Gene/Protein Disease Symptom Drug Enzyme Compound
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Query: UMLS:C0040822 (tremor)
 18,428 document(s) hit in 31,850,051 MEDLINE articles (0.00 seconds)

Pigs in which venous catheters were positioned for long-term use were injected i.v. with high doses of nicotine in physiol. saline. The LD50 was 2.656 mg/kg body weight. Clinical symptoms were mainly: forced respiration, muscular tremor to tetanoid spasms, cyanosis of the skin, salivation and sometimes vomiting. The degree and duration of symptoms were dose-dependent. Ecg changes in anaesthesized pigs following intravenous nicotine injections of 0.126 mg/kg and 0.378 mg/kg at 15 minutes' interval were immediately commencing disturbances of the heart rate in form of bradycardia and asystolia. After 5 sec we observed extrasystoles, tachycardia, sino-auricular block and AV-block of first and second degree as well as a number of T- and P-changes. Changes of the ecg were observed generally for 10 to 15 min, however, the T-wave remained sometimes negative or biphasic-preterminal negative for some hours.
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PMID:Effect of high doses of nicotine in pigs. I. Changes of the electrocardiogram. 125 87

In healthy volunteers the emetic effect of apomorphine (5-10 mg, i.m.) was prevented by haloperidol (2 mg), metoclopramide (10 mg) and sulpiride (100 mg), injected intramuscularly. In parkinsonian patients, apomorphine (1 mg) given alone ameliorated the neurological symptoms (30% improvement in the disability score), but the improvement was accompanied by nausea, vomiting, sedation or sleepiness. Haloperidol (2 mg) prevented not only the emetic effect of apomorphine (10 mg), but also its therapeutic efficacy in parkinsonism. Indeed, the disability score was worsened by the drug combination in some patients. Moreover, after haloperidol, apomorphine produced deep sedation and sleep. By contrast, in parkinsonian patients pretreated with metoclopramide (10 mg) or sulpiride (100 mg), apomorphine (10 mg) markedly diminished tremor and rigidity and failed to produce nausea, vomiting and sleepiness.
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PMID:Therapeutical efficacy of a combination of apomorphine with sulpiride or metoclopramide in Parkinsonism. 127 13

The effect of arotinolol, a peripherally acting beta-adrenergic-blocking agent, on postural or kinetic tremor was studied in monkeys with 1-methyl-4-phenyl-1,2,3,6-tetrahydropyridine (MPTP)-induced parkinsonism. Male cynomolgus monkeys (Macaca fascicularis) were treated with three injections of MPTP hydrochloride (0.3 mg/kg, i.v.) at an interval of 3-4 days, followed by several injections of the same dose every 7 days. Four monkeys with persistent parkinsonian symptoms manifested for greater than 1 year were used. The animals developed mild to moderate degrees of postural or kinetic tremor, and their motor activity was reduced. Arotinolol (20-30 mg/kg, s.c.) significantly suppressed postural tremor in a dose-dependent manner. Propranolol (20-30 mg/kg) was also effective in suppressing the tremor. However, the application of propranolol induced emesis, whereas arotinolol had no adverse effects. These results suggest that arotinolol is a useful adjunct to dopaminergic therapy for tremor in Parkinson's disease.
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PMID:Therapeutic effects of arotinolol, a beta-adrenergic blocker, on tremor in MPTP-induced parkinsonian monkeys. 138 70

Bulimia nervosa represents a serious public health problem in the United States. We performed an 8-week, double-blind trial comparing fluoxetine hydrochloride (60 and 20 mg/d) with placebo in 387 bulimic women treated on an outpatient basis. Fluoxetine at 60 mg/d proved superior to placebo in decreasing the frequency of weekly binge-eating and vomiting episodes at end point. Fluoxetine at 20 mg/d produced an effect between that of the 60-mg/d dosage and that of placebo. Depression, carbohydrate craving, and pathologic eating attitudes and behaviors also improved significantly with fluoxetine, with the higher dosage again showing a more robust effect than the lower dosage. Several adverse events (ie, insomnia, nausea, asthenia, and tremor) occurred significantly more frequently with fluoxetine (60 or 20 mg/d) than with placebo. However, there was no statistically significant difference among treatment groups in the proportion of patients discontinuing the study because of adverse events.
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PMID:Fluoxetine in the treatment of bulimia nervosa. A multicenter, placebo-controlled, double-blind trial. Fluoxetine Bulimia Nervosa Collaborative Study Group. 155 Apr 66

The cause of postanesthesia shaking (PS) is unknown. PS develops spontaneously and unpredictably in up to 67% of patients emerging from general anesthesia, and it continues for minutes to hours when not treated with medications or radiant heat lamps. The purposes of this study were to (1) examine whether butorphanol tartrate (Stadol; Anaquest, Madison, WI/Bristol-Meyers Squibb, Evansville, IN), meperidine (Demerol; Winthrop, NY, NY), and morphine are differentially effective in suppressing PS, (2) compare PS suppression by sex, and (3) determine time to PS development. PS, measured on a 0 to 3 visual scale, developed in 120 of 533 patients (23%). Medication treatment was initiated for 66 of 120 patients by PACU nurses following standard policies and procedures for intravenous doses of 1 mg butorphanol (n = 12), 15 to 30 mg meperidine (n = 18; n = 23), or 2 to 4 mg morphine (n = 13). Treatment effect was measured in units on a 0 to 2 visual scale. By t test, butorphanol is more effective within 2 minutes than meperidine for suppressing shaking alone (P less than .02) or shaking among patients also complaining of pain (P less than .02). Morphine does not relieve shaking. The chi 2 test indicates women suppress PS more rapidly than men (P less than .01), and PS develops within 5 minutes of PACU arrival (P less than .001). Findings suggest that butorphanol is an alternative PS treatment to meperidine, since it relieves shaking within 2 to 5 minutes without producing nausea, vomiting, or recurrence of shaking.
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PMID:Butorphanol tartrate (Stadol) relieves postanesthesia shaking more effectively than meperidine (Demerol) or morphine. 157

Limited toxicity information is available in the medical literature on the antidepressant fluoxetine (Prozac, Dista Products Co, Indianapolis, IN). The goal of this prospective multicenter study was to develop a toxicity profile of initial signs and symptoms observed in an acute fluoxetine overdose. A prospective study was made of patients reported to one of four American Association of Poison Control Centers' regional poison control centers after ingesting an acute overdose of fluoxetine. A standard data collection form was used on all patients ingesting fluoxetine. Information obtained included age, current medications, dose, coingested drugs, presenting symptoms, vital signs, electrocardiogram abnormalities, outcome, and fluoxetine levels. The authors collected 272 cases; 234 cases met the criteria of the study. Fluoxetine was ingested alone in 87 cases and with ethanol or other drugs in the remaining 147 cases. Of the 87 cases where fluoxetine was ingested alone, 67 patients were adults and 20 were children. Symptoms that were seen in the adult group included: tachycardia (15/67), drowsiness (14/67), tremor (five/67), vomiting (four/67), or nausea (four/67). Thirty patients did not develop symptoms. Twelve of the adult overdose patients had total fluoxetine levels ranging from 232 to 1390 ng/mL. The authors conclude that symptoms that develop after an acute overdose of fluoxetine appear minor and of short duration. Aggressive supportive care is the only intervention necessary.
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PMID:Acute fluoxetine overdose: a report of 234 cases. 158 2

Acute oral toxicity of (-)-(S)-9-fluoro-2,3-dihydro-3-methyl-10-(4- methyl-1-piperazinyl)-7-oxo-7H-pyrido [1,2,3-de][1,4]benzoxazine-6-carboxylic acid hemihydrate (levofloxacin, DR-3355, CAS 100986-85-4), a new quinolone antibacterial agent, was studied in ddy mice, SD rats and cynomolgus monkeys. LD50 values were 1,881 mg/kg for males and 1,803 mg/kg for females in mice, 1,478 mg/kg for males and 1,507 mg/kg for females in rats and more than 250 mg/kg in females monkeys. Toxic signs included the decrease in locomotor activity, ptosis, tremor, tonic convulsion and respiratory depressed in rodents and soft feces or vomiting in monkeys. At necropsy, no treatment-related changes were observed in any species except for the enlargement of the cecum in rats.
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PMID:Acute oral toxicity of the new quinolone antibacterial agent levofloxacin in mice, rats and monkeys. 162 33

Acute i.m. injections of benzodiazepine receptor ligands were administered to baboons before 1-h observational sessions. The agonist midazolam produced sedative effects, the antagonist flumazenil produced no behavioral effects, the inverse agonist FG7142 produced tremor and the inverse agonist 3-carboethoxy-beta-carboline hydrochloride (beta CCE) produced tremor, vomiting, jerks and seizures. Co-administration of these drugs (midazolam + beta CCE, midazolam + flumazenil or flumazenil + beta CCE) produced a mutual antagonism of these effects. Compared to the non-dependent condition, in the diazepam-dependent condition (baboons maintained on 20 mg/kg per day diazepam) and withdrawn condition (dependent baboons tested during withdrawal), midazolam produced decreased sedative effects, flumazenil produced increased effects (i.e., tremor, vomiting and jerks), and beta CCE produced increased frequency of seizures. Taken together, these data suggest that (1) benzodiazepine receptor ligands lie on a continuum of behavioral activity, and (2) chronic diazepam administration alters the behavioral effects of these benzodiazepine ligands, producing a shift in the direction of the inverse agonist.
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PMID:Behavioral effects of benzodiazepine ligands in non-dependent, diazepam-dependent and diazepam-withdrawn baboons. 166 65

Citalopram is an antidepressant belonging to a new class of drugs which enhance serotoninergic neurotransmission through potent and selective inhibition of serotonin reuptake. Preliminary trials suggest that its short term therapeutic efficacy is significantly greater than that of placebo and mianserin, and comparable to that of amitriptyline, maprotiline and imipramine. It appears to be a weaker antidepressant agent than clomipramine, but better tolerated. Its elimination half-life of 33 hours permits once daily oral administration. Symptomatic improvement obtained with short term treatment has been maintained when therapy has been extended for up to 1 year; in the few patients studied for this extended period, the relapse rate was lower than with fluvoxamine, fluoxetine or imipramine. Compared to standard antidepressant agents, citalopram is well tolerated. It does not appear to be cardiotoxic, has not been associated with seizures in humans, and is relatively nonsedating. Unlike the tricyclic antidepressants, citalopram has minimal anticholinergic effects. Mild and transient nausea, with or without vomiting, is the most frequent adverse effect--occurring in 20% of patients--and increased perspiration, headache, dry mouth, tremor and insomnia are experienced by 15 to 18% of patients. Citalopram thus offers similar therapeutic efficacy and a more favourable tolerability profile than the tricyclic antidepressants. Preliminary data suggest that it may be particularly useful in patients who cannot tolerate the anticholinergic or cardiovascular side effects of tricyclic antidepressants and in those for whom sedation is not indicated.
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PMID:Citalopram. A review of its pharmacodynamic and pharmacokinetic properties, and therapeutic potential in depressive illness. 171 47

The levels of histamine (HA) and tele-methylhistamine (t-MH) were determined in five brain regions of Suncus murinus (suncus) and the effects of motion stimulus or drugs influencing the turnover of these amines were studied to elucidate the role of histamine in motion sickness. Shaking the animals for 2 min increased HA contents in telencephalon and diencephalon without significantly changing the t-MH levels. alpha-Fluoromethylhistidine (alpha-FMH), which is presumed to deplete the neuronal HA, tended to raise the HA levels. alpha-FMH slightly alleviated the vomiting response to motion stimulus and suppressed the HA increase in diencephalon caused by shaking. Compound 48/80, which releases HA from mast cells, did not alter the control HA levels, but effectively prevented the motion sickness and completely suppressed the motion-induced rises in HA levels. These results provide further evidence that brain HA plays an important role in the development of motion sickness.
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PMID:Role of histamine in motion sickness in Suncus murinus. 174 19


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