Gene/Protein Disease Symptom Drug Enzyme Compound
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Query: UMLS:C1323099 (sympathomimetic)
 2,957 document(s) hit in 31,850,051 MEDLINE articles (0.00 seconds)

1. In a double-blind study forty abstinent hospitalized male patients with an alcoholic organic brain syndrome (OBS) were treated for 6 weeks with either 200 mg modafinil or placebo. 2. Modafinil (CRL 40476) is a putative central alpha-1 adrenergic agonist. It's pharmacological profile is quite different from that of amphetamine, which can be seen by the lack of peripheral sympathomimetic effects. The vigilance promoting effect of modafinil has been shown previously in pharmaco-EEG and psychometric studies as well as in clinical studies involving treatment of daytime sleepiness in idiopathic hypersomniacs and narcoleptics. 3. The present clinical investigations demonstrated that the spontaneous restitution of the alcoholic OBS was significantly augmented and accelerated by modafinil. 4. Psychometric tests did not show significant intergroup differences. Modafinil- and placebo-treated patients improved continously over the 6-week period. 5. Psychophysiological and autonomous nervous system parameters were affected neither by placebo nor by modafinil. 6. Neurophysiological investigations by means of quantitative pharmaco-EEG showed partly inconsistent findings. However, superimposed dosages of modafinil (on the top of 6 weeks chronic administration) induced a decrease of slow activity and an increase of alpha activity suggesting an improvement of vigilance after the daily drug intake. 7. Considering the beneficial effects of modafinil in abstinent chronic alcoholic patients, it may be said that activation and improvement of adaptive behaviour by an alpha-adrenergic agonist could be regarded as a therapeutic principle in the treatment of the OBS, eventually due to noradrenergic deficits.
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PMID:On the treatment of the alcoholic organic brain syndrome with an alpha-adrenergic agonist modafinil: double-blind, placebo-controlled clinical, psychometric and neurophysiological studies. 196 72

Among the most common of health problems, allergies afflict more than one of every six Americans. In the allergic reaction, mast cells degranulate, releasing inflammatory mediators such as histamine. These mediators in turn cause smooth muscle contraction, itch, mucus secretion, and vascular leakage. A number of pharmacologic agents, including the H1 receptor antihistamines and the sympathomimetic decongestants, have been developed in an attempt to minimize such effects. Antihistamines were first used clinically 50 years ago. Currently taken by approximately 30 million Americans each year, they are grouped by structure into six classes. Until recently, all of the classes, or first-generation antihistamines, were thought to be relatively equal in efficacy and, because of their ability to cross the blood-brain barrier, they all caused varying degrees of sedation. The effects of antihistamines on psychomotor reflexes and driving skills, antihistamine-induced drowsiness, and the interaction of antihistamines with alcohol and tranquilizers are reviewed. The centrally acting first-generation agents, and the performance decrements these agents commonly induce, are compared with the newer, nonsedating, second-generation antihistamines (eg, terfenadine, astemizole, cetirizine, and loratadine). Although decongestants do not appear to cause impaired performance, this needs to be evaluated further, particularly with regard to decongestant-induced insomnia.
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PMID:Antihistamine- and decongestant-induced performance decrements. 197 Aug 34

In a placebo controlled double-blind multicenter trial, 245 patients with bronchial asthma (131 male and 124 female patients) between 6 and 51 years of age were treated in two parallel groups. A slow-release oral formulation containing 2 mg of ketotifen or placebo was administered daily for a duration of 12 weeks. Over a period of four weeks before the study, 94 percent of the patients had asthmatic attacks. 78 percent had cough, and 62 percent had nasal symptoms. In the group treated with slow-release oral ketotifen, there were 3.9 asthmatic attacks (range, 0 to 20) per week, and in the placebo group, there were 2.9 (range, 0 to 12) (mean values during four weeks prior to start of treatment). At the end of treatment, asthmatic attacks were significantly reduced in the group treated with slow-release oral ketotifen compared with placebo. Significant reduction was also evident for cough and sputum production, as well as nasal discharge and obstruction; however, slow-release oral ketotifen did not significantly improve pulmonary function indices when compared to placebo. The use of concomitant medication (beta-sympathomimetic drugs) was also significantly reduced in the group receiving slow-release oral ketotifen. The overall efficacy assessed by the investigators was "very good" and "good" in 76 percent of the group receiving slow-release oral ketotifen and 30 percent in the group receiving placebo (p less than 0.001). Tolerability rated by the investigators was "very good" and "good" in 90 percent of the group with slow-release oral ketotifen and in 96 percent of the group with placebo (p less than 0.10). The most frequent side effects were "mild" and "moderate" sedation, sleepiness and drowsiness reported in 44 percent of the patients receiving slow-release oral ketotifen and in 26 percent of the patients receiving placebo. This difference was statistically significant (p less than 0.01).
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PMID:Ketotifen in the prophylaxis of extrinsic bronchial asthma. A multicenter controlled double-blind study with a modified-release formulation. 268 51

Tricyclic antidepressants are among the commonest causes of both non-fatal and fatal drug poisoning in the world. Their toxicity is due to effects on the brain, the heart, the respiratory system and the parasympathetic nervous system. Symptoms usually appear within 4 hours of an overdose and all but the most seriously poisoned patients recover within 24 hours. The most common clinical features are dry mouth, blurred vision, dilated pupils, sinus tachycardia, pyramidal neurological signs, and drowsiness. In severe poisoning, there may be coma, convulsions, respiratory depression, hypotension and a wide range of electrocardiographic (ECG) abnormalities. The most frequent findings on the ECG are prolongation of the PR and QT intervals; the tracing may resemble bundle branch block or supraventricular or ventricular tachycardias. Treatment of poisoning due to the tricyclic antidepressants is essentially supportive, there being insufficient evidence at present to recommend the use of methods to increase elimination of the drug from the body. Gastric aspiration and lavage should be performed if more than 750 mg of drug have been taken. There must be regular monitoring for hypoxia, acidosis and hypokalaemia and these complications should be corrected enthusiastically. Convulsions should be treated with diazepam or chlormethiazole. Muscular paralysis and artificial ventilation should be employed if anticonvulsants are ineffective. Hypotension should be treated firstly by fluid replacement and then with sympathomimetic agents (dopamine or dobutamine). Antiarrhythmic drugs should only be employed if there is evidence of circulatory failure which fails to respond to correction of hypotension. Sodium bicarbonate infusions should be given to cardiotoxic patients who are acidotic and are worth trying even if the patient is not acidotic. Although physostigmine salicylate will reverse most of the features of tricyclic antidepressant poisoning, its effects are short-lived in serious toxicity and it can produce dangerous side effects; physostigmine should therefore be reserved for those patients who have complications of coma or who have resistant cardiotoxicity or convulsions. Drug screening and quantitative determination of tricyclic antidepressant serum concentrations are useful in a minority of patients who have severe, unusual or prolonged symptoms.
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PMID:Poisoning due to tricyclic antidepressant overdosage. Clinical presentation and treatment. 353 21

1. The haemodynamic mechanism of action of guanfacine 4 mg intravenously was investigated in resting conditions and during exercise for up to 20 h after administration of the drug. Cardiac output and pulmonary arterial pressure were determined by the Swan-Ganz thermodilution method. Blood pressure was measured directly. 2. During and immediately after intravenous administration of guanfacine, blood pressure peripheral resistance and pulmonary arterial pressure increased (in keeping with an alpha-sympathomimetic effect of the compound), whereas heart rate and cardiac output decreased. 3. Subsequently blood pressure fell as a result of a decrease in cardiac output. From the third hour peripheral resistance decreased, whereas cardiac output increased again, sometimes exceeding the control value. 4. During exercise blood pressure was reduced from the third hour after administration, as in resting conditions, as a result of the reduction in peripheral resistance. 5. In resting conditions guanfacine reduced heart rate at the beginning and during the whole course after administration of the drug. 6. Side-effects noted included fatigue, drowsiness and bradycardia.
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PMID:Haemodynamic effects of guanfacine. 699 66

The pharmacology, pharmacokinetics, therapeutic and diagnostic uses, toxicity, adverse reactions, and contraindications of metoclopramide are reviewed. Metoclopramide enhances the rate of gastric emptying by (1) augmenting esophageal peristalsis, gastric antral contractions, and small intestine transit time and (2) increasing resting pressures of the lower esophageal and pyloric sphincters. The drug does not stimulate gastric acid secretions. The injectable form is approved for use to facilitate intubation of the small intestine and the passage of barium into the intestine for radiographic procedures. Tablets are approved for the treatment of symptoms associated with diabetic gastroparesis. The drug has been used in the treatment of vomiting of various etiologies. The side effects of metoclopramide are usually mild, transient, and reversible with discontinuation of the drug. They include drowsiness, GI disturbances, extrapyramidal reactions, and increased lactation. Metoclopramide should not be given in combination with MAO inhibitors, tricyclic antidepressants, sympathomimetic amines, or to patients with pheochromocytoma, GI hemorrhage, obstruction, or perforation. Metoclopramide appears to be an effective drug in stimulating the mobility of the upper gastrointestinal tract without increasing gastric secretions. Further studies are needed to assess its value in the treatment of vomiting secondary to anesthesia and chemotherapy, and to assess its precise role in the treatment of diabetic gastroparesis.
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PMID:Review of a new gastrointestinal drug--metoclopramide. 701 32

Complications from mydriatic and cycloplegic drugs are rare compared with their extensive use. Adverse effects are often related to dosage or other factors. The ocular complications include increased intraocular pressure, pigmentation of the conjunctiva and cornea, pigment in the anterior chamber, lacrimal duct blockage, macular edema, corneal endothelium damage, hyperemia, allergy, discomfort, and blurred vision. The systemic complications are those common to sympathomimetic and parasympatholytic drugs and include tachycardia, hypertension, headache, faintness. pallor, trembling, excessive sweating, palpitations, arrhythmias, confusion, hallucinations, drowsiness, ataxia, flushed skin, high fever, dysarthria, thirst, dry mouth, convulsions, disorientation, nervousness, coma, and death. An understanding of all possible side effects is of paramount importance to those using these drugs in the treatment of anticholinesterase poisoning. This review is intended as a ready reference to the adverse effects of mydriatic and cycloplegic drugs.
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PMID:Mydriatic and cycloplegic drugs: a review of ocular and systemic complications. 703 29

Naphazoline, a sympathomimetic and an imidazoline derivative, is used as 0.05-0.1% solution for local decongestion of the nasal and ocular mucosa. In excessive dosage, or if ingested by accident, may cause depression of the central nervous system (disturbances of consciousness progressing to coma), hypothermia, bradycardia and sweating. These naphazoline effects are particularly strongly pronounced in children. Anglo-Saxon pharmacotherapy excludes the application of naphazoline nasal drops in children younger than six years, whereas the Croatian pharmacotherapeutic literature (and practice) allows its use even in infancy. At the Kantrida Paediatric Clinic, Clinical Hospital Centre in Rijeka, 11 children with signs of intoxication with naphazoline nasal drops were hospitalized from 1990 to 1992. The symptoms pertaining to the central nervous system i.e. disturbances of consciousness in the form of somnolence were clearly marked in all children. Some children developed skin pallor, bradycardia, bradypnoea and hypothermia. Resolution occurred within 24 hours and the findings returned to normal values. Clinical picture followed by rapid resolution and normal findings, with a personal history of drug taking, is a safe indication for diagnosis. There are several reasons to account for intoxication (drops difficult to use with children, containers inadequate for proper dosage), but the major factor is the age of the patient--all hospitalized children were younger than six years. It is pointed out that administration of naphazoline drops at an early age is not advisable.
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PMID:Naphazoline nasal drops intoxication in children. 806 10

In sleep, the eyelids are closed and the pupils narrow. The pupil width indicates alertness and, if it is narrow, sleepiness. The deeper the sleep, the narrower the pupil: miosis during drowsiness, sleep, sedation and general anesthesia relies on reduced inhibition of the oculomotor nucleus and, even more, on reduced sympathetic tone (it is as sympatholysis that accounts for the miosis exerted by the famous "cocktail lytique" onto an iris whose sphincter is weakened from briskly elevated IOP in angle-closure glaucoma). For whatever reason a lack of sympathetic tone occurs, a poor response to anticholinergic mydriatics will be the consequence. This communication is concerned with children who received tropicamide, cyclopentolate or atropine for diagnostic pupil dilation and cycloplegia but, during subsequent sleep, exhibited an unsatisfactory mydriatic response that could be overcome by additional administration of phenylephrine. Thus, parasympatholytic mydriasis can be proven to be a function of the sympathetic tone. The pupil shrinks during deep sleep even after atropine. If the conditions of deep sleep, sedation or general anesthesia are present and mydriasis needs to be maintained, an additional administration of a sympathomimetic compound is mandatory.
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PMID:[Sleep modifies anticholinergic mydriasis]. 896 50

Narcolepsy, a lifelong disorder, requires long-term management of symptoms. Interventions may be nonpharmacologic, such as lifestyle changes, and pharmacologic for relief of daytime sleepiness. Pharmacologic treatment of narcolepsy has depended on the use of CNS stimulants to increase wakefulness, vigilance, and performance. The medications considered effective in the treatment of narcolepsy include dextroamphetamine, pemoline, methylphenidate, methamphetamine, and modafinil; only methylphenidate hydrochloride and dextroamphetamine are approved for use in the United States. The currently available stimulants are associated with sympathomimetic side effects, limitations in efficacy, and negative effects on nighttime sleep. This has led to the development of alternative agents. Modafinil, a new wake-promoting agent, has been shown to be effective in reducing daytime sleepiness in patients with narcolepsy. The results of a United States 18-center randomized, placebo-controlled, 9-week trial of modafinil in the treatment of patients with narcolepsy has recently been reported. Patients receiving modafinil demonstrated significant improvement in all subjective and objective measures of sleepiness. Treatment with modafinil 200 mg and 400 mg daily significantly reduced mean scores on the Epworth Sleepiness Scale compared with baseline and placebo (p < 0.001) and significantly increased mean scores on the Maintenance of Wakefulness Test (p < 0.001) and the Multiple Sleep Latency Test (p < 0.001) compared with baseline and placebo. More improvement, as recorded on the Clinical Global Impression of Change scale, was seen in the modafinil group than in the placebo group at all time points (p < 0.001). Modafinil was well tolerated, with headache the only adverse event to occur significantly more often in the active treatment group (p < 0.05). These results suggest that modafinil is an important new therapeutic option for the treatment of narcolepsy.
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PMID:Treatment modalities for narcolepsy. 948 23


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