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Query: UMLS:C0011570 (depression)
 172,036 document(s) hit in 31,850,051 MEDLINE articles (0.00 seconds)

This literature review covers the effects of the contraceptive injectable depot medroxyprogesterone acetate (DMPA) on depression and mood changes, on weight, on bone metabolism, and on lipid and carbohydrate metabolism. Limited data from various settings indicate no adverse effect of DMPA on depression although, in some studies, women have complained of mood changes. The only comparative longitudinal study of weight gain followed a young population of contraceptors using DMPA and oral contraceptives for a year and found no significant weight change in any of the treatment groups. Weight gain and appetite improvement have been observed in studies of the use of MPA as treatment for disease. Some studies show a decreased bond density in DMPA users but these changes and their possible reversibility require further research. DMPA has little or no effect on glucose tolerance but may result in an increase in insulin levels. Observed increases in low-density lipoprotein cholesterol and decreases in high-density lipoprotein cholesterol have not been followed to determine if they increase the longterm risk of cardiovascular disease. Women using DMPA should understand the health benefits of proper diet and exercise as well as the adverse effects of smoking because healthy behavior can minimize the occurrence or sequelae of the side effects of DMPA.
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PMID:Depot medroxyprogesterone acetate contraception. Metabolic parameters and mood changes. 872 2

The haemodynamic and gas exchange abnormalities occurring in neurogenic pulmonary oedema (NPO) were examined retrospectively in 20 patients admitted to the Intensive Therapy Unit (ITU) over a 45-month period (February 1992 to November 1995). In 12 patients, where vasoactive therapy with dobutamine was employed, its effect on haemodynamics was examined. Cardiac index (CI median 2.2 l min-1 m-2) and left ventricular stroke work index (LVSWI 20 g.m.m-2) were markedly depressed, while pulmonary artery wedge pressure (PAWP 17 mmHg), mean pulmonary artery pressure (MPAP 30.5 mmHg), systemic vascular resistance index (SVRI 2852 dyne.s.cm-5.m2) and pulmonary vascular resistance index (PVRI 393 dyne.s.cm-5.m2) were substantially elevated above normal values. Mean arterial pressure (MAP 82.5 mmHg) and heart rate (HR 102 bpm) were within normal limits. The poor oxygenation is indicated by a median PaO2/fiO2 ratio of 18.0 kPa. Patients treated with dobutamine showed significant increases in CI and LVSWI and significant falls in SVRI and PAWP at 2 and 6 h after institution of therapy, and there was a significant rise in PaO2/fiO2 ratio to 27.8 kPa at 6 h. NPO was generally associated with severe depression of myocardial function and elevation of pulmonary vascular pressures. This dysfunction was readily reversed by dobutamine.
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PMID:Haemodynamic changes in neurogenic pulmonary oedema: effect of dobutamine. 884 33

This study was performed to determine the cardiovascular responses to isoflurane in euthyroid and hypothyroid dogs. Four healthy mixed-breed dogs were studied prior to thyroidectomy (PRE), 6 months after thyroidectomy (HYP), and after 2 months of oral supplementation with 1-thyroxine (SUP). Heart rate (HR), cardiac output (Q), stroke volume (SV), systolic, diastolic, mean arterial blood pressure (SAP, DAP, MAP), and total peripheral resistance (TPR) were determined in awake dogs and in the same dogs when end-tidal isoflurane concentration were 1.28%, 1.92%, and 2.56%. Ventilation was controlled in anesthetized dogs and PACO2 maintained between 38 to 42 mm Hg. Isoflurane caused significant (P < .05) dose-dependent reduction in Q, SV, SAP, DAP, and MAP in the PRE, HYP, and SUP dogs. Cardiac output was lower in the HYP dogs than in the PRE or SUP dogs during awake measurement. TPR was increased in the awake HYP dogs compared with the PRE or SUP dogs. During anesthesia, HYP dogs tended to have lower Q, SV, SAP, and MAP PRE or SUP groups, but the only significant reduction was SAP during 1.5 MAC. The cardiovascular responses to isoflurane in hypothyroid dogs are similar to euthyroid animals with a dose-dependent depression in Q, SV, and arterial pressure.
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PMID:Cardiovascular effects of 1.0, 1.5, and 2.0 minimum alveolar concentrations of isoflurane in experimentally induced hypothyroidism in dogs. 892 95

Our study investigated the effects of moderate doses of fentanyl and sufentanil versus high-dose sufentanil on cerebral hemodynamics by using transcranial Doppler ultrasonography (TCD). Thirty American Society of Anesthesiologists (ASA) II and III patients scheduled for elective coronary artery bypass graft (CABG) were studied after Institutional Review Board (IRB) approval and informed consent. The evening before surgery, all patients received oral flurazepam (1 mg/kg), Atropine (0.4 mg/70 kg s.c.) and a combination of droperidol (70 micrograms/kg s.c.) plus fentanyl (1.5 micrograms/kg s.c.) were given as preanesthetic medication 1 h before induction of anesthesia. Anesthesia was induced with either 25 micrograms/kg fentanyl i.v. (group 1, n = 10), 3 micrograms/kg sufentanil i.v. (group 2, n = 10) or 6 micrograms/kg sufentanil i.v. (group 3, n = 10). All patients received 100 micrograms/kg pancuronium i.v. With the induction of respiratory depression, assisted ventilation was performed followed by controlled ventilation to maintain normoxia and normocapnia (FiO2, 1.0). Cerebral blood flow velocity (CBFV, cm/s) was measured continuously in the middle cerebral artery by using a bidirectional 2-MHz TCD system. Monitoring included heart rate (HR, beats/min), direct mean arterial blood pressure (MAP, mm Hg), and PaCO2. Physiologic variables including arterial blood gases were measured at baseline, 5 min, and 10 min after infusion of fentanyl or sufentanil. In all patients, HR, MAP, end-tidal carbon dioxide tension (PetCO2), and PaCO2 were constant over time and did not differ between groups. CBFV did not change with moderate doses of fentanyl (group 1) or sufentanil (group 2). In contrast, infusion of high-dose sufentanil (group 3) was associated with 27 to 30% decreases in CBFV (p < 0.05). Our results suggest that sufentanil decreases CBFV in a dose-related fashion with a threshold effect. Increases in CBFV and CBF seen in previous studies may be related to an increasing PaCO2 when maintenance of normocarbia is based on only real-time capnography with a constant PetCo2 rather than additional arterial blood gas monitoring.
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PMID:The effects of fentanyl and sufentanil on cerebral hemodynamics. 923 83

The product labeling for Depo-Provera cites depression as an infrequent side effect. Previous research on this topic has documented self-reported depression or mood changes in 1-5% of Depo-Provera users. These studies were limited, however, by a lack of measurement of baseline depression. In the present study, 495 new acceptors of Depo-Provera enrolled in a broader prospective cohort study conducted at three US hospitals (Texas, Pennsylvania, New York) were interviewed at enrollment and again after 12 months of use. Included in both the initial and follow-up questionnaires were six questions on depressive symptoms in the past month taken from the Mental Health Inventory. At 12 months, 172 women were still using Depo-Provera, 221 had discontinued the method, and 102 were lost to follow-up. Women who were still using Depo-Provera at 12 months had lower depressive symptom scores at baseline than women who discontinued use or were lost to follow-up. Between baseline and the 12-month follow-up, the mean depression score dropped from 7.4 to 6.7 among continuing users and remained steady at 8.0 among discontinuers. The mean depression score in the quintile of women with the highest depression scores at baseline also decreased after 12 months of use, from 15.4 to 9.5. These results suggest that Depo-Provera use is not likely to exacerbate symptoms in women with pre-existing depression.
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PMID:Depressive symptoms and Depo-Provera. 964 14

The temporolimbic structures of the brain that subserve emotional representation are highly epileptogenic and play an important role in the modulation of hormonal secretion and mediation of hormonal feedback. Estrogen is highly epileptogenic and exerts energizing and antidepressant effects. Excessive estrogen influence produces anxiety, agitation, irritability, and lability. It can promote the development of anxiety manifestations (e.g., panic, phobias, and obsessive-compulsive disorder). Progesterone and its metabolites inhibit kindling and seizure activity. They have potent anxiolytic effects, possibly by virtue of their GABAergic activity. Excessive progesterone influence produces sedation and depression. Testosterone has two major metabolites: estradiol, which can exacerbate seizures, and dihydrotestosterone, which blocks NMDA-type glutamate transmission and may be responsible for antiseizure effects. Testosterone has energizing effects and increases sexual desire in both men and women. In excess, however, it may promote aggressive, impulsive, and hypersexual behavior. Hormonal effects tend to be exaggerated or idiosyncratic in the setting of an abnormal or anomalous temporolimbic substrate, especially temporolimbic epilepsy. This may reflect altered neuronal responsivity to hormonal exposure perhaps by virtue of changes in the number of dendritic spines and receptors.
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PMID:Psychoneuroendocrine aspects of temporolimbic epilepsy. Part I. Brain, reproductive steroids, and emotions. 1010 Apr 30

Propofol may cause profound bradycardia and asystole, which are mediated indirectly via cardiac innervation but could involve direct effects on the sino-atrial (SA) node and the conducting system of the heart. To test the hypothesis that propofol may also activate Bezold-Jarisch reflexes to cause bradycardia, 5-hydroxytryptamine (5-HT), veratridine and propofol were injected into the left ventricle of the heart in both intact and vagotomized rabbits. 5-HT and veratridine produced an acute, rapid, dose-dependent decrease in mean heart rate (delta HR) and a decrease in mean arterial pressure (delta MAP) together with transient but severe depression and abolition of renal sympathetic nerve activity (RSNA). Bilateral vagotomy greatly attenuated these responses; for example, at the highest dose of 5-HT (8 micrograms kg-1), delta HR, delta MAP and duration of abolition of RSNA were reduced by 57% (P < 0.001), 53% (P < 0.05) and 79% (P < 0.05), respectively. In contrast, reductions in delta HR and delta MAP produced by propofol were statistically significant only at very high doses (8 mg kg-1). Propofol depressed but did not abolish RSNA, and bilateral vagotomy had no effect on any of these responses. These results indicate that the cause of acute bradycardia after administration of propofol does not involve the Bezold-Jarisch reflex.
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PMID:Propofol, bradycardia and the Bezold-Jarisch reflex in rabbits. 1043 26

Tetanic stimuli to layer I-II afferents in rat prefrontal cortex induced long-term depression (LTD) of layer I-II to layer V pyramidal neuron glutamatergic synapses when tetani were coupled to bath application of dopamine. This LTD was blocked by the following metabotropic glutamate receptor (mGluR) antagonists coapplied with dopamine: (S)-alpha-methyl-4-carboxyphenylglycine (MCPG; group I and II antagonist), (RS)-1-aminoindan-1,5-dicarboxylic acid (AIDA; group I antagonist), or (RS)-alpha-methylserine-O-phosphate monophenyl ester (MSOPPE; group II antagonist). This suggests that the dopamine-facilitated LTD requires synaptic activation of groups I and II mGluRs during tetanus. LTD could also be induced by coupling tetani to bath application of groups I and II mGluR agonist (1S, 3R)-1-aminocyclopentane-1,3-dicarboxylic acid (1S,3R-ACPD). In the next series of experiments, coapplication of dopamine and 1S,3R-ACPD, but not application of either drug alone, consistently induced LTD without tetani or even single test stimuli during drug application, suggesting that coactivation of dopamine receptors and the mGluRs is sufficient for LTD induction. Immunoblot analyses with anti-active mitogen-activated protein kinases (MAP-Ks) revealed that D1 receptors, D2 receptors, group I mGluRs, and group II mGluRs all contribute to MAP-K activation in prefrontal cortex, and that combined activation of dopamine receptors and mGluRs synergistically or additively activate MAP-Ks. Consistently, LTD by dopamine + 1S, 3R-ACPD coapplication, as well as the two other forms of LTD (LTD by dopamine + tetani and LTD by 1S,3R-ACPD + tetani), was blocked by bath application of MAP-K kinase inhibitor PD98059. LTD by dopamine + 1S,3R-ACPD coapplication was also blocked by postsynaptic injection of synthetic MAP-K substrate peptide. Our results suggest that dopamine receptors and groups I and II mGluRs cooperate to induce LTD through converging postsynaptic activation of MAP-Ks.
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PMID:Dopamine receptors and groups I and II mGluRs cooperate for long-term depression induction in rat prefrontal cortex through converging postsynaptic activation of MAP kinases. 1055 88

The effects of several doses of progesterone on FSH and LH concentrations were used to study the role of the gonadotropins on deviation in growth rates of the two largest follicles during the establishment of follicle dominance. Progesterone was given to pony mares at a daily dose rate of 0 mg (controls), 30 mg (low dose), 100 mg (intermediate dose), and 300 mg (high dose). All follicles > or = 6 mm were ablated at Day 10 (Day 0 = ovulation) to initiate a new follicular wave; prostaglandin F(2alpha) was given to induce luteolysis, and progesterone was given from Days 10 to 24. The low dose did not significantly alter any of the ovarian or gonadotropin end points. The high dose reduced (P < 0.05) the ablation-induced FSH concentrations on Day 11. Maximum diameter of the largest follicle (17.2 +/- 0.6 mm) and the second-largest follicle (15.5 +/- 0.9 mm) in the high-dose group was less (P < 0.04) than the diameter of the second-largest follicle in the controls (20.0 +/- 1.0 mm) at the beginning of deviation (Day 16.7 +/- 0.4). Thus, the growth of the two largest follicles was reduced by the high dose, presumably through depression of FSH, so that the follicles did not attain a diameter characteristic of deviation in the controls. The intermediate dose did not affect FSH concentrations. However, the LH concentrations increased in the control, low, and intermediate groups, but then decreased (P < 0.05) in the intermediate group to pretreatment levels. The LH decrease in the intermediate group occurred 2 days before deviation in the controls. The maximum diameter of the largest follicle was less (P < 0.0001) in the intermediate group (27.3 +/- 1.8 mm) than in the controls (38.9 +/- 1.5 mm), but the maximum diameter of the second-largest follicle was not different between the two groups (19.0 +/- 1.1 vs. 20.3 +/- 1.0 mm). Thus, the onset of deviation, as assessed by the second-largest follicle, was not delayed by the decrease in LH. Diameter of the largest follicle by Day 18 in the intermediate group (23.1 +/- 1.6 mm) was less (P < 0.05) than in the controls (28.0 +/- 1.0 mm). These results suggest that circulating LH was not involved in the initiation of dominance (inhibition of other follicles by the largest follicle) but was required for the continued growth of the largest follicle after or concurrently with its initial expression of dominance.
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PMID:Role of luteinizing hormone in follicle deviation based on manipulating progesterone concentrations in mares. 1056 94

Clinical and laboratory studies suggest that progesterone reduces epileptic seizure activity. The mechanisms underlying this effect are not known. The present study determined the effects of progesterone on extracellular evoked responses recorded in the CA1 field of hippocampal slices, as well as epileptiform responses recorded from tetanized slices. Slices were prepared from ovariectomized rats, with or without estrogen replacement. Hippocampal slices were superfused in vitro with one of the following treatments: progesterone with or without RU486 (a progesterone receptor antagonist); allopregnanolone (a progesterone metabolite that potentiates GABA action at GABA(A) receptors); RU5020 (a high-affinity progesterone receptor agonist); or cholesterol (control). In non-tetanized slices, a twofold increase in the excitatory postsynaptic field potential and population spike amplitude occurred during both cholesterol and progesterone superfusion. In contrast, under the same conditions, exposure to allopreganolone caused a 25% reduction in both field potential and population spike amplitude of evoked responses within 30min of treatment. In tetanized slices, progesterone and RU5020, but not allopregnanolone or cholesterol, caused significant reductions in the field potential and population spike amplitude of evoked responses. Progesterone and RU5020 also significantly reduced the duration of tetanic stimulus-induced afterdischarges and the frequency of spontaneous interictal discharges. The effects of allopregnanolone were restricted to a reduction in the primary afterdischarge duration. Estrogen replacement slightly attenuated progesterone's suppression of spontaneous discharges and depression of evoked responses. All responses to progesterone were blocked by prior or concurrent exposure to RU486. These data indicate that allopregnanolone suppresses evoked potentials in non-tetanized hippocampal slices, consistent with previous reports that this neurosteroid has marked anxiolytic and anticonvulsant effects. After tetanization, however, progesterone receptor-mediated responses become quantitatively more important as a mechanism for suppressing hippocampal electrical activity.
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PMID:Progestin receptors mediate progesterone suppression of epileptiform activity in tetanized hippocampal slices in vitro. 1111 38


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