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)

In patients with chronic respiratory insufficiency the treatment of the underlying pulmonary disease is of primary importance. However, many patients often also need symptomatic management to recompensate or stabilize impaired pulmonary gas exchange. The most suitable measures for this purpose are (1) ventilatory support by periodic intermittent positive pressure breathing (IPPB), (2) long-term oxygen administration and (3) respiratory stimulant drugs. IPPB provides good results if restricted to well defined indications (paO2 below 60 mm Hg, paCO2 above 45 mm Hg, forced expiratory volume [FEV1] below 40% of vital capacity or below 1000 ml). Long-term domiciliary oxygen therapy for at least 15 h daily prevents the early decompensation of cor pulmonale and improves physical performance. With the introduction of industrial O2-concentrators this form of therapy becomes more practicable and less expensive compared with the conventional method delivering compressed oxygen. However, the indication should be confined to patients with chronic and severe hypoxemia (paO2 below 50 mm Hg), pulmonary hypertension and secondary polycythemia. Respiratory stimulant drugs are useful in protecting patients from central respiratory depression during oxygen breathing. Aminophylline seems to be the most suitable drug simultaneously acting as a bronchodilator and vasodilator in the pulmonary circulation. To achieve a potent stimulant effect, serum theophylline levels above 10 microgram/ml through repeated intravenous administrations of aminophylline are required. Individual differences in the pharmacokinetic action of theophylline may sometimes need drug monitoring to prevent toxic side effects.
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PMID:[Therapy of chronic respiratory insufficiency]. 701 May 78

ATP induced a concentration-dependent reduction of the velocity of propulsion in isolated segments of rabbit colon as assessed by the aboral displacement of an intraluminal rubber balloon, and delayed the onset of the propulsive wave. ATP depressed both the reflex contraction of the circular coat above the distended balloon and the response of the circular muscle to transmural (cholinergic) stimulation. On the contrary, ATP (up to 200 muM), while causing relaxation of the circular muscle, had no effect on either the muscular contractile response induced by carbachol and histamine or the non-adrenergic inhibitory responses elicited by electrical stimulation and by radial distension of the gut wall. Within the concentration range used (10-200 muM), ATP concentration-depression curves for propulsion and transmural excitatory stimulation were shifted to the right in the presence of theophylline (10 muM). Theophylline, however, had no influence on either the direct inhibitory action of ATP on circular smooth muscle or the non-adrenergic relaxation in response to electrical stimulation. These data are consistent with the concept that at least two populations of purinergic receptors are present in intestinal tissue. Those populations located presynaptically, unlike those located postsynaptically, are blocked by theophylline. Since the contractile machinery does not appear to be affected by ATP concentrations up to 200 muM, the mechanism by which ATP impairs propulsive activity is probably dependent on activation of presynaptic purinergic receptors located on the nervous pathways subserving the wave of contraction, without having any appreciable influence on descending inhibition.
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PMID:Mode of action of ATP on propulsive activity in rabbit colon. 712 78

Aminophylline (an inhibitor of animal phosphodiesterases) interferes with a pleiotypic program in embryos and seedlings of Haplopappus gracilis, inducing a specific and reversible block of the cell cycle in G1 and G2, partial depression of RNA and protein synthesis and inhibition of the uptake of nucleosides and leucine. The analogy between these effects and those evoked in animal cells by various treatments leading to a rise in cAMP level is discussed.
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PMID:Interference of the phosphodiesterase inhibitor aminophylline with the plant cell cycle. 728 61

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

We have used the isolated brainstem-spinal cord preparation of the neonatal rat to study the effects of theophylline on the ventilatory response to hypoxia. The brainstem-spinal cord was isolated from neonatal rats (0-4 days) and superfused with mock cerebrospinal fluid (CSF), equilibrated with a gas mixture (FO2, 0.90; FCO2, 0.02; FN2, 0.08; control CSF) at 27 degrees C. We recorded phrenic nerve discharge from C4 roots, using suction electrodes, and measured respiratory frequency (fR) and the amplitude of the integrated phrenic neurogram (integral of phr). We examined how theophylline and the specific adenosine antagonist, 8-p-sulfophenyltheophylline (SPT), modify the ventilatory response to hypoxia. The response during superfusion with hypoxic CSF (FO2, 0.06) consisted of a marked decrease in fR (to 60% of control) and a slight decline in integral of phr (to 85% of control). By contrast, in the presence of theophylline (30 mg/L = 165 microM) and SPT (5 mg/L = 15 microM) in the superfusate hypoxia reduced fR only moderately (to 87% of control) and exerted virtually no effect on integral of phr (105% of control). Theophylline and SPT attenuated the rate of decrease in fR and completely blocked the decrease in integral of phr. There was no difference between the effects of theophylline and those of SPT. The results suggest that theophylline attenuates hypoxic respiratory depression, and that this effect is mediated by the blockade of adenosine.
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PMID:Theophylline and hypoxic ventilatory response in the rat isolated brainstem-spinal cord. 760 81

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

Spreading depression (SD) is known to be involved in the N-methyl-D-aspartate receptor-mediated neuronal damage. In urethane-anesthetized rats, we examined the release of adenosine and glutamate during SD induced by microdialysis of high K+ perfusate through the hippocampal CA1 area. The effects of endogenous adenosine upon SD were studied by applying an adenosine antagonist, theophylline (1 mM) and by a simultaneous application of adenosine uptake blockers, dipyridamole (DPR) (100 microM) and nitrobenzylthioinosine (NBI) (50 microM). The dialysates were sampled every 5 or 10 min and analyzed by HPLC. SD was identified by flattening of background EEg and disappearance of population spikes recorded from the pyramidal cell layer of CA1 area by a glass microelectrode. Adenosine and glutamate release was enhanced significantly in association with the occurrence of SD. Theophylline increased the release of glutamate and the incidence of SD and decreased the latency of the SD occurrence. DPR+NBI decreased the release of glutamate and the occurrence of SD, but increased extracellular adenosine concentration. The effects of DPR+NBI were blocked by application of a selective antagonist of adenosine A1 receptor, 8-cyclopentyl-1,3-dipropylxanthine (DPCPX, 0.1 microM). These findings suggest that endogenous adenosine exerts inhibitory influences upon the development of SD and the glutamate release through the A1 receptor in rat hippocampus.
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PMID:Endogenous adenosine exerts inhibitory effects upon the development of spreading depression and glutamate release induced by microdialysis with high K+ in rat hippocampus. 783 53

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


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