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)

Eighty-six depressed inpatients were divided into four groups: patients in each of three groups were treated, respectively, with identical capsules of verapamil, amitriptyline, or placebo, whereas the fourth group was treated eclectically by the ward physician with so-called state-adjusted treatment (SAT). Each treatment period lasted 5 weeks. Psychopathology was assessed with the Hamilton Rating Scale for Depression, by the Zung self-rating scale, by the 100-mm analog scale, and by general clinical impression. Results indicated that amitriptyline and SAT were superior to verapamil or placebo. There was no significant difference between verapamil and placebo or between SAT and amitriptyline. This finding was more definitive in the homogeneous subgroup of 55 women with DSM-III diagnosis of Major depression. In addition, 12 manic inpatients (DSM-III) were treated orally with verapamil, 24 with neuroleptics, and 11 with both neuroleptics and lithium carbonate. The decline of their psychopathology, assessed by the Brief Psychiatric Rating Scale (BPRS) and general impression, was fully comparable. Using Analysis of Variance (ANOVA), the statistical difference among courses of psychopathology expressed as total BPRS scores reaches borderline significance in favor of verapamil. In contrast to neuroleptics, verapamil did not induce any sedative, hypnotic, or cataleptic effects, and was well tolerated.
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PMID:Verapamil in affective disorders: a controlled, double-blind study. 264 56

A female patient born in 1941, who suffers from affective psychosis and Addison's disease, first received lithium carbonate in 1983 during a severe, therapy-resistent depression. With lithium treatment she showed a considerable improvement. In the following months, with a daily dosage of 24.4 mmol, the blood lithium levels were between 0.8 and 0.9 mmol/l. One year later she suffered a severe lithium intoxication after a virus infection. Shortly afterwards, she had a manic and then a depressive phase. She was now put on a regimen of with 12.2 mmol lithium carbonate per day, which produced blood levels between 0.3 and 0.4 mmol/l. In the following years, values of about 0.9 mmol/l were observed several times, therapy and clinical condition remaining unchanged. These spontaneous fluctuations of the blood lithium level, a hitherto unreported phenomenon are discussed as a possible cause of the lithium intoxication. The consequences for clinical practice are outlined.
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PMID:Lithium treatment of a patient with Addison's disease and affective psychosis. 271 62

Somatostatin is a hypothalamic tetradecapeptide with many central nervous system actions. We investigated a potential role for altered somatostatin activity in affective disorder by measuring somatostatin in the cerebrospinal fluid (CSF) of 47 patients with affective disorder and of 39 normal volunteers. Medication-free depressed patients showed significantly lower levels of CSF somatostatin than normal volunteers (p less than .001) or patients during the improved state (p less than .01). Somatostatin levels were significantly and inversely correlated with duration of sleep on the night of the lumbar puncture (p less than .05). Treatment with carbamazepine reduced CSF somatostatin (p less than .01) in contrast to the absence of effect of imipramine, desmethylimipramine, and lithium carbonate and the significant increase in CSF somatostatin seen in a small group of patients treated with zimelidine. The implications of these findings with respect to attempts to explore the neurobiology of depression are discussed.
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PMID:CSF somatostatin in affective illness and normal volunteers. 286 61

An analysis of the phenomenology and treatment course of 52 subjects with delusional depression suggests that there may be various subtypes: bipolar, early-onset unipolar and possibly a late-onset unipolar. The bipolar subgroup tended to relapse in different but always psychotic directions, and was resistant to lithium carbonate treatment alone. Treatment refractoriness, delusional depressive recurrences, and a dementia-like presentation were associated with a small late-onset subgroup. A high rate of delusionally depressive relapses also characterized the early-onset unipolar group, however, patients with single episodes were found only in this subgroup.
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PMID:Proposed delusional depression subtypes: preliminary evidence from a retrospective study of phenomenology and treatment course. 289 70

Thirty-four hospitalized manic patients were randomized to treatment with either lithium carbonate or an average series of nine bilateral electroconvulsive treatments (ECTs), followed by maintenance with lithium carbonate. Weekly ratings of manic, depressive, and psychotic symptoms were obtained for eight weeks, and patients were followed up monthly for up to two years. Ratings by nonblind and blind observers indicated that the patients who underwent ECT improved more during the first eight weeks than did patients who were treated with lithium carbonate. This was especially true of patients with mixed symptoms of mania and depression and/or extreme manic behavior. Clinical ratings after eight weeks showed no significant differences between the lithium carbonate- and ECT-treated patients. Likewise, the two groups had comparable rates of relapse, recurrence, and rehospitalization during the follow-up period.
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PMID:Electroconvulsive treatment compared with lithium in the management of manic states. 289 25

Patients studied at peak severity of a manic episode showed substantial degrees of depression (dysphoria) and anxiety. Compared with nondysphoric manics (n = 26), the dysphoric manics (n = 22) had a significantly greater number of previous hospitalizations, and they displayed less rapid cycling both in the year before and during the index hospitalization admission. The severity of manic dysphoria tended to correlate with the number of previous hospitalizations, a finding that was highly significant in women (n = 27). Medication-free manic patients (n = 22) had significant elevations in cerebrospinal fluid norepinephrine concentrations compared with depressed and euthymic patients and normal volunteers, and the degree of elevation correlated significantly with the degree of manic dysphoria, anger, and anxiety rated at the time of the lumbar puncture. Patients with dysphoric mania, recognized by Kraepelin to have poor prognoses, have been reported to respond poorly to lithium carbonate but may be among those who respond to carbamazepine. Clinical, biologic, and pharmacologic response characteristics of manic subgroups, particularly those with extreme dysphoric components to their illness, appear to be clinically meaningful and deserving of further investigation.
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PMID:Dysphoric mania. Clinical and biological correlates. 293 Mar 31

Nephrotoxicity is a serious side effect that limits the use of cyclosporine (CyA) as an immunosuppressive agent. The purpose of this study was to develop a model of CyA nephrotoxicity in the isolated perfused rat kidney and to evaluate the effects of adenosine triphosphate (ATP)-MgCl2 and verapamil treatment on this model. Kidneys were perfused for 90 minutes in a 7.5% albumin-Krebs-HCO3 solution containing 3H-inulin (glomerular marker) and 5.0 micrograms/ml 14C-cytochrome C (cyt) (marker of tubular protein absorption). After 10-minute equilibration, perfusate and urine samples were collected with 10-minute clearance periods. After two control clearance periods, 500 ng/ml CyA was added to the perfusate. In some experiments, 1 micrograms/ml of verapamil was added 10 minutes before CyA and in others 2 mmol/l ATP-MgCl2 was added with CyA. Cyt and inulin radioactivity, [Na+] and [K+], were measured in perfusate and urine. Tissue ATP levels were also determined. The results demonstrate that CyA treatment leads to a marked depression of glomerular filtration rate (GFR), tubular absorption of protein, urine output, and renal flow. ATP-MgCl2 cotreatment improved GFR, tubular absorption, and renal perfusate flow but the increase in urine output was not dramatic. Verapamil pretreatment markedly improved GFR and urine and renal perfusate flow but not tubular function. The combination of verapamil and ATP-MgCl2 treatment with CyA returned GFR to control values, significantly improved tubular absorption, urine and renal perfusate flow, and enhanced renal tissue ATP of isolated kidneys to levels seen in vivo. These data lead us to conclude that ATP-MgCl2 cotreatment with CyA after verapamil pretreatment greatly reduces the nephrotoxic potential of this immunosuppressive agent.
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PMID:Treatment with verapamil and adenosine triphosphate-MgCl2 reduces cyclosporine nephrotoxicity. 295 Jun 8

The acute effects of lead in the rat CNS in vitro were studied on synaptic transmission in the isolated hemisected spinal cord from newborn rats and on the transport of exogenous GABA, acetylcholine and cis-3-aminocyclohexane carboxylic acid (ACHC) from slices of cerebral cortex from adult rats. Lead had quite variable effects on monosynaptic reflexes and synaptic potentials. When it occurred, the depression of synaptic transmission by lead (typically at 18.5 mumol/liters of added lead acetate) was reversible provided exposure times were less than 15 min; furthermore, depression could be antagonised by increasing the external calcium concentration. Lead had no effect on the postsynaptic responses of motoneurons to the putative transmitters L-glutamate, GABA and glycine or to eledoisin-related peptide. The effects of lead on uptake and release of exogenous GABA and ACHC were dependent on the perfusion buffer employed: minimal effects were seen in solutions buffered with either phosphate or carbonate. When Tris HCl was used as buffer, lead inhibited the uptake of GABA and potentiated the spontaneous release of GABA with an EC50 = 50 mumol/liters as added lead acetate. In Tris HCl buffer, lead acetate (100 mumol/liters) produced a two-fold enhancement in the spontaneous release of acetylcholine under conditions where choline and acetylcholine re-uptake was blocked by hemicholinium. The availability of free lead cations in solution is highly dependent on the concentrations of other ions (particularly phosphates) and the pH. Under the appropriate conditions, lead can inhibit CNS synaptic function acutely in a manner consistent with lead competing with calcium ions in transmitter release processes as has been established for acetylcholine release at peripheral synapses.
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PMID:Acute effects of lead at central synapses in vitro. 298 66

Thirty-six dehydrated diarrheic neonatal calves were used to study the effects of various alkalinizing compounds on acid-base status, the changes in central venous pressure (CVP) in response to rapid IV infusion of large volumes of fluid, and the correlation of acid-base (base deficit) status, using a depression scoring system with physical determinants related to cardiovascular and neurologic function. Calves were allotted randomly to 4 groups (9 calves/group). Over a 4-hour period, each calf was given two 3.6-L volumes (the first 3.6 L given in the first hour) of a polyionic fluid alone (control group) or were given the polyionic fluid with sodium bicarbonate, sodium L-lactate, or sodium acetate added (50 mmol/L). Acid-base status, hematologic examination, and biochemical evaluations were made immediately before infusion of each fluid (at entry) and after 3.6, 4.8, and 7.2 L of fluid had been given. Compared with control values, bicarbonate, lactate, and acetate had significantly greater alkalinizing effects on pH (P less than 0.01) and base deficit (P less than 0.01) after 3.6, 4.8, and 7.2 L of fluid were given. Bicarbonate had the most rapid alkalinizing effect and induced greater changes in base deficit (P less than 0.01) than did acetate or lactate at each of the 3 administered fluid volumes evaluated. Acetate and lactate had similar alkalinizing effects on blood. Rehydration alone did not improve acid-base status. The CVP was elevated in 10 (28%) of the 36 calves after 1 hour of fluid (3.6 L) administration, but significant differences in body weight, PCV, and clinical condition or depression score at entry were not found between calves with elevated CVP and those with normal CVP.(ABSTRACT TRUNCATED AT 250 WORDS)
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PMID:Clinical evaluation of sodium bicarbonate, sodium L-lactate, and sodium acetate for the treatment of acidosis in diarrheic calves. 299 12

To examine the cellular mechanism of urinary acidification in detail, micropuncture studies were performed on the in situ bullfrog proximal tubule with nigericin-based pH microelectrodes. Pencil-type double-barreled antimony microelectrodes were also used for monitoring pHs of the tubular fluids. Luminal perfusion of 10(-3) M cyanide caused a biphasic change in cell pH (pHi): i.e., early acidification by 0.04 pH unit in 2 min and later alkalinization by 0.04. A profound depolarization of 30-35 mV was observed in the peritubular membrane potential (EM Peri), although the tubular fluid pH (pHTF) was elevated by 0.11 unit. Luminal substitution of 100 mM Na+ by Li+ acidified the cell by 0.06 pH unit with a depolarization of EM Peri by 8 mV and an alkalinization of pHTF by 0.10 unit. It is a fact that cellular acidification and luminal alkalinization are in good agreement with the depression of luminal H+ secretory mechanism. Perfusion of 10(-4) M SITS from the peritubular side caused a rise in pHi by 0.04 without appreciable changes in EM Peri in the short period application. Peritubular perfusion of 10(-4) M ouabain lowered the pHi by 0.07 with a resulting depolarization of EM Peri by 15.4 mV, meanwhile, the pHTF, while initially lowered by 0.07 unit, was elevated 4 min later by 0.12. Inhibitions of the peritubular ion transport mechanism caused some pH changes in the same direction, both in the cell interior and the tubular fluid. Further, from the ouabain experiment, it is inferred that some linkages, mediated by Na+ and H+(or HCO3-), would exist between the peritubular and luminal membranes.
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PMID:Regulatory mechanism of cell pH in the renal proximal tubule of bullfrog nephron. 300 93


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