disorder (alcohol-only group). Symptoms of alcohol withdrawal were measured on admission to an in-patient treatment program and throughout treatment (days 0, 2, 7, 14 and 21) using the revised Clinical Institute Withdrawal Assessment for Alcohol (CIWA-Ar) scale. The dual-diagnosed group exhibited more severe alcohol withdrawal, as indicated by higher total CIWA-Ar scores, at all time points than the alcohol-only group. The possibility that anxiety disorders and alcohol withdrawal share a common neurochemical basis and that the CIWA-Ar scale may be useful as a screening instrument for anxiety disorders in alcoholics is discussed.

Adult↗
PubMed1991

Effect of ibuprofen on alcohol-induced teratogenesis in mice.

The purpose of the present study was to examine the effect of the prostaglandin synthetase inhibitor ibuprofen (IBU) on the teratogenic actions of alcohol. On day 10 of pregnancy, C57BL/6J mice were injected subcutaneously with 25 mg/kg IBU or vehicle control. One hour later, the mice were intubated with 5.8 g/kg alcohol or an isocaloric control solution. A group injected subcutaneously with 150 mg/kg aspirin, followed by 5.8 g/kg alcohol 1 hr later, served as a positive control. The results showed that maternal alcohol treatment resulted in significantly decreased fetal weight and an increased number of fetuses with limb and kidney defects. Implantation sites and prenatal mortality were not affected. IBU did not have any effect on these dependent variables. IBU statistically antagonized the teratogenic effects of alcohol on fetal weight and dysmorphology. These effects, however, were not as marked as in the Aspirin-Alcohol positive control group. These results are discussed in the context of clarifying the role of prostaglandins in the etiology of alcohol-induced birth defects.

Abnormalities, Drug-Induced↗
PubMed1990

Thyrotropin and prolactin response to thyrotropin-releasing hormone in depressed and nondepressed alcoholic men.

Thyrotropin-releasing hormone (TRH) stimulation tests were performed on 81 alcoholic men after at least 3 weeks of abstinence. Subjects were given 500 micrograms of TRH intravenously, and thyroid-stimulating hormone (TSH) and prolactin (PRL) were measured at baseline, and then 15 and 30 min later. Comparisons were made among alcoholics with (n = 27) and without (n = 54) a lifetime history of depression as determined by the Diagnostic Interview Schedule. Nine nondepressed, nonalcoholic subjects served as controls. Alcoholics with or without a depression history did not differ from each other or from control in TSH or PRL response area under the curve. Blunted TSH responses were present in 10 (12%) of the alcoholics and none of the controls when blunting was defined as a delta max TSH less than 5 microU/ml. When blunting was defined as a delta max TSH less than 7 microU/ml, 18 (22%) of the alcoholics and 1 (1%) of the controls were blunted. Conversely, 2 (2.5%) of the alcoholics had a delta max TSH greater than 32 microU/ml. All subjects were clinically euthyroid. Contrary to expectation, depressed subjects were slightly less likely to show blunted responses than nondepressed subjects. No relationship was found between neuroendocrine measurements and several measurements of alcoholism or depression. Some alcoholic subjects show a blunted TSH response to TRH injection, which may be a function primarily of the alcoholism itself. The precise mechanism remains unknown.

Adult↗
PubMed1990

Ethanol increases PGE and thromboxane production in mouse pregnant uterine tissue.

The teratogenic effect of ethanol in the C57BL/6J mouse can be attenuated by pretreatment with aspirin (ASA). One prominent effect of ASA is to inhibit prostaglandin (PGE) and thromboxane (TXB2) production. We examined the effect of in vivo ethanol exposure on PGE and TXB2 production in a uterine-embryo tissue sample of C57BL/6J mice either before or after in vivo ASA pretreatment on day 10 of gestation. Ethanol increased both PGE and TXB2 production by approximately 20%. ASA caused a marked reduction of PGE and TXB2 in both control and ethanol groups by approximately 80-90%. The mouse strain, gestation time, and study parameters used in this study were the same as in the previously reported ASA attenuation of the teratogenic effect of ethanol. Therefore, the present data add additional support to the hypothesis that prostaglandin and/or thromboxane production may be involved in at least some aspects of fetal alcohol syndrome.

Analysis of Variance↗
PubMed1990

Valproate potentiates and picrotoxin antagonizes the anxiolytic action of ethanol in a nonshock conflict task.

The purpose of this study was to examine the effects of the indirect GABA agonist valproate and the indirect GABA antagonist picrotoxin on the anxiolytic (anti-conflict) activity of ethanol in a behavioral conflict task that does not employ electroshock. This task (negative contrast) quantifies how animals respond to an abrupt, unexpected reduction in reward. Treatment with valproate alone did not elevated depressed behavior engendered by abrupt reduction in reward. However, when administered together with a sub-effective dose of ethanol (0.5 g/kg), valproate (50-200 mg/kg) dose-dependently potentiated the anxiolytic action of ethanol. Picrotoxin (2 mg/kg) antagonized the anxiolytic effects of a larger dose of ethanol (1.0 g/kg) given alone, as well as the ability of valproate to enhance the anxiolytic effects of smaller dose of ethanol (0.5 g/kg). As such, these data support a role for GABA in mediating the anxiolytic activity of ethanol.

Animals↗
PubMed1990

Perspectives on the pathophysiology of fetal alcohol syndrome.

Fetal alcohol syndrome (FAS) is a major known cause of fetal malformations and mental retardation. Prevention/intervention of FAS can only be achieved with identification of the mechanisms by which alcohol induces birth defects. The purpose of this paper is to discuss the data on possible mechanisms of FAS, and to give a number of suggestions for future research areas.

Acetaldehyde↗
PubMed1990

Amoxapine versus amitriptyline combined with perphenazine in the treatment of psychotic depression.

In a double-blind study lasting for 4 weeks, the authors compared the effectiveness of amoxapine, an antidepressant with potential antipsychotic properties, with a combination of amitriptyline plus perphenazine in the treatment of 38 patients who had the diagnosis of major depression with psychotic features (psychotic or delusional depression). Patients in each group showed similar improvement in depression and psychosis. There was a tendency for the patients treated with amitriptyline plus perphenazine to have higher global response rates. However, the patients given amoxapine had significantly fewer extrapyramidal side effects.

Adult↗
PubMed1989

The thyroid axis and desipramine treatment in depression.

Although there has been much recent investigation of the role of thyroid function in affective illness, few studies have addressed the effects of the tricyclic antidepressants on the pituitary-thyroid axis. In the present study, thyroid functions (TFTs) and thyrotropin-releasing hormone (TRH) stimulation of thyroid-stimulating hormone (TSH) were measured before and after treatment with desipramine (DMI) in 13 men with a diagnosis of major depressive disorder. All subjects had normal TFTs and baseline TSH measured in a drug-free state at the initiation of the study. Both mean free thyroxine index and baseline TSH decreased after DMI treatment. The amount of decrease in baseline TSH correlated with increase in delta TSH. Four subjects had blunted delta TSH (delta TSH less than or equal to 5 microIU/ml); three of these subjects "normalized" with treatment (delta TSH less than or equal to 5 microIU/ml; greater than or equal to 20 microIU/ml). Two subjects had a high delta TSH, and both "normalized" during treatment. The decrease in both free T4 index and TSH suggests a down-regulation of the thyroid axis at the hypothalamic level. "Normalization" of subtle dysregulation of the thyroid axis is suggested as a mechanism of antidepressant therapy in the treatment of some depressions.

Adult↗
PubMed1989

CSF prostaglandin-E in agoraphobia with panic attacks.

Prostaglandins are thought to act as neuromodulators of both central catecholamine and endocrine systems. Abnormalities of these systems have been described in affective disorders, in general, and in agoraphobia with panic attacks, in particular. This study measured basal prostaglandin-E (PGE) cerebrospinal fluid (CSF) levels in 20 patients with agoraphobia with panic attacks and 10 nonpsychiatric controls. In a subgroup of patients and controls, CSF levels of adrenocorticotrophic hormone (ACTH) and corticotropin-releasing factor (CRF) were also measured. There was no significant difference in CSF PGE levels between patients and controls. However, patients with higher depression scores had lower CSF PGE levels. CSF PGE levels tended to correlate with CSF ACTH, but not CSF CRF in the patient group, in general, and in the female patients, in particular. These findings do not support an abnormality in basal CNS PGE production in agoraphobia with panic attacks, but suggest further study of the PGE modulatory effect on the hypothalamic-pituitary-adrenal axis in this disorder.

Adrenocorticotropic Hormone↗
PubMed1989

The benzodiazepine receptor inverse agonist RO15-4513 exacerbates, but does not precipitate, ethanol withdrawal in mice.

RO15-4513, an imidazobenzodiazepine that has been reported to antagonize several behavioral and biochemical actions of ethanol, was given to C3H mice at various times during withdrawal from chronic (72 hours) continuous exposure to ethanol vapor. When administered immediately following chronic ethanol exposure, RO15-4513 (6 or 12 mg/kg) did not influence the withdrawal response. However, when given at subsequent times (3, 5, and 8 hours postethanol withdrawal), RO15-4513 significantly increased the severity of the withdrawal response in ethanol-exposed mice. Moreover, this exacerbation was completely reversed by pretreatment with the benzodiazepine receptor antagonist RO15-1788. Thus, these data indicate that the benzodiazepine inverse agonist, RO15-4513, is capable of exacerbating, but not precipitating, ethanol withdrawal.

Acoustic Stimulation↗
PubMed1988

Alcohol detoxification and withdrawal seizures: clinical support for a kindling hypothesis.

There has been speculation that a kindling model may have applicability to alcohol withdrawal syndromes and seizures, suggesting that repeated alcohol withdrawals may lead to increased severity of subsequent withdrawals. We evaluated historical and clinical variables of a group of male alcoholics with (n = 25) and without (n = 25) alcohol withdrawal seizures. We found that the number of detoxifications appeared to be an important variable in the predisposition to withdrawal seizures. The withdrawal seizure group had 12 of 25 (48%) patients with 5 or more previous detoxifications, compared to only 3 of 25 (12%) of the control group. A relationship between alcohol use history and withdrawal seizures was not supported by the data. These findings support the concept that previous alcohol withdrawals may "kindle" more serious subsequent withdrawal symptomatology, ultimately culminating in withdrawal seizures.

Adult↗
PubMed1988

PGE measurement in mouse embryos and uterine/embryo tissue.

Embryonic tissue of rodents and other species has been reported to produce prostaglandins (PG) of the E series during gestation. We attempted to establish the presence of PGE in C57BL/6J mouse embryos and peri-embryonic tissue as an initial step in examining the role of maternal ethanol treatment on PG production. Gestation day 10 embryos were found not to produce or degrade PGE. However, a tissue complex which included embryonic tissue, peri-embryonic membranes, placenta and uterus was capable of producing PGE from both endogenous and exogenous arachidonic acid. Furthermore, in vivo and in vitro aspirin was able to suppress PGE production from this tissue. It is concluded that gestation day 10 C57BL/6J mouse embryonic tissue, unlike that of rat, is not capable of measurable PGE production. However, uterine and peri-embryonic tissues, needed to support pregnancy, are capable of significant PGE production.

Analysis of Variance↗
PubMed1988

Role of alcohol-induced hypothermia in mediating the teratogenic effects of alcohol in C57BL/6J mice.

The purpose of this study was to determine the role of alcohol-induced maternal hypothermia in the teratogenic actions of alcohol. C57BL/6J mice were administered an acute dose of alcohol (5.8 g/kg orally) or isocaloric sucrose on day 10 of gestation. One half of each group was placed for 6 hr in an incubator set at 32 degrees C and the other half was housed in the incubator at room temperature (22 degrees C). As expected, acute prenatal alcohol exposure at this time of gestation was associated with decreased birth weight and an increase in limb and kidney malformations. The significant alcohol x environmental temperature interaction on these dependent variables indicated that the teratogenic insult was not attenuated, but was in fact even greater for the 32 degrees C/alcohol group. An absence of a main effect of environmental temperature indicated that the 32 degrees C environment, per se, was not teratogenic. Thus, maternal hypothermia is probably not an etiological factor in animal models of fetal alcohol syndrome. Moreover, antagonism of alcohol-induced maternal hypothermia exacerbates the teratogenic actions of alcohol observed at room temperature.

Abnormalities, Drug-Induced↗
PubMed1987

Effect of indomethacin on alcohol-induced morphological anomalies in mice.

The purpose of the present study was 1) to examine the effect of indomethacin (INDO), a prostaglandin synthesis inhibitor, on alcohol-induced growth and morphological impairment in C57BL/6J mice (Study 1) and 2) to determine if INDO crosses the placenta (Study 2). On day 10 of gestation, mice were injected (s.c.) acutely with either 0, 5, 10, or 20 mg/kg INDO, followed one hour later by alcohol (5.8 g/kg orally) or isocaloric sucrose. Fetuses were removed on day 19 of pregnancy, weighed, and examined for anomalous development. As expected, Study 1 demonstrated that maternal alcohol treatment decreased fetal weight and increased the number of fetuses with birth defects. INDO alone decreased fetal weight but did not affect morphologic development. More importantly, INDo antagonized alcohol-induced birth defects, but only at the highest dose. The results of Study 2 suggest that the relative ineffectiveness of INDO may be related to its inability to readily cross the placenta. Since high doses of INDO also caused maternal toxicity, the usefulness of this compound in future studies of this type was questioned.

Abnormalities, Drug-Induced↗
PubMed1987

Urinary free cortisol in psychotic depression.

Major depression with psychotic features may be associated with higher cortisol secretion and a greater probability of dexamethasone nonsuppression of serum cortisol than is found in major depression without psychotic features. In this study, urinary free cortisol (UFC), a sensitive parameter of 24-hr cortisol production, was examined both before and after dexamethasone administration in 32 patients with major depression, 18 with psychotic features (MDPF), and 14 without psychotic features (MDD). A significantly larger number of MDPF patients had UFC excretion greater than 90 micrograms/24 hr before dexamethasone administration and greater than 20 micrograms/24 hr after dexamethasone administration. Although some clinical variables other than psychotic features differed between the two groups, these could not account for the UFC differences. However, the older patients (greater than 55 years) in the MDPF group accounted for the high UFC excretion, suggesting an interaction between age and diagnosis.

Adult↗
PubMed1987

Central nervous system prostaglandins and ethanol.

There is growing interest in the effect of ethanol on cellular membranes, generally, and neuronal membrane systems, in particular. Perturbations of membranes have led to numerous enzymatically mediated processes, one of which is prostaglandin production. This paper reviews the nature and role of prostaglandins in the central nervous system, and what is known about the effect of ethanol on prostaglandin production in brain. Areas of central nervous system physiological function in which prostaglandins may mediate the actions of ethanol are discussed. Methodological considerations and future directions for research in the area of ethanol and prostaglandins are highlighted.

Animals↗
PubMed1987

Alcohol, pregnancy, and prostaglandins.

Basic scientists and clinicians alike are in agreement that children of alcoholic mothers are at risk for a variety of birth defects. These defects have been labeled fetal alcohol syndrome or, in a milder form, fetal alcohol effects. Prevention or therapeutic intervention of this disorder requires an understanding of the mechanism of action of alcohol on the developing fetus. This paper addresses the possible role of prostaglandins as biochemical mediators of the teratogenic actions of alcohol.

Abnormalities, Drug-Induced↗