Effect of Bupropion ( Wellbutrin SR ) SR on the Quality of Life of Elderly Depressed Patients With Comorbid Medical Disorders.

BACKGROUND: There is a need for additional studies of the quality of life (QOL) of elderly depressed subjects with medical comorbidity. METHOD: We conducted an 8-week, open trial of Bupropion ( Wellbutrin SR ) sustained release (SR) in 18 elderly (60-81 years) subjects with DSM-IV major depressive disorder and one or more serious medical illnesses (e.g., congestive heart failure, type 1 diabetes mellitus, irritable bowel syndrome) with a week-12 follow-up interview. The intent-to-treat method with the last observation carried forward was used to analyze depression and QOL measures. Dosing was initiated at 100 mg once daily and increased at weekly intervals to a maximum of 150 mg twice daily as clinically indicated. RESULTS: Bupropion ( Wellbutrin SR ) SR treatment was associated with reductions in Clinical Global Impressions-Severity of Illness scale (p <.0001) score and in the 17-item Hamilton Rating Scale for Depression (HAM-D) total score (p <.0001). QOL as measured by the Medical Outcomes Study Short Form-36 (SF-36) also tended to improve with treatment. The SF-36 "mental health" (p <.01) and "social functioning" (p <.0006) domains improved significantly by week 4. "Vitality" (p <.03) improved significantly by week 12. On the HAM-D, statistically significant improvement was noted on "depressed mood" (p <.0001), "feelings of guilt" (p <.01), "work and activities" (p <.001), "hypochondriasis" (p <.02), and "insomnia" (p <.01) at week 8. The mean dose of Bupropion ( Wellbutrin SR ) SR at endpoint was


The thermogenic and hypophagic effects of sibutramine's metabolite (metabolite 2), a 5-hydroxytryptamine (5-HT) and noradrenaline reuptake inhibitor, were investigated in rats and compared with duloxetine and Bupropion ( Wellbutrin SR ). Metabolite 2 increased colonic temperature for 2.5-4.5 h. Duloxetine was also thermogenic but was less effective than metabolite 2. Bupropion ( Wellbutrin SR ) similarly increased colonic temperature and was as efficacious, but less potent, than metabolite 2. At -8 degrees C, metabolite 2, duloxetine and Bupropion ( Wellbutrin SR ) all decreased response to heat reinforcement and reduced colonic temperature. Metabolite 2 produced a sustained increase in oxygen consumption (VO(2)) at 29 degrees C from 90 to 240 min, whereas duloxetine was far less effective. Bupropion ( Wellbutrin SR ) rapidly enhanced VO(2), but its effect was less prolonged than that of metabolite 2. Metabolite 2 markedly reduced 24-h food intake. Duloxetine decreased feeding although its effect was shorter-lived, but Bupropion ( Wellbutrin SR ) was without effect. Thus, sibutramine's antiobesity action is probably attributable to effects on energy intake and expenditure. Duloxetine shares these properties, but is generally less efficacious. Any potential weight-reducing effect of Bupropion ( Wellbutrin SR ) is probably due to thermogenesis.

Bupropion ( Wellbutrin SR ) inhibits nicotine-evoked [(3)H]overflow from rat striatal slices preloaded with [(3)H]dopamine and from rat hippocampal slices preloaded with [(3)H]norepinephrine.

Bupropion ( Wellbutrin SR ), an efficacious antidepressant and smoking cessation agent, inhibits dopamine and norepinephrine transporters (DAT and NET, respectively). Recently, Bupropion ( Wellbutrin SR ) has been reported to noncompetitively inhibit alpha3beta2, alpha3beta4, and alpha4beta2 nicotinic acetylcholine receptors (nAChRs) expressed in Xenopus oocytes or established cell lines. The present study evaluated Bupropion ( Wellbutrin SR )-induced inhibition of native alpha3beta2* and alpha3beta4* nAChRs using functional neurotransmitter release assays, nicotine-evoked [(3)H]overflow from superfused rat striatal slices preloaded with [(3)H]dopamine ([(3)H]DA), and nicotine-evoked [(3)H]overflow from hippocampal slices preloaded with [(3)H]norepinephrine ([(3)H]NE). The mechanism of inhibition was evaluated using Schild analysis. To eliminate the interaction of Bupropion ( Wellbutrin SR ) with DAT or NET, nomifensine or desipramine, respectively, was included in the superfusion buffer. A high Bupropion ( Wellbutrin SR ) concentration (100 microM) elicited intrinsic activity in the [(3)H]DA release assay. However, none of the concentrations (1 nM-100 microM) examined evoked [(3)H]NE overflow and, thus, were without intrinsic activity in this assay. Moreover, Bupropion ( Wellbutrin SR ) inhibited both nicotine-evoked [(3)H]DA overflow (IC(50) = 1.27 microM) and nicotine-evoked [(3)H]NE overflow (IC(50) = 323 nM) at Bupropion ( Wellbutrin SR ) concentrations well below those eliciting intrinsic activity. Results from Schild analyses suggest that Bupropion ( Wellbutrin SR ) competitively inhibits nicotine-evoked [(3)H]DA overflow, whereas evidence for receptor reserve was obtained upon assessment of Bupropion ( Wellbutrin SR ) inhibition of nicotine-evoked [(3)H]NE overflow. Thus, Bupropion ( Wellbutrin SR ) acts as an antagonist at alpha3beta2* a


Bupropion ( Wellbutrin SR ) and Paroxetine ( Paxil ) differentially influence cardiovascular and neuroendocrine responses to stress in depressed patients.

BACKGROUND: There exists a need to identify safe and effective treatments for depression in patients with coronary heart disease (CHD). METHODS: Using a cross-sectional design, 17 depressed patients being treated with Bupropion ( Wellbutrin SR ) (200-450 mg/day) were compared with 17 depressed patients being treated with Paroxetine ( Paxil ) (10-50 mg/day) and with a group of 15 unmedicated, non-depressed controls for cardiovascular, neuroendocrine and heart rate variability (HRV) measures at rest and in response to mental and physical stressors. RESULTS: Regardless of treatment, both treated groups exhibited blunted plasma cortisol, plasma epinephrine, systolic blood pressure, cardiac output, and pre-ejection period responses to mental stressors relative to controls. Bupropion ( Wellbutrin SR ) treated individuals exhibited greater total peripheral resistance (TPR) increases than either the Paroxetine ( Paxil ) or control groups, and greater plasma norepinephrine (NE) increases to mental stressors than the Paroxetine ( Paxil ) group. The Bupropion ( Wellbutrin SR ) group also displayed reduced HRV at rest relative to the controls and during orthostatic challenge relative to both the control and Paroxetine ( Paxil ) groups. LIMITATIONS: Despite the fact that the treated groups were well matched for depression and other psychiatric histories, lack of randomization into treatment arms may be associated with a selection bias in the two treated groups. CONCLUSIONS: Although both pharmacological treatments were associated with a blunting of some cardiovascular and neuroendocrine responses to stress relative to controls, which may be reflective of their therapeutic mechanisms of action, the results of our study also suggest that Bupropion ( Wellbutrin SR ) is associa