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)

Effective resuscitation of the newborn requires knowledge of the cause of depression. Four major causes are trauma, asphyxia, medication, and malformation. More than one of these may contribute to depression in a single infant. The first principles of resuscitation are to avoid cooling the infant and to establish an airway. Infants with an Apgar score of 3 to 4 at one minute usually need bag-and-mask ventilation, while those with scores of 0 to 2 require immediate ventilation, preferably by means of endotracheal intubation. Severely depressed infants may also require chemical resuscitation and closed cardiac massage. Fetal depression caused by narcotic analgesics given to the mother can be reversed with the use of naloxone hydrochloride (Narcan). Infants asphyxiated on the basis of malformations may benefit from expeditious diagnostic and therapeutic procedures performed in the delivery room.
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PMID:Resuscitation of the newborn. 55 8

A study was undertaken to determine the effect in man of naloxone on the central nervous system depression produced by IV thiopental. Eight normal volunteers were given 5 mg/kg thiopental IV. On a separate occasion the same 8 volunteers were given 50 microgram/kg naloxone IV 5 minutes prior to 5 mg/kg thiopental. Naloxone had no significant effect on the rate of return of consciousness following administration of thiopental. Naloxone also had no significant effect on the responses of blood pressure, heart rate, or respiratory rate to thiopental.
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PMID:Naloxone fails to antagonize thiopental anesthesia. 56 25

Morphine, levorphanol, dextrorphan and naloxone were applied microelectrophoretically to cells identified as either having nociceptive inputs or non-nociceptive inputs in the dorsal horn of the cat. Morphine excited non-nociceptive cells and depressed nociceptive cells. Naloxone reversed morphine excitations on non-nociceptive cells, but only reversed about one-third of morphine depressions on nociceptive cells. Levorphanol depressed nociceptive cells, whilst dextrophan ejected with similar currents caused less depression or had no effect. It is concluded that excitation of non-nociceptive cells may constitute a spinal action relevant to the analgesic action of opiates, acting synergistically with a depressant effect on nociceptive neurones.
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PMID:Differential excitatory and inhibitory effects of opiates on non-nociceptive and nociceptive neurones in the spinal cord of the cat. 63 89

The postoperative respiratory depressant effect of fentanyl in combination with flunitrazepam (Rohypnol) was assessed in awake and in unconscious patients. In awake patients respiratory function was measured with blood-gas analyses. For measurements in unconscious patients the administration of nitrous oxide/oxygen was continued postoperatively and the respiratory depression was judged from the increase in respiratory minute volume after the i.v. administration of 0.05 mg naloxone (Narcan). In the group of awake patients blood-gasvalues were within the normal range after anaesthesia with flunitrazepam (1 mg) and fentanyl (0.80 mcg/kg body weight/10 min anaesthesia; last fentanyl given 40 min before the end of the operation), and the administration of naloxone was without any effect. If, however, naloxone was given while the patients were kept under light nitrous oxide/oxygen anaesthesia, the effect was different. The respiratory minute volume was considerably less than its predicted value in all groups of patients having received fentanyl, and naloxone caused a marked increase in respiratory minute volume and in respiratory rate. In a group of patients which have received no opiate but enflurane, naloxone showed no effect. After premedication with pethidine as compared with flunitrazepam the effect of naloxone on ventilation was more pronounced. This marked difference in the postoperative effect of fentanyl on ventilation depending on the state of consciousness has to be attributed to an interaction between a residual respiratory depressant effect of fentanyl and the effect of unconsciousness. Since after the combined use of flunitrazepam and fentanyl deep postoperative sleep occurs quite frequent, a residual effect of fentanyl should always be antagonized with naloxone to protect the patients from a possible hazardous effect of this interaction.
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PMID:[Respiratory depression after fentanyl and antagonism by naloxone (author's transl)]. 67 31

After administration of fentanyl, 0.15 mg naloxone or levallorphan or placebo were given several times and in increased doses and at same intervals of time to six volunteers. The experiment has been done after the rules of a double blind study. Naloxone has shown its superiority to levallorphan. The study demonstrated a faster and better action of naloxone in the way of a return to initial conditions of respiratory frequency, blood gases, and EEG. The concentration and attention faculties after naloxone have become clearly better in contrary to the results after levallorphan. At the end of an anaesthetic procedure, the greatest care should be given to the patient. First of all effective antagonism of the respiratory depression should be obtained without concomitant sedative and psychomimetic effects. The use of antagonists with agonist properties to reverse respiratory depression due to a morphinomimetic drug is not justified and so naloxone should supplant levallorphan.
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PMID:[The effect of naloxone and levallorphane following fentanyl on the blood gases, EEG and psychodiagnostic tests (author's transl)]. 67 33

In five volunteers the sensitivity of the respiratory centre to carbon dioxide after naloxone and nalorphine injections was studied using "double blind" method and increments of doses. Alterations in the respiratory centre sensitivity were reflected by changes in respiratory minute volume, which was measured before and after drug injections, as well as after carbon dioxide stimulation. Comparison of results and their statistical verification showed that nalorphine alone causes respiratory depression and carbon dioxide stimulation is, beside the weak initial action, almost ineffective. Naloxone causes very small, if at all, respiratory depression and the respiratory centre answers efficiently to carbon dioxide stimulation.
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PMID:The sensitivity of the respiratory center and some circulatory and subjective responses after nalorphine and naloxone injections. 77 23

74 patients, undergoing gynaecological operations under neuroleptanesthesia were subdivided into 4 groups, each receiving Naloxone in different doses postoperatively. For a longer period of time tidal volume, respiratory rate, minute ventilation, blood gas volues and pain index were recorded. From the results one can conclude that 0.1-0.2 mg Naloxone i.v. seems to be the most effective dose to reverse opiate-induced respiratory depression. The initial i.v. dose should be followed by an i.m. dose of 0.2 mg, if required.
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PMID:[Changes of the blood gases following the application of naloxon (author's transl)]. 84 13

A consecutive series of 273 anaesthetics is presented. All patients were given moderate doses of droperidol and fentanyl intravenously to supplement nitrous oxide and oxygen anaesthesia. 28.6% of the patients needed reversal of the analgesic respiratory depressant effect at the end of anaesthesia to establish stable spontaneous respiration. The opiate antagonist, naloxone hydrochloride (Narcan), was found to give rapid and reliable reversal of the respiratory depression. A mean dose of 2 mug/kg body weight of naloxone was found adequate in that no patient required further doses in the post-operative period in order to maintain adequate ventilation. Neither does the dose seem to have been too large. Patients in the naloxone group had no need for additional analgesics during the first 5 3/4 hours postoperatively, as compared to the painfree interval of 3 1/4 hours in the control group.
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PMID:Postanaesthetic use of naloxone hydrochloride after moderate doses of fentanyl. 96 33

1 Intracellular recordings were made from smooth muscle cells of the mouse vas deferens. Excitatory junction potentials (e.j.ps) were evoked by stimulation of the intramural nerves. 2 Normorphine (50 nM-5muM) depressed the amplitude of the e.j.p. The ED50 was 430 nM. The latency of the e.j.p. and the resting membrane potential of the smooth muscle cells were unaffected by normorphine. 3 The depression of the e.j.p. by narcotic analgesic drugs was stereospecific. 4 Naloxone (100 nM) completely reversed the depression of the e.j.p. produced by normorphine (1 muM). Naloxone (100 nM) alone did not alter the amplitude of the e.j.p. 5 Normorphine (1 muM) did not prevent the depolarization of the smooth muscle cells produced by exogenous noradrenaline (10 muM). 6 It is concluded that narcotic analgesic drugs act directly upon the transmitter release sites to reduce the amount of noradrenaline liberated by each nerve impulse.
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PMID:Depression by morphine of excitatory junction potentials in the vas deferens of the mouse. 97 15

The effect of microelectrophoretically and systemically applied opiates on neuronal discharge activity in the sensorimotor cortex of naive and morphine tolerant/dependent rats has been studied. In naive rats depression of spontaneous discharge activity was the predominant effect of low doses of phoretically applied morphine. Higher doses and repeated application frequently converted this effect into excitation. Only the depressant effect was antagonised by naloxone. Naloxone itself had no effect on spontaneous discharge activity when applied at dose-levels sufficient to antagonise the depressant effect of morphine. Levorphanol mimicked the action of morphine whereas dextrorphan was inactive. Morphine depressed the excitatory action of L-glutamate and of acetylcholine by a naloxone-antagonisable mechanism. Systemic application of Fentanyl mimicked the inhibitory effect of phoretically applied morphine upon transcallosally evoked discharge activity. The late response was markedly depressed whereas the primary response was little affected. Phoretically applied naloxone antagonised the effects of systemically applied Fentanyl. In chronically morphinised rats the depressant effect of microelectrophoretically administered morphine was almost lacking and a naloxone-resistant excitation became the predominant effect. In these animals the excitant effect of naloxone was also increased and the anti-glutamate effect and the anti-acetylcholine effect of morphine was abolished. The present data speak in favour of a postsynaptically located stereospecific receptor which mediates the inhibitory effects of opiates and which may be involved in the development of acute and chronic tolerance to these drugs.
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PMID:Actions of opiates upon single unit activity in the cortex of naive and tolerant rats. 98 31


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