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)

Aminophylline, theophylline, etamiphylline and diprophylline have been tested as antagonists of neuronal inhibition produced by microiontophoretically applied adenosine, when ejected as cations or anions. Aminophylline proved to be an effective adenosine antagonist when ejected as an anion, especially from alkaline solution. Anionic theophylline was also effective but less so, and on a smaller proportion of neurones. Ethylenediamine and hydroxyl ions had no effect on adenosine responses. GABA depressions were unaffected by any of the methylxanthines at the time of adenosine blockade. Cationic ejection from aminophylline or ethylenediamine barrels produced a depression of unit firing on about one third of the cells tested, but no antagonism of adenosine was observed. It is concluded that the anionic ejection of aminophylline from alkaline solution, or of etamiphylline of diprophylline, yields potentially useful antagonists of adenosine for iontophoretic experiments.
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PMID:Aminophylline and theophylline derivatives as antagonists of neuronal depression by adenosine: a microiontophoretic study. 743 27

Dipyridamole thallium-201 imaging, using single-photon emission computed tomography, was evaluated for its safety and diagnostic efficacy in 109 patients with angiographically documented coronary artery disease and 35 normal subjects. The most common side effects after the intravenous administration of dipyridamole thallium-201 (0.56 mg/kg) included chest pain in 41 patients, dizziness in 20 patients, headache in 16 patients, and ST segment depression > or = 1 mm in 15 patients. Aminophylline was required to reverse the side-effects in 46 patients, and 45 of the 46 patients experienced complete relief of symptoms. Of the 109 patients with coronary artery disease, 104 had abnormal dipyridamole thallium images. The per patient sensitivity was 95%. Of the 35 normal subjects, 27 had normal thallium images. The per patient specificity was 77%. The sensitivity and specificity for the individual vessels were 84% and 87% for the left anterior descending artery, 67% and 97% for the left circumflex artery, and 89% and 85% for the right coronary artery, respectively. Dipyridamole thallium-201 imaging is a relatively safe noninvasive method and is an effective alternative to exercise thallium-201 scintigraphy for the diagnosis of coronary artery disease.
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PMID:Diagnosis of coronary artery disease using dipyridamole thallium-201 imaging. 763 92

The present paper delineates some of the current opinions as well as our own experiences with pharmacologic antagonists in anaesthetic practice. Non specific (Aminophylline, Physostigmine) as well as specific-opiate and benzodiazepine antagonists are therapeutic agents which cans shorten time of awakening or reverse respiratory depression induced by different anaesthetic drugs.
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PMID:[Antagonists in anesthesiology practice]. 796 32

1. Aminophylline (cumulative concentrations of 0.036-3.60 mmol/l) produced a concentration-dependent increase in both tension developed (Td) and the maximum rate of rise of tension (dT/dt max) of the isolated hemidiaphragm of the rat both during direct single-pulse and subtetanic stimulation. 2. The repeated series of additions of aminophylline into the bathing medium (the second and the third series) produced even further, more pronounced potentiation of both Td and dT/dt max during subtetanic stimulation only, the potentiation being the strongest after the third series of additions of the drug ("antifatigue effect"). The antifatigue effect of aminophylline was much more pronounced than the antifatigue effect of the equimolar concentrations of caffeine. 3. The presence of intact beta 1-adrenergic receptors seems to be essential for the antifatigue action of aminophylline under our experimental conditions. 4. The antifatigue effect of aminophylline was not affected by reserpine or 6-OHDA pretreatment of rats. 5. In a Ca(2+)-free medium the stimulatory effect of aminophylline on Td and dT/dt max was abolished or depressed (single-pulse and subtetanic stimulation, respectively). After returning the muscle into the medium containing Ca2+, the effect of aminophylline was significantly potentiated during both types of the stimulation. 6. The antifatigue action of aminophylline was preserved even in the presence of nicardipine or its solvent in the bathing medium. 7. In the presence of heparin (which produced a significant depression of both Td and dT/dt max by itself during direct subtetanic stimulation) the stimulatory effects of aminophylline on Td and dT/dt max (the second and third series of additions) were significantly potentiated in comparison with the effects of the first series of additions of aminophylline (with no heparin in the bathing medium). 8. The dose-response curves for the effects of aminophylline in the presence of Ni2+ on Td and dT/dt max during direct single-pulse stimulation were significantly shifted to the right. Ni2+ by itself produced significant and dose-related depression of both Td and dT/dt max during single-pulse and subtetanic stimulation, the subtetanic stimulation being much more sensitive. The antifatigue effect of aminophylline during subtetanic stimulation was preserved in the presence of Ni2+. 9. Our results indicate the important role of the extracellular calcium and the involvement of intact beta 1-adrenergic receptors in the antifatigue action of aminophylline. Also, the potentiating effect of heparin on the antifatigue action of aminophylline is presumably due to the influx of extracellular calcium through L-type Ca2+ channels during subtetanic stimulation. Our results indicate the possibility of the presence of T-type calcium channels (which can be blocked by Ni2+) in the isolated hemidiaphragm of the rat, but they do not seem to be involved in the antifatigue action of aminophylline.
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PMID:Some new evidence on antifatigue action of aminophylline on the isolated hemidiaphragm of the rat. 809 40

Adenosine is a purine nucleoside with a rapid onset and brief duration of action after intravenous bolus administration. Its most prominent cardiac effect is impairment or blockade of atrioventricular nodal conduction, but other effects are depression of automaticity of the sinus node and attenuation of catecholamine-related ventricular after-depolarizations. The cardiac cell surface receptor is the A1 purinoceptor. The therapeutic value of adenosine is predominantly in those arrhythmias in which the atrioventricular node forms part of a reentry circuit, as clearly demonstrated by the high success rate for termination of atrioventricular nodal reentry tachycardia and of atrioventricular reentry tachycardia involving an accessory pathway in the Wolff-Parkinson-White syndrome. Ventricular tachycardias are generally unresponsive, with the exception of right ventricular outflow tract tachycardia. A diagnostic role has emerged for adenosine. The transient blockade of the atrioventricular node that it causes can reveal important electrocardiographic features in arrhythmias, such as atrial flutter, or can unmask latent preexcitation. In wide-QRS tachycardias, adenosine can help to distinguish ventricular tachycardia from supraventricular tachycardia with QRS aberration. Unlike verapamil, adenosine is safe in ventricular tachycardia. A suggested dosing scheme is to give incremental doses at 1-minute intervals, starting at 0.05 mg/kg and continuing until complete atrioventricular block is induced or a maximum of 0.25 mg/kg is reached. Side effects are transient, sometimes uncomfortable, and not hazardous; dyspnea and chest discomfort are most frequent. A history of asthma is a relative contraindication. Aminophylline antagonizes and dipyridamole potentiates the effects of adenosine.
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PMID:The therapeutic and diagnostic cardiac electrophysiological uses of adenosine. 848 69

Peripheral chemoreceptors may be immature in neonatal animals, exhibiting maturational changes in the perinatal period. Even though methylxanthines are respiratory stimulants, many premature neonates do not respond to them. Thus, we hypothesized that carotid body activity is necessary for aminophylline to reverse hypoxia-induced respiratory depression. We exposed 16 anesthetized newborn piglets (age 2-7 days) to hypoxia (inhalation of 12% oxygen) for 5 min. Aminophylline (15 mg/kg iv) was administered either prior to (11 piglets) or following (5 piglets) carotid body denervation (CBD). Before CBD, hypoxia elicited transient initial increases in tidal volume (from 79 +/- 4 to 99 +/- 1% of maximum, mean +/- SE), minute ventilation (from 64 +/- 5 to 93 +/- 4%), and peak phrenic electroneurogram (from 63 +/- 8 to 91 +/- 6%, all P < 0.05). This was followed by a decrease in tidal volume, minute ventilation and phrenic electroneurogram (all P < 0.05). Prior to CBD, aminophylline pretreatment prevented the decrease in all the measures of respiratory output during late hypoxia. After CBD, hypoxia induced an initial and sustained depression of ventilation (tidal volume from 100 to 33 +/- 14%; frequency from 94 +/- 4 to 42 +/- 17%; minute ventilation from 100 to 32 +/- 14%, all P < 0.05) and phrenic electroneurogram (peak phrenic from 100 to 47 +/- 18%; minute phrenic from 85 +/- 6 to 55 +/- 21%, both P < 0.05). Administration of aminophylline after CBD did not prevent the profound respiratory depression elicited by hypoxia in the chemodenervated piglets.(ABSTRACT TRUNCATED AT 250 WORDS)
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PMID:Carotid bodies and ventilatory response to hypoxia in aminophylline-treated piglets. 857 Mar 9

Diminished myocardial function can be seen in chronic coronary stenosis (CS) even in the presence of normal resting myocardial blood flow. We hypothesized that adenosine contributes to myocardial depression in this setting, predominantly through activation of the A(1) adenosine receptor. To test this hypothesis we used aminophylline, a nonselective adenosine receptor antagonist, and 8-cyclopentyl 1,3 dipropylxanthine, a selective A(1) adenosine receptor antagonist, in a canine model of chronic CS. Chronic CS was produced by placement of ameroid constrictors on the left anterior descending and left circumflex coronary arteries in 17 adult mongrel dogs, which resulted in severe left ventricular dysfunction 6 weeks later. Eight dogs without ameroid placement were used as controls (C). Closed-chest echocardiographic short-axis images at the low midpapillary level, hemodynamics, and radiolabeled microsphere-derived myocardial blood flow were obtained before and immediately after injection of either 5 mg/kg(-1) of aminophylline (7 left ventricular dysfunction and 4 C dogs) or 1 mg/kg(-1) of 8-cyclopentyl 1,3-dipropylxanthine (10 left ventricular dysfunction and 4 C dogs). Both 8-cyclopentyl 1,3-dipropylxanthine and aminophylline had no effect in C animals but resulted in a significant transient increase in regional percent wall thickening (P <.05) with a concomitant decrease in end-systolic wall stress (P <.05) in CS animals. There was no change in transmural myocardial blood flow or systemic hemodynamics to explain these results. Thus, adenosine plays a significant role in myocardial dysfunction in chronic ischemia by activation of the A(1) receptor. Aminophylline or a selective A(1) adenosine receptor antagonist can be used to detect viable myocardium and may be safer than dobutamine in severe chronic ischemic heart disease.
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PMID:A1-receptor blockade: a novel approach for assessing myocardial viability in chronic ischemic cardiomyopathy. 1283 64

1. Theophylline and aminophylline have been widely used as inhibitors of phosphodiesterase when examining the role of cAMP in regulating cell function. In reality, however, these phosphodiesterase inhibitors may have additional sites of action that could complicate the interpretation of the results. These additional sites of action could include antagonism of inhibitory adenosine autoreceptors and release of intracellular calcium. The purpose of the present study was to determine which of the above three is the primary mechanism by which theophylline and aminophylline affect transmitter release at the mammalian neuromuscular junction. 2. Quantal release measurements were made using intracellular recording techniques. A variety of drugs were used to elucidate this pathway. Isoproterenol, an adenylate cyclase activator, was first used to establish the effect of enhanced levels of cAMP. Theophylline application on its own or in the presence of a drug combination that blocked the adenosine receptor and phosphodiesterase pathways caused significant release depression, opposite to what is expected if it was functioning to enhance cAMP levels. However, when applied in the presence of a drug combination that blocked the adenosine receptor, phosphodiesterase and intracellular ryanodine calcium pathways, theophylline was unable to depress release. Therefore, it was concluded that the major mechanism of action of theophylline is depression of transmitter release by causing the release of intracellular calcium. 3. Aminophylline application alone resulted in a significant enhancement of release. However, when coupled with an adenosine receptor blocker, the ability of aminophylline to enhance transmitter release was blocked, suggesting that its dominant mechanism of action is adenosine receptor inhibition. 4. Taken together, these results indicate that the use of theophylline and aminophylline is inappropriate when examining the role of cAMP at the mammalian neuromuscular junction.
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PMID:Effect of theophylline and aminophylline on transmitter release at the mammalian neuromuscular junction is not mediated by cAMP. 1670 Aug 79

Introduction: Comorbidities of epilepsy may significantly interfere with its treatment as diseases in the general population are also encountered in epilepsy patients and some of them even more frequently (for instance, depression, anxiety, or heart disease). Obviously, some drugs approved for other than epilepsy indications can modify the anticonvulsant activity of antiepileptics. Areas covered: This review highlights the drug-drug interactions between antiepileptics and aminophylline, some antidepressant, antiarrhythmic (class I - IV), selected antihypertensive drugs and non-barbiturate injectable anesthetics (ketamine, propofol, etomidate, and alphaxalone). The data were reviewed mainly from experimental models of seizures. Whenever possible, clinical data were provided. PUBMED data base was the main search source. Expert opinion: Aminophylline generally reduced the protective activity of antiepileptics, which, to a certain degree, was consistent with scarce clinical data on methylxanthine derivatives and worse seizure control. The only antiarrhythmic with this profile of action was mexiletine when co-administered with VPA. Among antidepressants and non-barbiturate injectable anesthetics, trazodone, mianserin and etomidate or alphaxalone, respectively, negatively affected the anticonvulsant action of some antiepileptic drugs. Clinical data indicate that only amoxapine, bupropion, clomipramine and maprotiline should be used with caution. Possibly, drugs reducing the anticonvulsant potential of antiepileptics should be avoided in epilepsy patients.
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PMID:Interactions of antiepileptic drugs with drugs approved for the treatment of indications other than epilepsy. 3330 39


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