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Biomedical subjects

C L DeVane

Publications and source records attributed to C L DeVane.

119 records · Page 7Linked to original sources
PubMedDate not supplied

Effect of bupropion on immunodensity of putative imidazoline receptors on platelets of depressed patients.

A substantial number of studies have demonstrated increased imidazoline receptors (I1 binding sites) on platelets of depressed patients and downregulation following antidepressant treatments. Herein, imidazoline receptor binding protein (IRBP) antiserum was used to quantify imidazoline receptors on platelets of depressed patients before and after treatment with the atypical aminoketone antidepressant, bupropion. Western blots revealed an increase in IRBP-immunodensity (p = 0.01, two-tailed) in a 33 kDa protein band in untreated depressed patients (n = 21) as compared with controls (n = 17). This band has been positively correlated with I1 binding sites on platelets. Following 6 weeks' treatment with bupropion, IRBP-immunodensity was downregulated in depressed patients (p = 0.03, paired t-test); predominantly in responders (p = 0.005). Patients non-responsive to bupropion (n = 5) were significantly different from responders (p = 0.05) by exhibiting no elevation in IRBP-immunodensity at pre-treatment and no downregulation of the 33 kDa band after treatment. IRBP-immunodensity was negatively correlated (r = -0.79, p = 0.01) with plasma concentrations of bupropion and its metabolites at week-4 of BUP treatment. Thus, a 33-kDa IRBP on platelet plasma membranes is elevated in depression and normalized in responders to bupropion.

Adolescent↗
PubMedDate not supplied

Distribution of phenobarbital and phenytoin in pregnant rats and their fetuses.

Studies were conducted to determine the extent of fetal exposure to phenobarbital (PB) and phenytoin (PHT) in pregnant rats. Two groups of rats determined to be in the third week of pregnancy received 30 mg/kg as a single intraperitoneal (i.p.) dose of either PB or PHT. At various times (from 15 min to 48 h for PB and from 20 min to 16 h for PHT), the rats were killed and whole blood, plasma, maternal brain, fetal brain and liver, whole fetuses, and placentas were rapidly collected. Concentrations of PB, PHT, and its major metabolite, p-hydroxyphenytoin (HPPH), were measured by high-performance liquid chromatography (HPLC). PB and PHT appeared rapidly in plasma and all tissues; the maximum HPPH concentrations appeared much later. The highest PB concentrations were detected in plasma, followed by placenta, whole fetus, maternal brain, fetal liver, and fetal brain. In contrast, PHT concentrations were higher in fetal brain and liver than in whole fetuses. HPPH concentrations were much lower than PHT and were not detected in maternal brain. These results show that PB and PHT readily distribute to the rat fetus, that drug distribution within the fetus is regional, and that changes in maternal plasma concentrations of these antiepileptic drugs (AEDs) are accompanied by parallel changes in fetal tissue.

Animals↗
PubMedDate not supplied

Pharmacokinetics of imipramine and its major metabolites in pregnant rats and their fetuses following a single dose.

The pharmacokinetic profiles of imipramine (IMI) and its major active metabolites were determined in pregnant rats following an acute 30 mg/kg ip IMI dose. At timed intervals from 10 min to 18 hr, groups of five animals were sacrificed and whole blood, plasma, maternal and fetal brain, fetal liver, placental tissue, and whole fetus were retained for measurements of drug concentrations. IMI, 2-hydroxyimipramine (2-OH-IMI), and desipramine (DMI) rapidly appeared in all tissues and showed complex disposition kinetics. The 2-hydroxydesipramine (2-OH-DMI) metabolite was detectable in occasional samples. The area under the drug concentration-time curve for both IMI and DMI was more than 7-fold greater in whole fetus than in maternal plasma. Drug concentrations were greater in fetal brain than in whole fetus. The DMI concentration exceeded that of IMI in all tissues and DMI persisted in tissues longer: mean residence time for DMI in whole fetus was 21.2 hr compared to 3.5 hr for IMI. The area under the curve of DMI in fetal brain was 5.35 times greater than that of IMI. These results demonstrate that IMI and two of its major metabolites freely distribute to the rat fetus, that drug distribution within the fetus is regional, and that the major drug to which the fetal brain is exposed following maternally administered IMI is DMI. Studies of the teratogenic effects of extensively biotransformed drugs like IMI should consider the effects of active metabolites.

Animals↗
PubMedDate not supplied

Drug interactions and antipsychotic therapy.

Various combinations of drugs may be used to treat psychotic disorders, but pharmacodynamic and pharmacokinetic interactions can result in adverse effects. In most cases, interactions are of clinical significance only when drug therapy is initiated or discontinued, or when major changes in dosage are made. A number of patient-related variables also affect the clinical significance of a drug-drug interaction. To help predict the occurrence of interactions, and therefore minimize or prevent them, the clinician should be familiar with each agent's pharmacokinetics, the enzymes involved in its metabolism, and the expected pharmacologic effects. With this knowledge, the clinician may consider decreasing the dosage of previous therapy or reducing the dosage of a coadministered drug to prevent or minimize the potential of an adverse interaction.

Antipsychotic Agents↗
PubMedDate not supplied

The place of selective serotonin reuptake inhibitors in the treatment of panic disorder.

Panic disorder is a frequently chronic condition with extensive patterns of psychiatric comorbidity. Optimum pharmacotherapy with traditional agents is limited by side effects, long-term tolerability, and other problems. Recent research findings support the characterization of panic disorder as an illness involving derangements of central serotonergic function. Selective serotonin reuptake inhibitors could become first-line treatment of the disorder, as they seem to have fewer side effects than tricyclic antidepressants and benzodiazepines.

Cognitive Behavioral Therapy↗