Gene/Protein Disease Symptom Drug Enzyme Compound
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Query: UMLS:C0011570 (depression)
 172,036 document(s) hit in 31,850,051 MEDLINE articles (0.00 seconds)

In 20 infarct patients, whose age varies from 43 to 78 years (m 59.6), continuous hemodynamic measurements were made to determine the cardiovascular effects of propranolol without and during a simultaneous infusion treatment with nitroglycerin. In cases of compensated ventricular function and pulmonary wedged pressures of 15 mm Hg or less (N = 10), a mean intravenous propranolol dose of 6.1 +/- 1.3 mg led to a significant reduction of the LVSWI and a simultaneous increase of the PCP by 31% of the control value (P less than or equal to 0.005). A simultaneously performed infusion treatment with nitroglycerin at a mean dose of 3.0 +/- 1.6 mg/h resulted in totally cutting off the propranolol-induced PCP increase, whereas a decrease of the heart rate and the LVSWI due to a beta-receptor-blockade remained completely unchanged. In the case of pre-existing congestion insufficiency of the left ventricle (N = 10) and of a pulmonary wedged pressure of above 15 mm Hg, the administration of a mean dose of propranolol of 5.8 +/- 1.1 mg for protection of the myocardium resulted in a partly disquieting decrease of the volume of cardiac output (P less than or equal to 0.005) which was 28% of the control value for the CI an 12% for the SVI. Correspondingly the left ventricular stroke work decreased to 18%. Nitroglycerin has a reducing influence on these changes, but not down to the initial level. In cases of sufficient ventricular function, propranolol has a favorable influence on the myocardial O2-metabolism via its depressor effect on heart rate and contractility. By means of nitroglycerin, an increase of the pulmonary wedged pressure occurring under this condition can be inhibited. However, in the case of a pre-existing congestion insufficiency, propranolol can lead to a partly disquieting depression of the circulation, which, apart from the hemodynamic risks, makes a rather unfavorable influence on the myocardial O2-metabolism seem likely.
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PMID:[The treatment of acute myocardial infarctions with beta-receptor-blockers. II. Hemodynamic effects of propranolol with and without combination therapy with nitroglycerin (author's transl)]. 679 41

Routine blood samples of 145 consecutive patients seen in the Los Angeles County Psychiatric Hospital Emergency Room during a 48-hour weekday period in June 1979 were examined for phencyclidine (PCP) using a sensitive and specific gas capillary gas chromatographic nitrogen detector (GC2-N) method. Of these 145 samples 63 (43.4%) were positive and PCP levels ranged 0.34 to 142.9 nanograms/ml (mean 14.6 ng/ml +/- 3.4 S.E.M.). An analysis of the records of these 63 patients revealed a wide variety of psychotic clinical pictures resembling mania, depression or schizophrenia with relatively few of the supposedly characteristic manifestations of PCP intoxication. Each of the 63 patients had at least one manifestation of toxic psychosis and/or acute delirium, in addition to the florid symptoms characteristic of functional states. PCP measurement, pharmacokinetics and the possible relationships of this intoxication to the psychiatric manifestations are discussed.
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PMID:The urban epidemic of phencyclidine (PCP) use: clinical and laboratory evidence from a public psychiatric hospital emergency service. 721 23

In 155 polydrug abusers, drug use patterns that were associated with serious suicidal behavior included preference for depressant drugs, history of withdrawal from barbiturates, and lower frequency of PCP use. Diagnostic factors associated with increased suicidal behavior included a history of depression in the subject's mother and a diagnosis of antisocial personality in the subjects themselves. These findings are discussed in relation to Winokur's concept of broad spectrum depressive disease.
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PMID:Factors associated with suicidal behavior in polydrug abusers. 744 May 11

1. The effects of the glycine/NMDA receptor partial agonists, D-cycloserine and (+)-HA-966 and the full agonist, D-serine, on focal seizure threshold and behaviour have been determined in amygdala-kindled rats, i.e. a model of focal (partial) epilepsy. The uncompetitive NMDA receptor antagonist, MK-801, was used for comparison. 2. The high efficacy glycine partial agonist, D-cycloserine, did not alter the threshold for induction of amygdaloid afterdischarges (ADT) at doses of 20-80 mg kg-1 i.p., but significant ADT increases were determined after application of higher doses (160 and 320 mg kg-1). The ADT increases after these high doses were long-lasting; significant elevations were still observed 2 days after drug injection. Determination of D-cycloserine in plasma and brain tissue showed that it was rapidly eliminated from plasma. Compared to peak levels in plasma, only relatively low concentrations of D-cycloserine were measured in brain tissue. 3. The low efficacy glycine partial agonist, (+)-HA-966, 10-40 mg kg-1 i.p., did not alter the ADT or seizure recordings (seizure severity, seizure duration, afterdischarge duration) at ADT currents. However, the drug dose-dependently increased the duration of postictal behavioural and electroencephalographic depression in kindled rats. At the higher dose tested, postictal immobilization was dramatically increased from 3 min to about 120 min. This might indicate that glutamatergic activity is decreased postictally, which is potentiated or prolonged by (+)-HA-966. 4. Like D-cycloserine, the glycine receptor full agonist, D-serine, injected bilaterally into the lateral ventricles at a dose of 5 mumol, significantly increased the ADT, while no effect was seen at a lower dose (2.5 mumol). 5. The anticonvulsant effects observed with D-cycloserine were completely antagonized by combined treatment with (+)-HA-966, indicating that the effects of D-cycloserine were mediated by the glycine/NMDA receptor complex. 6. MK-801, 0.1 mg kg-1, did not alter the focal seizure threshold or seizure recordings at ADT current, but induced marked phencyclidine(PCP)-like behavioural alterations, such as hyperlocomotion, stereotypies and motor impairment. No PCP-like behaviours were observed after D-cycloserine, D-serine or (+)-HA-966. High doses of (+)-HA-966 induced moderate motor impairment in kindled rats. 7. The long lasting increases in seizure threshold observed after the high efficacy glycine partial agonist,D-cycloserine but not the low efficacy partial agonist, (+)-HA-966, may suggest that the effects of D-cycloserine are mediated by adaptive changes in the NMDA receptor complex in response to glycine receptor stimulation.8. Pharmacological intervention at the strychnine-insensitive glycine receptor by high-efficacy partial agonists with systemic bioavailability may be an effective means of increasing seizure-threshold without concomitantly inducing PCP-like adverse effects.
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PMID:Anticonvulsant effects of the glycine/NMDA receptor ligands D-cycloserine and D-serine but not R-(+)-HA-966 in amygdala-kindled rats. 803 69

d-Amphetamine (DEX) and phencyclidine (PCP) increased motor activity in rats as measured in automated activity cages. Analysis of the stimulation indicated that both drugs increased horizontal activity (total activity), locomotion, and peripheral activity. However, DEX increased while PCP decreased the incidence of rearing. The ability of different drugs to antagonise DEX- and PCP-induced increases in total activity (called stimulation) was measured. Dopamine (DA) D1 receptor antagonists (SCH23390, NNC-01-0112) were 7-8 times more potent in blocking DEX than PCP. DA D2 receptor antagonists (raclopride, remoxipride, haloperidol) were only 1-2 times more potent against DEX-induced stimulation. Nonselective DA receptor antagonists were also tested. Chlorpromazine was more potent against DEX than against PCP. Buspirone and sertindole were slightly more potent in blocking PCP than DEX. Ritanserin (5-HT2 receptor antagonist) was inactive against both stimulants. 8-OH-DPAT (5-HT1A receptor agonist) potentiated the stimulant effects of DEX and PCP. Prazosin (alpha 1-adrenergic receptor antagonist) partially blocked both DEX and PCP. Most drugs tested depressed spontaneous motor activity. Remoxipride and sertindole, however, caused very little depression even at doses several times higher than those needed to block DEX or PCP. The data show clear pharmacological differences between DEX- and PCP-induced stimulation.
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PMID:Dopamine receptor antagonists block amphetamine and phencyclidine-induced motor stimulation in rats. 809 Aug 16

1. Immobility induced by forced swimming is well known as an animal model of depression. To develop an animal model for the negative symptoms of schizophrenia, in particular the depressive symptoms, the effect of phencyclidine (PCP) on immobility in the forced swimming test was investigated in mice, since PCP produces such negative symptoms in humans. 2. Repeated treatment with PCP (10 mg kg-1 day-1, s.c., once a day for 14 days) prolonged the immobility time in the forced swimming test 24 h after the final injection compared with saline treatment; the effect was not obtained by single or 5 treatments with PCP (10 mg kg-1, s.c.), or by repeated treatment with methamphetamine (0.5 and 1 mg kg-1 day-1, s.c., once a day for 14 days). 3. The enhancing effect of PCP (10 mg kg-1 day-1, s.c.) on the immobility persisted for at least 21 days after the withdrawal of the drug. 4. Haloperidol (0.3 and 1 mg kg-1, p.o.), ritanserin (3 and 10 mg kg-1, p.o.), risperidone (0.1-1 mg kg-1, p.o.), and clozapine (3 and 10 mg kg-1, p.o.) failed to attenuate the immobility induced by the forced swimming in mice repeatedly treated with saline when the drugs were administered 1 h before the forced swimming test. However, ritanserin (30 mg kg-1) and clozapine (30 mg kg-1) did attenuate this immobility. 5. The enhancing effect of PCP on the immobility was attenuated by ritanserin (3 and 10 mg kg-1, p.o.), risperidone (0.3 mg kg-1, p.o.), and clozapine (3 and 10 mg kg-1, p.o.), whereas haloperidol (0.3 and 1 mg kg-1, p.o.) had no effect. 6. These results suggest that the enhancement of immobility in the forced swimming test brought about by repeated PCP treatment could be used as a model of the negative symptoms, particularly the depression, of schizophrenia. This effect of PCP appeared to be mediated, at least in part, via 5-HT2A receptors.
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PMID:Enhancement of immobility in a forced swimming test by subacute or repeated treatment with phencyclidine: a new model of schizophrenia. 858 Dec 95

Frontal-subcortical circuits provide a comprehensive framework for understanding the anatomy, biochemistry, and pharmacology of behavior. The three principal behaviorally relevant circuits originate in the dorsolateral prefrontal cortex, orbitofrontal cortex, and anterior cingulate cortex, respectively. Circuit-specific marker behaviors associated with each circuit are executive dysfunction (dorsolateral prefrontal-subcortical circuit), disinhibition and OCD (orbitofrontal-subcortical circuit), and apathy (medial frontal-subcortical circuit). Environmental dependency is common to all prefrontal-subcortical syndromes and may reflect disruption of working memory. Depression, mania, and psychosis are mediated by structures involved in prefrontal-subcortical circuits and are circuit-related but not circuit-specific behaviors. The actions of PCP, LSD, serotonergic antidepressants, anxiolytics, sedative-hypnotics, antipsychotic agents, and ethanol may all be partially or primarily mediated through transmitter systems and receptor effects expressed through frontal-subcortical circuits.
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PMID:Anatomic and behavioral aspects of frontal-subcortical circuits. 859 19

Immobility induced by forced swimming is well known as an animal model of depression. To develop an animal model for the negative symptoms of schizophrenia, in particular, the depressive symptoms, the effect of phencyclidine (PCP) on immobility in the forced swimming test was investigated in mice, since PCP produces negative symptoms-like behavioral changes in humans. Repeated treatment with PCP (10 mg/kg/day, sc, once a day for 14 days) prolonged the immobility time in the forced swimming test 24 hr after the final injection compared with saline treatment; the effect was not obtained by single treatment with PCP (10 mg/kg), or by repeated treatment with methamphetamine (0.3 and 1 mg/kg/day, sc, once a day for 14 days). The enhancing effect of PCP on the immobility persisted for at least 21 days after the withdrawal of the drug. Desipramine (10 mg/kg, po) attenuated the immobility induced by the forced swimming in mice repeatedly treated with saline. The enhancing effect of PCP on the immobility was attenuated by risperidone (0.3 mg/kg), clozapine (3 and 10 mg/kg), and desipramine (20 and 50 mg/kg), whereas haloperidol (0.3 and 1 mg/kg) had no effect. These results suggest that the enhancement of immobility in the forced swimming test brought about by repeated PCP treatment could be used as a model of the negative symptoms, particularly the depression, of schizophrenia.
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PMID:[Behavioral assessment of neuroleptics (3)--Schizophrenia negative symptoms-like model induced by PCP]. 890 1

We have previously found that repeated phencyclidine (PCP) treatment enhances the immobility induced by forced swimming and suggested that this behavioral change could be used as a model of the negative symptoms, particularly depression, of schizophrenia. The present study attempted to examine the effects of antidepressants on the depressive states (immobility) induced by forced swimming in mice repeatedly treated with PCP, compared with those in mice repeatedly treated with saline. In mice repeatedly treated with saline, desipramine (5 and 10 mg/kg) and imipramine (5 and 10 mg/kg) significantly attenuated immobility, whereas mianserin (5-20 mg/kg) and clomipramine (10 and 50 mg/kg) had no affect. In mice repeatedly treated with PCP, the enhancing effect of PCP on immobility was attenuated by mianserin (5-20 mg/kg) at doses which did not have any effect in saline-treated mice, and by desipramine at higher doses (20 and 50 mg/kg). However, imipramine (5-20 mg/kg) and clomipramine (10-50 mg/kg) did not affect PCP-induced enhancement of immobility. In the biochemical study, the content of 5-hydroxyindoleacetic acid (5-HIAA) and the 5-HIAA/5-hydroxytryptamine (5-HT) ratio in the prefrontal cortex in mice repeatedly treated with PCP, but not with saline, following the forced swimming test were significantly increased, compared with those in the corresponding control mice (which did not perform the test). The present findings suggest that the depressive states induced by the forced swimming in mice repeatedly treated with PCP are less sensitive to acute treatment with tricyclic antidepressants, and this may be due to increase in 5-HT turnover. Antidepressants such as mianserin, which have the 5-HT2 receptor antagonist properties, may be useful for the treatment of negative symptoms of schizophrenia.
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PMID:Effects of antidepressants on phencyclidine-induced enhancement of immobility in a forced swimming test in mice. 914 63

The aims of the present study were to evaluate the extent to which primary care physicians' (PCPs) identification of psychiatric distress is related to a number of nonpsychopathological factors, such as patient sociodemographic and health-related characteristics, and to assess the impact of depression on PCP identification of psychiatric distress, controlling for patient sociodemographic and health-related characteristics. Two patient samples were chosen to explore these issues: 1) patients not fulfilling any ICD-10-defined or subthreshold psychiatric diagnosis and, 2) patients with an ICD-10 diagnosis of current depression. Patients attending 46 primary care clinics during an index period were screened by the General Health Questionnaire (GHQ)-12 and selected for a second stage interview according to GHQ score. Among the 559 interviewed patients, 123 had no mental disorder and 66 had an ICD-10 current depressive disorder. Identification of psychiatric distress by the PCP was associated with retirement among subjects without mental disorders but not among depressed patients. Patient's negative overall health self-perception and severity of physical illness were significantly related to identification of psychiatric distress in the two groups, whereas neither disability nor reason for medical consultation had a significant effect. Patients with current depression, compared with those without, were 4.3 times more likely to be identified by PCPs as having psychiatric distress when adjusting for all the above nonpsychopathological variables. Patients with depression and comorbid anxiety disorders were more likely to be recognized by the PCP as compared with those with pure depression. Finally, among depressive symptoms, diurnal variation and symptoms related to suicidal tendencies were predictive of identification of psychiatric distress, whereas increase of appetite was negatively associated with PCP recognition.
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PMID:Identification of psychiatric distress by primary care physicians. 943 85


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