Cancer patients need not only advanced therapeutic method but also spiritual counseling. Therefore clinical nurses need to analyze the negative psychological status and discuss the effect of psychological support and intervention on the improvement of patients' psychological burden, thus to establish effective intervention plans for patients. A total of 30 patients with cancer were selected for study. They were divided into blank group, intervention group and control group. Patients in three groups were orally administrated amitriptyline if necessary. Patients in blank group directlyfilled in the form of self-perceived burden and self-made questionnaire of general material of patients. Different groups were interfered with psychological support in different patterns for 3 months. The differences of SPB experience, MCMQ and QLQ-CCC in two groups werecompared respectively. It was found that SPBscore of cancer patients in blank group was in moderate level of burden, while SPB score in intervention group and control group were relatively lower, and score of MCMQ and QLO-CCC in intervention group were higher than that in control group. It was concluded that the experience of self-perceived burden existed in most cancer chemotherapy patients. Psychological support and intervention can obviously reduce the SPB experience of cancer patients and improve patients' living quality.
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Several factors correlate with the risk of suicide in people taking antidepressants. After controlling for these factors, the risk of suicide was similar among the 10 study antidepressants. Overdose with antidepressants accounted for only 14% of the suicides.
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We planned this study in order to investigate the effects of theophylline on cardiovascular parameters in an anaesthetized rat model of amitriptyline toxicity. In the preliminary study, we tested theophylline as 1 mg/kg of bolus, followed by a 0.5-mg/kg infusion. Toxicity was induced by the infusion of 0.94 mg/kg/min of amitriptyline up to the point of a 40-45% inhibition of mean arterial pressure (MAP). The rats were randomized to two groups: a group of 5% dextrose bolus followed by 5% dextrose infusion, and another group with theophylline bolus followed by infusion. Amitriptyline caused a significant decrease in MAP and prolongation in QRS; however, it did not alter heart rate (HR). When compared to the dextrose group, theophylline administration increased MAP, shortened prolonged QRS duration, and increased HR (P < 0.05, respectively). There was no statistically significant difference in the results of arterial blood-gas analyses among the groups (P > 0.05). Bolus doses followed by a continuous infusion of theophylline were found to be effective in reversing the hypotension and QRS prolongation seen in amitriptyline toxicity. One of the possible explanations of this beneficial effect is nonselective adenosine antagonism of theophylline. Further studies are needed to reveal the exact mechanism of the observed effect.
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This pilot study raises doubts regarding the feasibility of a randomized trial, presumably due to both clinician and patient bias toward LC and the lack of "gold-standard" nonoperative treatments. However, these prospective data indicate that, with careful patient selection (standardized symptom criteria/imaging methodology), LC results in pain relief and significant improvement in QOL in BD patients. Further prospective study of these findings is warranted.
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Amitriptyline may be more effective than propranololforprophylaxis of CVS. However, a randomized controlled trial is required to confirm this result. Children with CVS have a relatively favorable long-term outcome, particularly those who initially responded well to the prophylactic medications.
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The effects of antidepressant drugs in rats responding under a differential-reinforcement-of-low-rate 72-sec schedule were assessed. Seven clinically used tricyclic antidepressant drugs (imipramine, desipramine, chlorimipramine, protriptyline, nortriptyline, amitriptyline and doxepin), two atypical antidepressants (iprindole and mianserin) and a monoamine oxidase inhibitor (tranylcypromine) dose-dependently reduced response rate and increased reinforcement rate. Nomifensine, an atypical antidepressant which has been reported to have psychomotor stimulant properties and abuse potential, increased response rate and decreased reinforcement rate. Chlorpromazine, an antipsychotic agent, and diphenhydramine, an antihistamine, have been reported to produce effects similar to antidepressants in several behavioral tests, but neither of these drugs mimicked the actions of antidepressants on responding under a differential-reinforcement-of-low-rate 72-sec schedule. Chlorpromazine decreased response rate but did not increase reinforcement rate. Diphenhydramine did not have consistent effects but tended to decrease reinforcement rate. These findings suggest that behavior maintained by the differential-reinforcement-of-low-rate schedule may be selectively affected by antidepressants that have no psychomotor stimulant properties.
We investigated how the L-type calcium channel blockade (CCB) with nifedipine affects the cyclic AMP responses to noradrenaline or isoproterenol in cerebral cortical slices from rats receiving antidepressant treatments that induce (electroconvulsive shock, imipramine) or do not induce (amitriptyline) beta-downregulation. To assess the role of protein kinase C (PKC) in receptor crosstalk under CCB conditions, the cyclic AMP responses were tested also in the presence of a PKC activator, TPA. CCB alone induced no changes, but modulated the action of those antidepressants that down regulate the beta-adrenergic system. Chronic ECS and imipramine treatments were differently affected. ECS, under conditions of CCB, down regulated the response to isoproterenol in the presence of TPA, while imipramine ceased to block the TPA-potentiation of cyclic AMP responses. Thus, CCB affects the processes related to the antidepressant-induced changes on the crosstalk between alpha1- and beta-adrenergic receptors, depending on the specific properties of the antidepressant.
A double blind controlled trial involving 37 inpatients whose depression was judged clinically to require antidepressant medication revealed that amoxapine and amitriptyline was approximately equal in efficacy. In average daily doses of 139.7 mg and 123 mg respectively, there seemed little difference in speed of action, or in the frequency of side effects, though amoxapine had less central nervous system stimulating consequences (tremors and restlessness) than did amitriptyline.
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We describe a case of a 2-year-old boy who ingested 35 mg.kg(-1) of amitriptyline. He developed central nervous system toxicity, as demonstrated by coma and seizures and cardiac toxicity (cardiac arrest) within 1 h of ingestion. The cardiac toxicity was refractory to standard therapy. His cardiac rhythm alternated between ventricular tachycardia and pulseless ventricular tachycardia/ventricular fibrillation for a period of 17 h. Following prolonged cardiopulmonary resuscitation and aggressive supportive management, the patient recovered both cardiovascularly and neurologically. An echocardiogram and MRI brain were subsequently performed and were normal. The patient was discharged 2 weeks later with normal cognitive, behavioral and motor function. We discuss the benefit of prolonged and effective cardiopulmonary resuscitation in the management of this potentially fatal poisoning.
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The antinociceptive efficacy of systemic- (IV), spinal- (IT), and global supraspinal (ICV)-administered amitriptyline (AMIT) was compared in three different tests for nociception: the hot-plate test, the tail-flick test, and the withdrawal reflex test. Systemic AMIT inhibited the responses in each of the three tests, with distinct dose-effect relationships. Spinal AMIT reduced in a dose-dependent fashion the force of withdrawal to noxious electrical stimulation but was ineffective in the hot-plate test and facilitated the responses in the tail-flick test. Supraspinal AMIT inhibited in dose-dependent fashion the response to the stimulus of the hot plate, reduced the force of withdrawal after a dose that was effective by the IV route, and again facilitated the responses in the tail-flick test. The results suggest that spinal sites mediate the inhibition of the withdrawal reflex and the supraspinal site the inhibition of the hot-plate test. Two conclusion are drawn: First, AMIT's site of action varies among the pain modalities; and, second, augmentation of the reactions can occur. The complex interaction accords with the clinical experience that the benefits of AMIT in pain treatment are hard to predict.
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Many adverse drug reactions are caused by the cytochrome P450 (CYP) dependent activation of drugs into reactive metabolites. In order to reduce attrition due to metabolism-mediated toxicity and to improve safety of drug candidates, we developed two in vitro cell-based assays by combining an activating system (human CYP3A4) with target cells (HepG2 cells): in the first method we incubated microsomes containing cDNA-expressed CYP3A4 together with HepG2 cells; in the second approach HepG2 cells were transiently transfected with CYP3A4. In both assay systems, CYP3A4 catalyzed metabolism was found to be comparable to the high levels reported in hepatocytes. Both assay systems were used to study ten CYP3A4 substrates known for their potential to form metabolites that exhibit higher toxicity than the parent compounds. Several endpoints of toxicity were evaluated, and the measurement of MTT reduction and intracellular ATP levels were selected to assess cell viability. Results demonstrated that both assay systems are capable to metabolize the test compounds leading to increased toxicity, compared to their respective control systems. The co-incubation with the CYP3A4 inhibitor ketoconazole confirmed that the formation of reactive metabolites was CYP3A4 dependent. To further validate the functionality of the two assay systems, they were also used as a "detoxification system" using selected compounds that can be metabolized by CYP3A4 to metabolites less toxic than their parent compounds. These results show that both assay systems can be used to screen for metabolic activation, or de-activation, which may be useful as a rapid and relatively inexpensive in vitro assay for the prediction of CYP3A4 metabolism-mediated toxicity.
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Four different in vitro cytotoxicity tests were compared: the MTT assay, the NR assay, the uridine incorporation assay and the measurement of total cellular protein. The comparison was done using the BHK-21 cell line and nine selected test chemicals (colchicine, amitriptyline, cycloheximide, 2,5-hexandione, mercury chloride, cadmium chloride, copper chloride, 2,4-dinitrophenol and chloroquine diphosphate). The concentration that induced 50% inhibition relative to the controls (IC(50)) was calculated for each test and chemical. The results from the cytotoxicity tests were generally in good agreement. However, for some chemicals the IC(50) values varied significantly between two assays. The largest variation was found for chloroquine diphosphate, where the IC(50) value for the NR assay was approximately eight times lower than the IC(50) value for the protein measurement.
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We searched the Cochrane Neuromuscular Disease Group Register, MEDLINE, EMBASE, and LILACS (all to August 2005) and the Chinese Biomedical Retrieval System, the database of the Chinese Cochrane Center (The Cochrane Library, Issue 1 2005), conference paper databases and checked bibliographies. We handsearched ten Chinese journals.
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1 Mianserin is a tetracyclic piperazino-azepine compound synthesized in 1966 for its peripheral anti 5-hydroxytryptamine properties. Animal screening showed that mianserin was centrally active, but the profile did not indicate possible antidepressant activity. Following clinical observations of sedative and possible mood-lifting effects, a quantitative electroencephalogram (EEG) study showed that the EEG effects of mianserin are similar to those of amitriptyline. 2 Subsequent clinical and pharmacological studies have indicated that mianserin is an effective antidepressant which differs from the tricyclic antidepressants not only chemically but also in its pharmacological and clinical profile. Mianserin seems to lack anticholinergic and cardiotoxic properties, and has unusual effects on monoamine metabolism. 3 On the basis of the initial profile a series of clinical and pharmacological studies has been carried out, and the results of many of these studies are presented in these Proceedings.
Clinically important improvement was observed in both primary and secondary outcomes in all three study groups over time. The reduction in headache index scores during treatment compared with baseline was 49% for amitriptyline, 40% for spinal manipulation and 41% for the combined group; p = .66. During the posttreatment follow-up period the reduction from baseline was 24% for amitriptyline, 42% for spinal manipulation and 25% for the combined group; p = .05.
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An integrated workflow using LC-MS/MS was developed to comprehensively profile the metabolites of amitriptyline in human urine, in which five N-acetyl-l-cysteine conjugates were characterized as tentative biomarkers for idiosyncratic toxicity.
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Chronic migraine (CM) was first defined in the second edition of the International Headache Society (IHS) classification in 2004. The definition currently used (IHS 2006) requires the patient to have headache on more than 15 days/month for longer than 3 months and a migraine headache on at least 8 of these monthly headache days and that there is no medication overuse. In daily practice the majority of the patients with CM also report medication overuse but it is difficult to determine whether the use is the cause or the consequence of CM. Most the patients also have other comorbidities, such as depression, anxiety and chronic pain at other locations. Therapy has to take this complexity into consideration and is generally multimodal with behavioral therapy, aerobic training and pharmacotherapy. The use of analgesics should be limited to fewer than 15 days per month and use of triptans to fewer than 10 days per month. Drug treatment should be started with topiramate, the drug with the best scientific evidence. If there is no benefit, onabotulinum toxin A (155-195 Units) should be used. There is also some limited evidence that valproic acid and amitriptyline might be beneficial. Neuromodulation by stimulation of the greater occipital nerve or vagal nerve is being tested in studies and is so far an experimental procedure only.
Cells, constantly cultured or frozen, were assayed on the PatchXpress 7000A using tool compounds.
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Amitriptyline can cause tachycardia and arrhythmia associated with an excessive release of cardiac catecholamines. We have investigated its effects on norepinephrine release from adrenergic nerves by using the dog saphenous vein as a model of the sympathetic neuroeffector junction. Isolated strips of vein were mounted for isometric tension recording or incubated with [3H]norepinephrine and mounted for superfusion, tension recording and the superfusate. Amitriptyline (10(-6); 5 x 10(-6) M) increased the overflow of [3H]norepinephrine but decreased that of [3,4-3H]dihydroxyphenylglycol from electrically stimulated strips. The selective decreased in the overflow of this metabolite indicates that amitriptyline inhibits neuronal uptake. However, the increased overflow of [3H]norepinephrine caused by amitriptyline also occurred when neuronal uptake was blocked by cocaine (3 x 10(-5) M) but was abolished when prejunctional alpha receptors were blockade by phentolamine (10(-5) M). Amitriptyline attenuated the prejunctional inhibitory action of exogenous norepinephrine, this indicates that the drug interacts with prejunctional alpha receptors. Amitriptyline also antagonized the prejunctional inhibitory action of acetylcholine, both in the absence and presence of cocaine and phentolamine. These effects were not due to a nonspecific action of the drug as it did not reduce the prejunctional inhibitory effect of histamine. Thus, amitriptyline can increase the concentration of norepinephrine at the neuroeffector junction by blockade of neuronal uptake and by interacting with prejunctional alpha and muscarinic receptors. Since the cardiac adrenergic nerves also possess these receptors, the results could help to explain the cardiotoxic effects of the drug.
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Role of the level of alertness. Based upon 25 new cases. The author, after referring to the leg muscle bed syndrome associated with exercise, reports the frequency of painful spasticity of the calves, occurring initially at rest and in particular at night in the form of a restless legs syndrome, then secondarily during the day with varying degrees of persistence at rest and during exercise. This problem frequently has a lateral dominance and appears to be induced by self-maintained functional muscular spasticity of the gastrocnemii and soleus, explained by a study. It is frequently attributed to a venous etiology. This study based upon 25 cases enabled definition of the diagnosis and showed the probable links between EMG hyperactivity and a high level of alertness indicative of a predisposing situation.
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Out of 14 patients with severe, refractory, psychotic depression-7 patients were treated by UECT and the rest with amitriptyline or mianserin. Remission and improvement were recorded in 6 patients after a course of UECT but in none treated with antidepressants.
The effect of intravenous amitriptyline (0.5-2 mg/kg) on heart rate, blood pressure, ECG, and electrolytes in plasma and heart muscle was studied in rats. In addition, the effect on monophasic action potentials was studied in rats with open chest. Amitriptyline caused a significant decrease in blood pressure and heart rate and a significant prolongation of QRS and PQ duration. At the time of maximal QRS prolongation (mean +94%) the duration of monophasic action potentials was virtually unchanged. Beta-adrenergic blockade by means of pretreatment with 0.1 mg propranolol did not influence the amitriptyline-induced prolongation of QRS duration. Amitriptyline administration causing obvious QRS prolongation induced no detectable changes in plasma and heart muscle electrolytes. The results contradict adrenergic dominance or marked imbalance between intra- and extra-cellular electrolytes as a cause of the ECG changes. The present data indicate that the amitriptyline effect is compatible with a direct quinidine-like action on the heart, resulting mainly in a slowing of impulse propagation in the intracardiac conduction system.
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The influence of amitriptyline, fluoxetine and tianeptine upon transcallosal responses has been studied in male albino rats. It is established that amitriptyline does not influence, fluoxetine reduces, and tianeptine increases the amplitude of evoked potentials. These data show evidence that tianeptine facilitates, fluoxetine impairs, and amitriptyline does not affect the interhemispheric transmission.