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Query: UMLS:C0011570 (depression)
 172,036 document(s) hit in 31,850,051 MEDLINE articles (0.00 seconds)

Moderate to deep (67-99% single twitch depression) pancuronium-induced neuromuscular blockade was antagonised with neostigmine (30 micrograms/kg, 60 micrograms/kg, or 80 micrograms/kg) in combination with glycopyrronium. Twenty-seven patients were reversed from 91%-99% twitch depression. Recovery of the first twitch of a train-of-four to 95% of control twitch took at least 20 minutes with neostigmine 30 micrograms/kg. The higher doses were significantly faster (60 micrograms/kg p less than 0.05, 80 micrograms/kg p less than 0.01) and took 15.8 and 14.8 minutes respectively. Reversal to a train of four ratio of 0.75 was not consistently achieved in under 30 minutes with any dose of neostigmine. Nineteen patients were antagonised from a 67%-80% depression of first twitch and in all but two recovery to 95% of control took under 10 minutes. To achieve a train of four ratio of 0.75 took less than 12.5 minutes except in three patients, two of whom, both given neostigmine 30 micrograms/kg, took longer than 20 minutes. Neostigmine 60 micrograms/kg produced as rapid a degree of antagonism as 80 micrograms/kg. Heart rates after reversal decreased gradually in all groups, although the decrease was initially greater in the low dose neostigmine (30 micrograms/kg) group. A fixed 5:1 ratio of neostigmine and glycopyrronium will usually antagonise a moderate (70%-80%) pancuronium block to a train of four of greater than 75% within 12.5 minutes if at least 60 micrograms/kg of neostigmine is administered. More than 30 minutes may be required for reversal whatever the dose of neostigmine, for antagonism from greater than 90% twitch depression.
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PMID:Reversal of pancuronium. Neuromuscular and cardiovascular effects of a mixture of neostigmine and glycopyrronium. 340 68

1. Acetylcholine (ACh), other cholinomimetics, cholinesterase inhibitors and cholinergic antagonists were administered iontophoretically to medial geniculate (MG) neurones and their effects on chemically or neurally evoked responses recorded extracellularly.2. Acetylcholine had excitant actions on 45% of the neurones tested. Most of these were of a slow time course. Desensitization to the excitant effects was frequently observed.3. Acetylcholine excited 91% of neurones activated antidromically by stimulation of the auditory cortex, 71% of neurones activated synaptically from the auditory cortex, 74% of neurones activated from the inferior colliculus and 100% of geniculo-cortical relay neurones.4. Acetylcholine had depressant effects, which were generally of a rapid time course, on 29% of MG neurones. No desensitization to the depressant effects was observed.5. On 4% of neurones, ACh had both excitant and depressant effects. Such "dual" effects were manifested either as an initial excitation followed by a depression, or as a depression followed by an excitation.6. Eserine, neostigmine and edrophonium potentiated both excitant and depressant actions of ACh on many cells. Neostigmine and edrophonium occasionally antagonized the effects of ACh.7. Atropine, hyoscine, dihydro-beta-erythroidine, hexamethonium and (+)-tubocurarine antagonized both excitant and depressant effects of ACh. The muscarinic blocking agents were usually more effective than the nicotinic agents.8. Carbamylcholine, acetyl-beta-methylcholine, nicotine, butyrylcholine, arecoline and pilocarpine had excitant, depressant or no effects on MG neurones. Generally, carbamylcholine was more potent than acetyl-beta-methylcholine and ACh, which were more potent than nicotine. Butyrylcholine, arecoline and pilocarpine were even less potent, often having no effect.9. The cholinomimetics generally had similar effects to those of ACh on the same neurones, but sometimes were quite different. Carbamylcholine, acetyl-beta-methylcholine and nicotine antagonized the effects of ACh on some neurones.10. The results suggest that cholinoceptive receptors on MG neurones are not homogeneous. Although there are possibly some purely muscarinic and purely nicotinic receptors, the majority appear to be of intermediate muscarinic-nicotinic type. These mediate either excitation or inhibition.
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PMID:Properties of cholinoceptive neurones in the medial geniculate nucleus. 541 82

Sucrose gap recording technique was employed to record surface potentials from superior cervical ganglia (SCGs) of several species. Repetitive preganglionic stimulation (30 Hz, 1-2 sec) elicited in curarized rabbit, rat and cat SCGs, a biphasic response as the initial slow positive (P) potential, was followed by a late negative (LN) potential. In curarized guinea-pig SCG, a LN response with no detectable P potential was observed. Neostigmine (0.5-1 microM) increased the amplitude and duration of the P and LN responses in the majority of the rabbit, rat and cat SCGs. LN response of guinea-pig SCG was first enhanced by neostigmine; subsequently, it was converted into a hyperpolarizing potential. Alpha receptor antagonists, phenoxybenzamine, phentolamine and dihydroergotamine, and a beta receptor antagonist, propranolol, did not appreciably alter the P and LN responses of the rabbit, cat and rat SCG or neostigmine-induced hyperpolarization of the guinea-pig SCG. Dopaminergic receptor antagonists, haloperidol, chlorpromazine and metoclopramide, caused no significant depression of the P and LN responses in the rabbit SCG. Atropine (1 microM) consistently abolished the P and/or LN of all these ganglia, as well as the neostigmine-induced hyperpolarization of the guinea-pig SCG. These results demonstrate that muscarinic receptors are involved in the generation of P and LN potentials of mammalian sympathetic ganglia, while the adrenergic and disynaptic nature of P response remains to be clarified. Furthermore, there appears to be no correlation between the generation of P potential and elevation of cyclic AMP in the SCG.
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PMID:A comparative study of the pharmacological properties of the positive potential recorded from the superior cervical ganglia of several species. 610 60

1 Physostigmine (0.1-1 mM) induced dose-dependent negative and neostigmine (0.1-1 mM) positive inotropic effects on driven guinea-pig isolated atria. Physostigmine decreased and neostigmine increased cardiac frequency of spontaneously beating atria. 2 The depression of amplitude of contraction by physostigmine cannot be attributed to its inhibitory effect on tissue cholinesterase. The negative inotropic action of physostigmine is not influenced by preincubation with atropine. 3 The positive inotropic effect of neostigmine is not caused by a nicotine-like action of the drug. Neostigmine (1 mM) counteracts the negative inotropic effect of acetylcholine. The possible mechanisms of action are discussed.
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PMID:The inotropic and chronotropic effects of physostigmine and neostigmine on guinea-pig isolated atria. 711 61

The influence of physostigmine was studied on the effect of morphine on the cardiovascular and respiratory systems in conscious rabbits. Morphine (4 mg/kg i.v.) caused analgesia, bradycardia, hypotension and respiratory depression, as indicated by a fall in respiratory rate of 50%, a rise in blood PaCO2 from 25.1 to 37.2 mm Hg and a fall in pH from 7.40 to 7.24. These effects lasted 2 to 3 hr and were completely antagonized by naloxone. Physostigmine (2.5 or 5 microgram/kg/min) given by constant i.v. infusion did not significantly alter blood pressure or heart rate, but decreased blood PaCO2 from 25.1 to 19 mm Hg and increased pH from 7.40 to 7.46. Pretreatment of rabbits with physostigmine (5 microgram/kg/min) completely prevented both the fall in blood pressure and blood pH and the rise in PaCO2 induced by morphine (4 mg/kg) and also significantly reduced both the intensity and duration of bradycardia. Analgesics activity of morphine remained unimpaired by physostigmine. Neostigmine (2.5 microgram/kg/min) potentiated the bradycardia induced by morphine and did not antagonize its hypotensive and respiratory depressant effects. The results support the hypothesis that the respiratory and cardiovascular depressant effects of morphine, but not the analgesia, results from an inhibition of acetylcholine release from neurons in the central nervous system.
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PMID:Antagonism of the cardiovascular and respiratory depressant effects of morphine in the conscious rabbit by physostigmine. 725 49

The tetanic and single twitch responses of the adductor pollicis muscle were used to study the neuromuscular effects of neostigmine in 26 patients anaesthetized with thiopentone and nitrous oxide. Neostigmine 2.5 mg i.v. given 5 min after exposure to halothane antagonized non-depolarizing neuromuscular block, whereas a second dose give 2-5 min later depressed the peak tetanic contraction and re-established tetanic fade. In the absence of halothane the second dose of neostigmine had less effect. Recovery of the single twitch was not impaired by the second dose. A single dose of neostigmine 5 mg rapidly antagonized the competitive block of the tetanic response but the subsequent slight depression of the peak contraction and the brief reappearance of fade were less than after 5 mg given in two doses of 2.5 mg. In patients who were not given neuromuscular blocking drugs, one or two injections of neostigmine 2.5 mg caused a substantial reduction in the peak tetanic contraction and severe tetanic fade which persisted for about 20 min; the single twitch was slightly potentiated. The neostigmine block of the tetanic response could be antagonized by gallamine and potentiated by suxamethonium. These findings indicate that neostigmine in clinical doses can produce an acetylcholine-induced block which be a potential hazard in anaesthetic practice.
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PMID:Neuromuscular blockade by neostigmine in anaesthetized man. 737 32

The ability of physostigmine to antagonize the respiratory depressant effect of morphine was studied in conscious rabbits and ketamine-anaesthetized dogs pretreated with atropine methyl nitrate. Morphine 4 mg kg-1 increased PaCO2 in the rabbit from 3.43 +/- 0.16 to 4.95 +/- 0.28 kPa, decreased arterial pH from 7.45 +/- 0.01 to 7.31 +/- 0.01 and decreased respiratory frequency by 36%. Physostigmine 0.1 mg kg-1 reduced PaCO2 to control values within 10 min and significantly increased arterial pH and respiratory frequency. There was no antagonism of the analgesic effect of morphine. Neostigmine 0.1 mg kg-1 did not reverse the respiratory depressant effect of morphine. In dogs anaesthetized with ketamine, morphine 15 mg kg-1 caused loss of consciousness and marked analgesia, decreased the respiratory frequency by 47%, and increased PaCO2 by 47%. Physostigmine 0.1 mg kg-1 antagonized the effect of morphine on respiration and restored consciousness in the dogs, but did not impair analgesia. It is concluded that physostigmine reverses morphine-induced respiratory depression by prolonging the effect of acetylcholine released from brain-stem neurones. The possibility should be considered of replacing opiate antagonists by physostigmine to reverse postoperative respiratory depression and drowsiness induced by opiates.
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PMID:Physostigmine antagonizes morphine-induced respiratory depression but not analgesia in dogs and rabbits. 744 96

Dantrolene sodium, a muscle relaxant, does not have a clinically useful antagonist. The present study was undertaken to test the efficacies of germine monoacetate, 4-aminopyridine, neostigmine, and calcium chloride as possible agents for the reversal of the direct skeletal muscle depression produced by dantrolene sodium in the cat anesthetized with alpha-chloralose. Depression of the indirectly elicited twitch responses (0.1 Hz) of the tibialis anterior muscle by 25, 50, 75 and 84 per cent was produced by dantrolene, 0.16, 0.36, 0.88 and 1.13 mg/kg respectively; spontaneous recovery of twitch tension during the subsequent 30 min was negligible. After the 30-min observation period had elapsed, one of the reversal agents under study was given (iv) in divided doses at intervals of 10 min (five cats for each agent). Germine monoacetate (2 X 0.5 mg/kg) immediately reversed the dantrolene-induced twitch depression, with an over-shoot that persisted for an hour. 4-Aminopyridine (4 X 0.5 mg/kg) caused a steady but incomplete reversal to 17 per cent depression, 30 min after the last dose. Neostigmine (4 X 0.04 mg/kg) caused an immediate, but transient, reversal of the twitch depression, with overshoot. Calcium chloride (4 X 10 mg/kg) was without effect. It is concluded that germine monoacetate is the drug of choice for reversal of the muscle depression produced by dantrolene sodium in the cat.
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PMID:Reversal of dantrolene sodium-induced depression of skeletal muscle in the cat. 745 84

In modern anaesthesia various antagonists are used. They provide efficient tools to facilitate better control of pharmacological effects and side effects of drugs routinely used in anaesthesia. Naloxone is a competitive antagonist of opioids without any intrinsic activity. It counteracts respiratory depression, pruritus, sedation and analgesia caused by opioids. It is fast-acting with a duration of action of 45 to 90 min. Several investigators have reported severe side effects of naloxone including hypertension, tachyarrhythmias, left heart failure and cardiac arrest, and hence the use of naloxone must be carefully considered in every single patient. Flumazenil is a competitive antagonist of benzodiazepines. It is a remarkably safe drug and very effective to terminate all benzodiazepine effects in anaesthesia and intensive-care patients. Serious complications caused by flumazenil have been reported in patients receiving benzodiazepines in the treatment of seizure disorders and in patients with mixed intoxications. Neostigmine is one of several antagonists of neuromuscular blocking agents. Its side effects include bradycardia, increased bronchial secretions and increased peristalsis. Indication depends on the results of neuromuscular monitoring. Physostigmine is an unspecific antagonist of the central anticholinergic syndrome, an acute psychosis that may be caused by numerous drugs used in anaesthesia. Generally, antagonists should be carefully titrated. In emergency medicine the use of these antagonists is not recommended; the primary goal is to restore vital functions.
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PMID:[Antagonists in anesthesia]. 854 33

The effects of two calcium channel blockers (verapamil and nicardipine) on indirectly elicited muscle twitch and possible interactions between these drugs and non-depolarising muscle relaxants (vecuronium, atracurium, pancuronium) were investigated using isolated rat phrenic nerve-hemidiaphragm preparations. Both verapamil 10(-5) M and nicardipine 10(-6) M caused significant depression of twitch amplitude. Verapamil significantly increased vecuronium- and atracurium-induced neuromuscular block, but not that produced by pancuronium. Nicardipine potentiated atracurium-induced neuromuscular block but had no effect on pancuronium- and vecuronium-induced twitch depression. Neostigmine 10(-6) M did not produce any significant changes in the maximal recovery of twitch depression induced with calcium channel blockers and muscle relaxants combinations; also, neostigmine had no effect on maximal recovery time of twitch depression.
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PMID:Interactions of calcium channel blockers with non-depolarising muscle relaxants in vitro. 877 69


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