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)

Naloxone was used in 20 patients divided into two series: series A consisted of 10 adults with an average age of 50.6 years (+/- 12.03) and series B 10 children with an average age of 8.5 years (+/- 5.16). Naloxone was given in the treatment of postoperative respiratory depression related to persistence of morphine impregnation, the patients having received either fentanyl (mean dose 0.04 mg/kg/h) or dextromoramide (mean dose 1.15 mg/kg/h). The mean dose of naloxone was 0.26 mg +/- 0.10, i.e. 3.9 microgram/kg in series A, and 0.13 mg +/- 0.11, i.e. 5.3 microgram/kg in series B. In both series, study of ventilatory function showed correction and stabilisation of the various parameters (F/min, Vt and V) up to 180 minutes after the injection. Recovery was rapid in both groups (7 to 10 min) and of good quality. Whilst it was accompanied in a number of cases by the recurrence of pain, the latter never required specific relief. The administration of naloxone was associated with an increase in heart rate (non-significant) at 10 min in series A and 30 min in series B. Apart an episode of nausea in one case of series A, no disagreeable side effects were observed.
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PMID:[The use of naloxone in neuroleptoanalgesia]. 2 36

The object of this study was the use of naloxone to correct hypoventilation related to the use of morphinomimetics without suppressing the analgesic effect of these agents. The study involved ten patients undergoing gynaecological surgery under neuroleptanalgesia and who at the end of surgery had hypoventilation due to the use of fentanyl (average dose : 4.87 microgram/kg/h) or phenoperidine (average dose : 48.7 microgram/kg/h). Naloxone was administered intravenously in an average dose of 1.37 microgram/kg (in one or two injections) followed by an intramuscular injection of an average of 0.73 microgram/kg. Under these conditions, respiratory depression was completely corrected in all cases, the effect being durable. Good analgesia was retained and there was a normal return to consciousness without undesirable effects.
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PMID:[Antagonistic effects of naloxone against morphinomimetic agents. Apropos of 10 cases in gynecologic surgery]. 2 37

The effectiveness of naloxone and doxapram in reversing the respiratory depressant actions of fentanyl and droperidol in the rabbit has been examined. Both drugs did not reverse fully the depression of respiratory frequency produced by the neuroleptanalgesic agents. Doxapram also failed to reverse fully the depression of minute volume produced by fentanyl and droperidol, although naloxone was adequate in this respect. However, analysis of arterialized venous blood showed that both naloxone and doxapram not only prevented the increase in PCO2 caused by fentanyl and droperidol, but caused also a significant decrease. A reduction in PCO2 was seen also when either naloxone or doxapram was given to untreated rabbits. With doxapram this appeared to be a result of pure respiratory stimulation. Naloxone also produced a reduction in standard bicarbonate.
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PMID:A study of naloxone and doxapram as agents for the reversal of neuroleptanalgesic respiratory depression in the conscious rabbit. 3 Apr 67

Naloxone has been accepted as a potent antagonist towards several narcotic analgesics, e.g. morphine, heroin and pethidin. Its effect as an antagonist and its potency against ketobemidone have not been tested in man. We have described the antagonistic effect of naloxone towards the respiratory depression caused by the administration of ketobemidone to patients anesthetized with N2O/O2 and methohexitone.
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PMID:Naloxone: a potent ketobemidone antagonist in man. 4 Mar 93

The influence of serotonergic system on the changes in locomotor activity of mice and rats brought about by morphine, fentanyl, codeine and pentazocine and on morphine induced catalepsy in rats was studied. p-Chlorophenylalanine (pCPA) did not affect the behavioral changes produced in mice by morphine, fentanyl, codeine and pentazocine but reduced the behavioral depression produced by these drugs in rats. 5-Hydroxytryptophan (5-HTP) but not tryptophan (TP) reversed the action of pCPA on the effect of morphine and fentanyl. After reserpine the depression produced in rats by morphine and fentanyl was more pronounced. TP did not change the depression produced by combination of reserpine and morphine but counteracted the depression observed after combination of reserpine and fentanyl. In mice reserpine protected against hypermotility produced by morphine or fentanyl and TP potentiated the depression produced by the combination of reserpine and morphine or reserpine and fentanyl. Serotonin precursors, 5-HTP and TP evidently potentiated the morphine induced catalepsy. pCPA counteracted only the enhancement of the catalepsy observed after TP administration. Naloxone abolished the catalepsy after combined treatment with morphine and TP. Similarly but weaker acted cyproheptadine. The results suggest that the serotonin system plays a role in the effects of morphine and fentanyl on rat locomotor activity. An increase in the cerebral serotonin level increases the morphine catalepsy in rats.
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PMID:Central action of narcotic analgesics. V. Participation of serotonin in the mechanism of action of narcotic analgesics. 4 45

Behavioral effects and blood or plasma levels of d-amphetamine, ethanol, cocaine, and diazepam were examined in rhesus monkeys treated chronically with alpha-l-acetylmethadol (LAAM), methadone, or vehicle. Chronic treatment with the opiates failed to alter blood or plasma levels and behavioral effects of d-amphetamine or ethanol. LAAM-maintained monkeys were somewhat less sensitive to rate-decreasing effects of cocaine on schedule-controlled responding, but cocaine plasma levels and half-lives generally did not differ across the chronic treatment conditions. Behavioral depression after diazepam was prolonged substantially in LAAM- and methadone-maintained monkeys, but blood levels of diazepam and metabolites were not increased prolonged in those animals. Naloxone partially antagonized the residual depression LAAM- and methadone-maintained monkeys 24 hr after diazepam, but had no effect on the weaker sesidual depression in vehicle-maintained aniamals. Thus, diazepam appeared to interfere with the metabolic inactivation of the opiates. One LAAM-maintained monkey showed recurrent episodes of LAAM overdose and eventually died during the course of the study.
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PMID:Interactions of acetylmethadol or methadone with other drugs in rhesus monkeys. 10 65

The pesticide chlordimeform (CDM) depressed the electrically-induced twitch responses of the guinea pig longitudinal muscle ED50 = 3 X 10(-5)M). Naloxone reversed twitch depression induced by morphine but not by CDM. Phentolamine reversed twitch depression induced by either norepinephrine or clonidine, but not by CDM. PGE2 completely reversed twitch depression induced by either CDM or indomethacin, but only partially reversed twitch depression induced by lidocaine. The actions of CDM best resemble those of the nonsteroidal anti-inflammatory agents. The reversibility of the CDM depression by washing indicates that the guinea pig ileal preparation is a convenient screen for distinguishing reversible from irreversible inhibitors of prostaglandin biosynthesis.
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PMID:Reversible depression of electrically-induced contractions of guinea pig longitudinal muscle by a reversible inhibitor of prostaglandin synthetase. 12 9

Narcotic analgesics and related drugs act as agonists on several receptors that are responsible for their effects on pain perception, mood and feeling state, and respiration, as well as other pharmacologic actions. Naloxone is the first discovered antagonist that is devoid of agonistic activity and appears to be a competitive antagonist at several receptors. The ability of naloxone to displace or prevent the binding of agonistic narcotics is partly responsible for its antagonistic effects. The ability of naloxone to rectify narcotic-depressed homeostats and precipitate abstinence is also related to its antagonistic activity. Certain cautions and principles apply in the use of naloxone in treating narcotic overdose, reversing surgical analgesia, and the treatment of neonates and children. Unapproved uses of naloxine include reversing the psychotomimetic effects of certain agonists-antagonists, terminating narcotic-induced convulsions and coma, reversing non-narcotic depression, diagnosing physical dependence, and treating narcotic addicts.
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PMID:Naloxone. 18 95

The vast majority of morphine-sensitive single units in the area examined were localized to the locus coeruleus. This corresponds well with the known distribution of the highest densities of opiate receptor sites in this region of the midbrain. The effect of iontophoretically applied morphine was a marked and prolonged depression of spontaneous activity. Levorphanol, an opiate agonist, produced an effect similar to that of morphine while comparable doses of dextrorphan, it's clinically inactive stereoisomer, did not. Naloxone and levallorphan prevented as well as reversed the depression due to application of agonists. While the units were depressed following the application of opiate agonists, the cells were still excited by the neurotransmitter acetylcholine. We conclude that (1) neuronal sensitivity to opiates has a high positive correlation with autoradiographically determined opiate receptor sites, and (2) this sensitivity to opiates is blocked by opiate antagonists and is stereospecific in nature.
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PMID:Iontophoretic application of opiates to the locus coeruleus. 19 Nov 43

1 In spinal cats anaesthetized with alpha-chloralose, a study was made of the effects of morphine and naloxone, administered electrophoretically from micropipettes, on the responses of dorsal horn neurones to noxious (raising of skin temperature above 45 degrees C) and innocuous (deflection of hairs) peripheral stimuli.2 Administered near cell bodies, morphine reduced the nociceptive responses of only 2 of 37 cells. Excitation occurred more commonly than depression and abnormalities in action potentials were commonly observed following ejection of morphine. None of these effects of morphine was antagonized by electrophoretically applied naloxone.3 Administered in the substantia gelatinosa from one micropipette while recording responses of deeper neurones with a second micropipette, morphine reduced the nociceptive responses of 15 of 19 neurones. Firing in response to deflection of hairs was not reduced by morphine. Depression of nociceptive responses by morphine was long lasting (>20 minutes). Naloxone ejected into the substantia gelatinosa or given intravenously in doses as low as 0.1 mg/kg antagonized the effects of morphine. The effectiveness of this dose of intravenous naloxone suggests that the concentrations of morphine in the substantia gelatinosa which reduced nociceptive responses were not unlike those present after analgesic doses of systemic morphine. Naloxone alone, and excitant and depressant amino acids ejected into the substantia gelatinosa had little effect on cell firing.4 Both the selective action of morphine on nociceptive responses and the reversal of this action by intravenous naloxone suggest that the opiate receptor present in the substantia gelatinosa is relevant to analgesia produced by opiates given systemically.
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PMID:Suppression of transmission of nociceptive impulses by morphine: selective effects of morphine administered in the region of the substantia gelatinosa. 19 11


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