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)

We designed experiments to evaluate changes in ventral medullary (VM) extracellular fluid (ECF) PCO2 and pH during hypoxemia-induced ventilatory depression (VD). Our aim was to investigate effects of aminophylline on VD and VM ECF acid-base variables. We used aminophylline because it inhibits adenosine, which is released within the brain during hypoxemia and could mediate VD. Experiments were performed in seven cats with acute bilateral denervation of carotid sinus nerves and vagi. Cats were anesthetized with chloralose-urethan and breathed spontaneously at a regulated and elevated arterial PCO2 (PaCO2). Measurements were made during normoxemia, hypoxemia, and recovery before (phase I) and after (phase II) aminophylline. By use of strict criteria for definition of VD, during phase II two kinds of responses were observed. Aminophylline prevented VD in five cats. In these cats in phase I, with mean arterial PO2 (PaO2) = 105 and PaCO2 = 42.2 Torr, VM ECF PCO2, [H+], and [HCO3-] were 59.5 +/- 8.6 Torr (mean +/- SD), 60.2 +/- 9.4 neq/l, and 23.1 +/- 3.7 meq/l, respectively. When mean PaO2 dropped to 49 Torr, ventilation decreased 21%, with only small changes in VM ECF acid-base variables. Studies were repeated 30 min after aminophylline (17 mg/kg iv). In phase II, during normoxemia (PaO2 = 110 Torr) VM ECF Pco2, [H+], and [HCO3-] were 55.4 +/- 8.1 Torr, 62.0 +/- 8.0 neq/l and 20.7 +/- 2.5 meq/l, respectively. During hypoxemia (PaO2 = 48 +/- 4 Torr) mean ventilation, VM ECF PCO2, [H+], and [HCO3-] did not change significantly.(ABSTRACT TRUNCATED AT 250 WORDS)
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PMID:Effects of aminophylline on hypoxemia-induced ventilatory depression in the cat. 339 87

Neonates of animals and humans exhibit a paradoxical ventilatory response to hypoxia characterized by an initial increase in minute ventilation followed by a late, sustained decrease. Exogenous adenosine analogues cause respiratory depression, and the xanthine derivative aminophylline, a competitive inhibitor of adenosine receptors, decreases the amount of hypoxic ventilatory depression in the newborn piglet. Other xanthine derivative such as enprofylline are weak adenosine antagonists. The purpose of this report is to test the hypothesis that enprofylline would not reverse ventilatory depression caused by hypoxia, supporting the suggestion that adenosine contributes to hypoxic ventilatory depression. To confirm the weak adenosine antagonism of enprofylline, L-N6-(phenylisopropyl)adenosine (PIA) was administered to six newborn piglets until respiratory depression was achieved. Either aminophylline or enprofylline was then administered. Aminophylline, but not enprofylline, reversed the respiratory depression caused by PIA. In seven additional piglets, respiratory depression was first produced by 10% oxygen breathing and the ability of saline, aminophylline, and enprofylline to reverse the decrease in ventilation was evaluated. The administration of either saline or enprofylline produced little change in minute ventilation (9.8% +/- 3.7% and -11.7% +/- 7.7%, respectively), whereas aminophylline consistently produced an increase (43.5% +/- 7.3% [P less than 0.001]). Both aminophylline and enprofylline increased heart rate (P less than 0.01), whereas saline produced no significant change. Blood pressure was increased by enprofylline but not by aminophylline or saline. These findings suggest that, in the anesthetized newborn piglet, adenosine contributes to ventilatory depression caused by hypoxia.
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PMID:Effects of adenosine and xanthine derivatives on breathing during acute hypoxia in the anesthetized newborn piglet. 358 54

A 17-year old boy presented with severe, predominantly central sleep apnoeas secondary to structural damage in the medulla. At low O2 saturation, the electroencephalogram showed the sudden onset of slow waves. Hypercapnic ventilatory response was low and hypoxic ventilatory response was absent. Low flow oxygen therapy dramatically improved the apnoea score, probably by relieving hypoxic brain depression. Slow waves also disappeared with oxygen therapy. Aminophylline was effective on apnoea score and duration (p less than 0.001). This beneficial effect could be explained by an improvement of the normal oscillations of respiration at the onset of sleep, a change in arousability or a stimulation of the ascending reticular system. These findings suggest a possible role of hypoxic depression in the manifestations of central sleep apnoeas and demonstrate the beneficial effect of low flow oxygen and aminophylline in treating certain central sleep apnoeas.
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PMID:Effect of aminophylline and relief from hypoxia on central sleep apnoea due to medullary damage. 360 31

The analgesic agent, tramadol, was tested on motor and sensory responses of the nociceptive system in rats. The tail-flick response to radiant heat was dose dependently depressed by tramadol (1-10 mg/kg i.p.), and the antinociceptive effect of the drug was reduced by naloxone in the same range of doses that antagonized the effect of morphine. Tramadol (100 micrograms) microinjected into the periaqueductal grey (PAG) prolonged the tail-flick latency and this effect was abolished by naloxone (0.2 mg/kg i.p.). Aminophylline (25 mg/kg i.p.) did not prevent the antinociceptive effect of tramadol (5 mg/kg i.p.). Tramadol (20 and 40 mg/kg injected i.v.; 100 and 200 micrograms injected intrathecally (i.t.); 100 micrograms injected into the PAG) depressed both the spontaneous activity in ascending axons and their activity due to stimulation of afferent C fibres and co-activation from afferent A delta fibres in the sural nerve. Naloxone injected i.v. at a dose (0.2 mg/kg) that had proven fully effective against the effects of morphine antagonized only the effect on spontaneous activity caused by i.v. injection of tramadol. A high dose of naloxone (1 mg/kg i.v.) not only abolished the depression of spontaneous activity caused by an i.t. injection of tramadol (200 micrograms) but also significantly reduced (but did not abolish) the activity in ascending axons evoked from afferent C fibres while the depression of co-activation from afferent A delta fibres remained unchanged. Aminophylline (50 micrograms i.t.) failed to abolish the depression by tramadol of ascending nociceptive activity. The activity elicited in ascending axons by stimulation of afferent A beta fibres was not changed by i.t. injection of tramadol (200 micrograms), which was evidence that the antinociceptive effect of tramadol is not due to a local anaesthetic action. It is concluded that tramadol produces its antinociceptive and analgesic effects through spinal and supraspinal sites of action. Since the effects of tramadol and morphine differ in some respects, it must be assumed that they are due to binding to different opiate receptors or that some of the effects of tramadol are not mediated by opiate receptors alone.
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PMID:Effects of tramadol on motor and sensory responses of the spinal nociceptive system in the rat. 365 36

1. Dibutyryl cyclic AMP, injected towards the superior cervical ganglion of the cat, produced no consistent responses.2. Imidazole, injected towards the ganglion, regularly produced facilitation, both during intermittent and continuous preganglionic stimulation. This effect was dose-dependent and lasted 2-10 minutes.3. Aminophylline, injected towards the ganglion, regularly produced depression of ganglionic transmission, both during intermittent and continuous preganglionic stimulation. This effect was also dose-dependent and lasted 1-4 minutes. Papaverine produced the same type of response as aminophylline.4. Imidazole potentiated the ganglionic response to 1,1-dimethyl-4-phenylpiperazinium iodide (DMPP), while aminophylline depressed it.5. The results of the present experiments are consistent with the view that cyclic AMP may have a mediating role in the process of ganglionic transmission.
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PMID:The effect of N6-2'-O dibutyryl 3',5' cyclic adenosine monophosphate, imidazole and aminophylline on ganglionic transmission in the superior cervical ganglion of the cat. 436 81

The effect of intrathecal (i.t.) and systemic (i.p. and i.v.) administration of morphine, aminophylline, dibutyryl cyclic adenosine monophosphate (DBcAMP) and dibutyryl cyclic guanosine monophosphate (DBcGMP) on motor and sensory responses of the spinal nociceptive system was studied in rats. Motor responses were assessed in the tail-flick test performed on rats with an intact spinal cord, or as flexor reflex activity elicited in the electromyogram of the tibialis anterior muscle by supramaximal electrical stimulation of the sural nerve in rats in which the spinal cord was transected at the lower thoracic level. The sensory response consisted of activity in single ascending axons of the spinal cord evoked by electrical stimulation of afferent C fibres in spinal rats. Morphine (20 micrograms i.t. or 2 mg/kg i.p.) prolonged the tail-flick latency and aminophylline (25 mg/kg i.p. or 50 micrograms i.t.) prevented the antinociceptive effect of morphine. Aminophylline alone, administered by i.t. injection, reduced the tail-flick latency in a dose-dependent way. Morphine (2 mg/kg i.v. or 10 micrograms i.t.) reduced flexor reflex activity, and this reduction was abolished by aminophylline (25 mg/kg i.v. or 50 micrograms i.t.). Morphine (2 mg/kg i.v.) depressed spontaneous and evoked activity in single ascending axons responding to stimulation of afferent C fibres. This depressant effect of morphine was not abolished by aminophylline (50 micrograms i.t.); the depression was antagonized by naloxone (10 micrograms i.t.). DBcAMP (5 to 100 ng i.t.) dose-dependently prolonged the tail-flick latency. The antinociceptive effect of DBcAMP (50 ng i.t.) was prevented by aminophylline (50 micrograms i.t.) or naloxone (5 micrograms i.t.).(ABSTRACT TRUNCATED AT 250 WORDS)
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PMID:Cyclic nucleotides and aminophylline produce different effects on nociceptive motor and sensory responses in the rat spinal cord. 609 67

The action of aminophylline on anti-nociceptive effects of morphine in rats was tested on the tail-flick response to noxious heat and on the activity evoked in ascending axons of the spinal cord by stimulation of nociceptive afferents. The depression of the tail-flick response produced by an intraperitoneal (i.p.) injection of morphine 2 mg/kg in intact and spinal rats was abolished by an i.p. injection of aminophylline 25 mg/kg. The activity evoked in ascending axons of spinal rats by electrical stimulation of afferent C fibres of the sural nerve was depressed by an intravenous (i.v.) injection of morphine 2 mg/kg. Aminophylline 25 mg/kg injected i.v. after morphine produced a slight and transient increase in the ascending activity immediately after its administration but did not abolish the depressant effect of morphine. Naloxone 0.2 mg/kg administered after aminophylline antagonized the depressant effect of morphine on the ascending activity. It is suggested that morphine exerts its depressant effect on the two nociceptive responses (the motor and the sensory response) by different mechanisms, one being sensitive to aminophylline, the other being relatively resistant to the action of the purine derivative.
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PMID:Aminophylline differentiates between the depressant effects of morphine on the spinal nociceptive reflex and on the spinal ascending activity evoked from afferent C fibres. 616 88

1. The effect of intravenous aminophylline on the contractility of adductor pollicis has been studied in three subjects both in the fresh state and following the induction of muscle fatigue. 2. Aminophylline had no influence on the frequency-force relationship and relaxation rate of adductor pollicis in the fresh state. 3. Fatigue resulted in a selective depression of the force response to low and moderate frequencies of stimulation and a slight effect on maximum force production 10 and 35 min afterwards. 4. Aminophylline given prior to, during and/or after fatigue did not influence this selective low-frequency fatigue at 10 or 35 min. 5. Aminophylline at the concentrations obtained has no significant effect on muscle contractility or fatiguability in man.
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PMID:Aminophylline and fatigue of adductor pollicis in man. 683 38

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

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


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