UMLS:C0011570 - FACTA Search

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Query: UMLS:C0011570 (depression)
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1. The carotid body and the carotid nerve were removed from anaesthetized cats and placed in a small Perspex channel through which Locke solution (at various pH values and usually equilibrated with 50% O(2) in N(2)) was allowed to flow. The glomus was immersed in the flowing solution while the nerve was lifted into oil covering the saline. Sensory discharges were recorded from the nerve and their frequency was used as an index of receptor activity. At times, a small segment of carotid artery, containing pressoreceptor endings, was removed together with the glomus. In this case, pressoreceptor discharges were recorded from the nerve.2. The amplitude of either chemo- or pressoreceptor discharges was not changed by strong acid solutions. Acid decreased the frequency of the baroreceptor discharges only when pH fell to less than 4.0. Solutions at low pH increased the chemosensory discharge, but acid depressed the increased chemoreceptor discharge elicited by KCl. These experiments indicated that H(+) ions probably acted as membrane ;stabilizers' without depolarizing either the nerve fibres or endings.3. Acid solutions increased the action of acetylcholine chloride (AChCl) (100-200 mug) on chemoreceptors. This effect probably was due either to inactivation of tissue cholinesterase or to enhanced sensitivity of the sensory endings to ACh.4. Choline chloride (10(-3)M), which favours ACh synthesis, protected the preparation against decay during prolonged experimentation. Hemicholinium-3 (HC-3), which blocks ACh synthesis in low concentrations (10(-5)M), depressed the chemosensory response to acid and to hypoxia when such stimuli were applied repeatedly. This concentration of HC-3 did not change effects of applied ACh.5. Substances which affect ACh release markedly changed the chemoreceptor discharge increase induced by acidity and other forms of stimulation. In the absence of Ca(2+), acid, anoxia, and interruption of flow provoked receptor depression while receptor excitation induced by ACh and KCl persisted. All stimuli excited and showed increased effectiveness as the Ca(2+) concentration was raised, but their effects declined as Ca(2+) was increased above normal values. Mg(2+) ions depressed the chemoreceptor effects induced by all these stimuli. The action of Mg(2+) was not due entirely to nerve ending block. Morphine sulphate (which decreases ACh release in other structures) also depressed the receptor response to acid and flow interruption.6. Cholinergic blocking agents such as mecamylamine, hexamethonium, atropine, dihydro-beta-erithroidine (DHE), HC-3 (10(-4)M), choline and acetylcholine (in combination with choline) depressed the effects of acid and ACh on the chemoreceptors. The effect induced by interruption of flow was depressed only by mecamylamine and DHE.7. Agents which affect the fate of released ACh, such as acetylcholinesterase and eserine salicylate, did not affect clearly the response of chemoreceptors to acid.8. The results suggest that acid stimulates chemoreceptor fibres through an indirect mechanism, viz. through increased release and/or decreased destruction of a presynaptic transmitter from the glomus cell. This transmitter is probably ACh (see following paper, Eyzaguirre & Zapata, 1968).
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PMID:Pharmacology of pH effects on carotid body chemoreceptors in vitro. 429 75

1. In the unanaesthetized cat, an injection of 0.75 mg of morphine into a lateral cerebral ventricle produced strong hyperglycaemia; on intravenous injection, 10 to 30 times larger doses were required. Other effects produced with both injections were shivering, pupillary dilatation, opening of the eyes, miaowing, periods of excitation, and analgesia. Between the periods of excitation the cat did not react to objects moving in front of its eyes and it had a vacant stare.2. Noradrenaline, adrenaline, and 5-hydroxytryptamine (5-HT) injected intraventricularly (250 mug, twice) depressed the hyperglycaemia due to intraventricular morphine, and noradrenaline also depressed the hyperglycaemia due to intravenous morphine. Adrenaline produced the strongest and 5-HT the weakest depression. 5-HT did not depress the other effects of morphine, but the catecholamines depressed most of them; only analgesia and the vacant stare appeared to be unaffected.3. Reserpine injected intraventricularly (0.5 mg, twice) greatly accentuated the hyperglycaemia as well as the other effects produced by intraventricular morphine, but pupillary dilatation and opening of the eyes no longer occurred; the protrusion of the nictitating membranes produced by the reserpine persisted.4. Pentobarbitone sodium injected intraperitoneally in an anaesthetizing dose practically abolished the morphine hyperglycaemia, but injected intraventricularly in a dose of a few milligrammes, it had a two fold effect: depression followed by enhancement of the morphine hyperglycaemia. The enhancement may be due to sensitization of the effect of the adrenaline released by morphine, since adrenaline hyperglycaemia was enhanced as well.5. Morphine did not seem to act on structures in the walls of either the lateral or third ventricle when producing its hyperglycaemic effect on intraventricular injection. The action may therefore be on more caudally situated parts of the neuro-axis, on the central grey, on structures in the floor of the fourth ventricle or of the lateral recesses, or even on structures near the ventral surface of the brain stem.
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PMID:The hyperglycaemic effect of morphine. 465 65

1. Morphine-like analgesic drugs caused depression of twitches of the isolated guinea-pig ileum in response to transmural electrical stimulation. The drugs tested were the narcotic analgesics codeine, diamorphine, fentanyl, morphine, morphine-N-oxide, normorphine, oxymorphone, pethidine, phenazocine and phenoperidine and the analgesic narcotic antagonists nalorphine and pentazocine.2. With the first application of one of these drugs the extent of depression of twitches was proportional to concentration. Except in the case of pethidine, there was no further depression when additional drug was added to the organ bath. With the second application of a drug after washing out the first dose, the depressant effect was less; that is, tolerance developed. With pethidine, the depression of twitches was proportional to concentration and tolerance could not be observed.3. When tolerance had been produced by cumulative addition of these drugs, a concentration was reached at which further addition resulted in increased activity of the ileum.4. With codeine, morphine and normorphine, the twitches were increased in height and regular.5. With diamorphine, fentanyl, oxymorphone, pentazocine, phenazocine and phenoperidine there were increased but irregular responses to transmural stimulation.6. Having reached the concentration at which these effects were observed, washout of the drug resulted in reduction of activity; the twitches became smaller or the irregular responses ceased.7. Readministration of a drug after activity of the ileum had been depressed by withdrawal of that drug resulted in restoration of activity, the ileum being dependent on the presence of the drug for its activity.8. Codeine and nalorphine did not produce as great an increase in activity on readministration to a dependent ileum as did morphine: they seem to act as partial agonists in producing this effect.9. In similar experiments with the isolated urinary bladder of the rat and guinea-pig, morphine was less active in depressing responses to stimulation than it was on the ileum, and tolerance to the drug and dependence on it did not occur.10. These observations have been discussed in relation to analgesic activity, tolerance and dependence in man.
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PMID:Comparison of effect of morphine-like analgesics on transmurally stimulated guinea-pig ileum. 534 30

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

Methionine-, leucine-enkephalin and beta-endorphin produced dose-related depression followed, not regularly, by stimulation of the spontaneous rhythmic activity of rabbit isolated ileum. The stimulant effect was obtained in one third to one half of the experiments. Naloxone antagonized the depressant, but not the stimulant effects of enkephalins and beta-endorphin. Morphine depressed or stimulated the spontaneous rhythmic activity of rabbit isolated ileum, but only when this narcotic analgesic was used in extremely large amounts. Naloxone had no effect or potentiated the depressant effect, while it potentiated the stimulant effect of morphine. It is apparent, therefore, that only enkephalins and beta-endorphin depressed the spontaneous rhythmic activity of rabbit isolated ileum by acting on enkephalinergic receptors. Further, these results suggest that these enkephalinergic receptors may be involved in the modulation or transmission of spontaneous rhythmic activity of rabbit isolated ileum.
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PMID:[Differences in the action of enkephalins, beta-endorphin, and morphine on spontaneous rhythmic movements of the isolated rabbit ileum]. 609 50

The inhibitory effects of various opiates on developing rat vas deferens were studied by determining the degree of depression of mechanical responses elicited by electrical field stimulation. All agonists showed decreased effects with maturation, but the decrease occurred at different times. With normorphine the loss of agonist activity was greatest at days 12-16, while with D-Met2,Pro5-enkephalinamide it was greatest at days 16-30. beta-Endorphin also was less effective in adult than 30-day preparations, but methionine enkephalin was ineffective at all ages. Morphine and normorphine were weak antagonists of opiate agonists in the adult preparations. These results indicate that the nature and pharmacologic sensitivity of opiate actions change with development.
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PMID:Opioid effects in developing rat vas deferens. 610 Oct 80

The effects of bolus and infusion of ciramadol, dezocine, morphine and pentazocine were examined in anesthetized dogs. Cardiopulmonary parameters, blood PCO2, PO2 and pH and plasma histamine determinations were made. Ciramadol (2 and 8 mg/kg) did not exhibit any major activity. Dezocine produced slight respiratory depression at 2 mg/kg but no cardiopulmonary effects were observed at this dose. At 8 mg/kg there were also reductions in pulmonary compliance (Cdyn) and resistance (RL), tidal volume (VT) and a marked arterial hypotension. Morphine (2 mg/kg) elicited significant effects on all parameters examined: marked bronchoconstriction, increased arterial PCO2 and pH and corresponding decrease in PO2, slight increase in heart rate and dramatic arterial hypotension. Morphine was the only agent studied to elevate plasma histamine. Histamine (0.015 mg/kg) mimicked the cardiopulmonary actions of morphine but was virtually devoid of effect on blood gases and pH. Pentazocine (8 mg/kg) did not produce bronchoconstriction but did increase VT and reduce respiratory frequency. It produced increases in arterial PCO2 and reductions in pH and PO2. There was a slight bradycardia and hypotension within this dose. These results demonstrate that both ciramadol and dezocine possess less potential than either morphine or pentazocine for producing bronchoconstriction, respiratory depression, hypotension and histamine release.
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PMID:A comparison of the cardiorespiratory effects of ciramadol, dezocine, morphine and pentazocine in the anesthetized dog. 611 23

1. Adenosine and its analogs depress the firing of neurons in various brain regions. The primary mode of action of adenosine in exerting this effect appears to be the depression of transmitter release from presynaptic nerve terminals. This is a result of reduced calcium mobilization. 2. Adenosine uptake inhibitors and deaminase inhibitors depress the firing of central neurons. Adenosine antagonists, caffeine and theophylline, excite central neurons. Adenosine is therefore likely to be released in sufficient quantities to exert an ongoing modulation of synaptic transmission in the intact brain. 3. A number of groups of centrally active drugs inhibit adenosine uptake by brain synaptosomal preparations. These include the benzodiazepines, phenothiazines, various other sedatives and hypnotics, tricyclic antidepressants, non-steroidal anti-inflammatory analgesics, some steroids, diphenylhydantoin, puromycin and toyocamycin. 4. It is proposed that many agents with anxiolytic, sedative, analgesic or anti-convulsant actions may achieve their effects by inhibiting adenosine uptake and thus potentiating extracellular adenosine levels. 5. Morphine also elevates extracellular adenosine levels but achieves this by enhancing adenosine release.
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PMID:The effect of various centrally active drugs on adenosine uptake by the central nervous system. 612 37

Saphenous vein rings mounted in organ chambers containing Krebs-Ringer solution were used to determine if the venodilator effects of morphine, nalbuphine, and butorphanol are the result of interference with adrenergic neurotransmission or are caused by direct depressant actions on venous smooth muscle cells. Morphine (5 X 10(-5) M and 2 X 10(-4) M) caused a dose-dependent depression of the contractile response to transmural electrical stimulation. H1- and H2- histamine antagonists did not attenuate the inhibitory effect of morphine. Concentrations of morphine and nalbuphine lower than 5 X 10(-5) M had no effect, whereas 5 X 10(-6) M butorphanol significantly depressed the evoked tension response to electrical stimulation. The contractile responses of the veins to exogenous norepinephrine (NE) were not altered by morphine, indicating a presynaptic site of action rather than a direct action on the venous smooth muscle. Transmural electrical stimulation was used to evoke release of endogenous NE. Morphine (5 X 10(-5) M and 2 X 10(-4) M), nalbuphine (2 X 10(-4) M), and butorphanol (4 X 10(-6) M) significantly decreased release of NE. Naloxone did not alter NE release and did not attenuate the inhibition of NE release observed with the opiates, indicating that the effect of morphine on this neuroeffector junction is not mediated by a naloxone-sensitive opiate receptor. Blockade of presynaptic alpha receptors by phenoxybenzamine or phentolamine augments NE release caused by transmural electrical stimulation; morphine inhibited this augmentation. The results of these experiments indicate that high concentrations of morphine may decrease NE release, an effect that may contribute to the venodilation and hypotension observed following administration of high doses of morphine in humans. In the usual analgesic doses, the venodilatory effects of morphine cannot be explained by local action on either NE release or venous smooth muscle contractility.
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PMID:The effects of morphine, nalbuphine, and butorphanol on adrenergic function in canine saphenous veins. 612 20

It has been proposed that various opiate receptor subtypes mediate different cardiovascular responses to centrally administered opioids. We evaluated this hypothesis in chloralose-urethane anesthetized cats by monitoring the cardiovascular and respiratory responses to relative mu [morphine, morphiceptin, D-Ala2, MePhe4, Gly-ol5 enkephalin (DAGO)] and delta [D-Ala2, D-Leu5enkephalin (DADL)] agonists microinjected (0.5 ul/kg) into the caudal region of the Nucleus of Tractus Solitarius (NTS). Dynorphin (1-13), an endogenous opioid which exhibits selective affinity towards the kappa receptor, was also tested. Dynorphin at a dose of 50 nMol/kg did not alter cardiovascular or respiratory variables. Morphine (10-54 nMol/kg) and DAGO (50 nMol/kg) had no effect on blood pressure, heart rate or respiratory rate; morphiceptin (100-320 nMol/kg) caused tachycardia only at the highest dose. DADL (10-100 nMol/kg) elicited a dose-dependent depression of blood pressure. High doses of DADL depressed heart rate and respiratory rate. The depressor effects of DADL were reversed by low doses of naloxone (0.1 mg/kg). This dose of naloxone also elicited pressor responses in cats treated with the other opioids and reversed the morphiceptin-induced tachycardia. These data indicate that opioid agonists differ with regard to their cardiovascular and respiratory effects following microinjection into the NTS of anesthetized cats, with the delta agonist DADL showing greatest activity.
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PMID:Cardiovascular responses to opioid agonists injected into the nucleus of tractus solitarius of anesthetized cats. 613 54

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