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Query: UMLS:C0030193 (pain)
 261,466 document(s) hit in 31,850,051 MEDLINE articles (0.00 seconds)

Lorazepam, a new benzodiazepine, was compared with morphine for premedication. Ten patients received morphine 10 mg/70 kg i.m. and 10 received lorazepam 4 mg/70 kg i.m. Respiratory effects were assessed from the change in slope (S) and intercept (B) of the carbon dioxide response line, using a development of Read's rebreathing method. Morphine depressed S by 47% (P less than 0.01), but after lorazepam S increased by 27% (P less than 0.05), neither drug altering B significantly. In two volunteers lorazepam was assessed by both the rebreathing and the steady-state methods; after lorazepam S was smaller by the steady-state than by the rebreathing technique. The findings for lorazepam are consistent with the known effects of sleep on carbon dioxide sensitivity. Amnesia lasting 4-8 h occurred in all patients who received lorazepam so that pain and nausea during this period were not recalled, but no patient who received morphine experienced amnesia. We conclude that lorazepam merits further study, particularly where sedation without respiratory depression is needed, as in obstetrics, and where amnesia for uncomfortable procedures is required.
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PMID:Respiratory effects and amnesia after premedication with morphine or lorazepam. 1 25

Prostaglandin E1 (PGE1), prostaglandin E2 (PGE2) and arachidonic acid have been demonstrated to potentiate the peritoneal writhing response in the mouse induced by benzoquinone. The resultant dose-response relationships were bell shaped with a maximum activity of 10 ng/kg i.p. of potentiating agent. Floctafenine, indometacin and acetylsalicylic acid (ASA) blocked the potentiation induced by arachidonic acid but not that induced by PGE2. This suggests that it is prostaglandin that causes the potentiation and that the mechanism of action of ASA-like drugs against hyperalgesia associated with inflammation is blockade of prostaglandin synthesis. Morphine reduced the potentiation by PGE2 and arachidonic acid but the bell shaped hyperalgesia was still evident using both agonists. These results indicate that morphine does not inhibit prostaglandin synthetase but may modify the effect of prostaglandin. This method may be useful to distinguish between ASA-like and morphine-like analgesic compounds using a pain response in vivo.
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PMID:Hyperalgesia after treatment of mice with prostaglandins and arachidonic acid and its antagonism by anti-inflammatory-analgesic compounds. 31 5

In chronic experiments on rats it was established that electric stimulation of certain areas of the midbrain depresses pain reactions of different genesis. Morphine in subanalgetic doses (2--2.5 mg/kg) reveals and potentiates the antinociceptive effect of central stimulation shown first of all by depression of the complex highly integrated components of an emotionally behavioral conductive reaction to pain.
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PMID:[Change in the antinociceptive effect occurring in stimulation of the rat midbrain under the influence of morphine]. 44 1

The effect of immunization of rats with the conjugated antigen morphine-bovine serum albumin synthetized by the authors on the analgetic activity of morphine hydrochloride has been investigated. Morphine binding antibodies were shown to appear in the blood of rats during immunization. The spleen demonstrated mononuclear cells also capable of morphine binding. It has been established that immunization of rats with the above synthetic antigen makes them tolerate the pharmacological effects of the narcotic. Morphine at a dose of 5 mg/kg is not capable of inducing an inherent increase in the threshold of pain sensitivity in immunized rats. Immunization also slightly diminishes the morphine effect at a dose of 20 mg/kg on the EEC. Prolonged daily administration of morphine does not remove morphine tolerance due to immunization.
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PMID:[Attenuation of the action of morphine in rats immunized with a conjugated morphine-protein antigen]. 49 68

The relationship between stimulus intensity and analgesic effectiveness of morphine was investigated by means of an operant technique. Various doses of morphine were tested in rats trained to press a bar to escape from shocks of varying intensity. Under control conditions a good linear relationship between the log of the stimulus intensity and the log of the speed to press the lever was found. Morphine showed inhibitory effects upon this escape behavior, which were greater at any given dose with greater intensity of the shock. These effects were dose related, that is, the slopes of the shock-response lines decreased by increasing the dose. The data obtained do not appear to be a consequence of a general depressant effect of the drug upon behavior and are in line with several experimental observations showing that in animals, as well as in humans, the magnitude of the analgesic effect of morphine tends to increase as pain severity increases.
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PMID:Stimulus-response relationships in a quickly learned escape from shock: effects of morphine. 50 95

Morphine sulphate 2 to 4 mg was given by epidural injection for analgesia in eleven patients whose pain was ischaemic, traumatic or post-operative. Excellent analgesia was obtained in ten of the eleven patients without significant side effects. This technique appears to offer relief in post-operative and other types of severe pain and has been continued for up to five days.
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PMID:Epidural analgesia with morphine a preliminary communcation. 52 63

It was established in chronic experiments on rats that electric acupuncture of the acupuncture point noticeably decreases pain reaction to electric stimulation of the tail. Morphine given in a subanalgetic dose (5 mg/kg) potentiated acupuncture analgesia, while 5 mg/kg of naloxone completely abolished it. Potential mechanisms of analgesia realization during electric acupuncture are discussed.
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PMID:[Acupuncture analgesia in rats and its changes under the effect of morphine and naloxone]. 54 Jan 43

Experiments were performed to evaluate the effects on the levels of aspartate, GABA and glutamate in the periaqueductal central gray matter, hypothalamus, midbrain reticular formation and cortex of mouse brain following various treatments. The results indicate that only glutamate among the 3 neurohumors is systematically altered relative to the experimental manipulations. Moreover, among the 4 brain areas examined, the data implicate only the periaqueductal central gray matter as a locus of morphine's antinociceptive action. Morphine also appears to produce a drug-specific effect in hypothalamus which, however, is not analgesia-related. There were no significant pain, stress or drug-related effects on the levels of glutamate in either the midbrain reticular formation or the cortex.
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PMID:Morphine and pain: effects on aspartate, GABA and glutamate in four discrete areas of mouse brain. 93 43

In protriptyline (25 mg/kg) pretreated rats stereotactic 5,7-dihydroxytryptamine (5,7-DHT) lesions of the medial plus laternal 5-hydroxytryptamine (5-HE) bundles in the mesencephalon increased the 5-HT fluorescence in these bundles, and reduced the in vitro uptake of [3H] 5-HT in the hypothalamus to 16% of control values after 2 mug 5,7-DHT/4mul and 12% after 4 mug 5,7-DHT/4mul, and in the cortex cerebri to 35 and 34% of control values, respectively. Selective lesion of the medial 5-HT bundle reduced [3H] 5-HT uptake both in hypothalamus and in cortex cerebri to 45-48% of control values, while selective lesion of the lateral 5-HT bundles significantly reduced [3H] 5-HT uptake only in cortex (to 73-75%). No significant change was observed in [3H] noradreanaline uptake after any injection, or in [3H] 5-HT uptake after vehicle injections. Locomotor activity in an open field 3-10 days postoperatively was significantly reduced by lesions of the medial plus lateral 5-HT bundles. 5-Hdroxytryptophan (50 mg/kg) and a peripheral decarboxylase inhibitor (MK 486, 75 mg/kg) 17 days postoperatively induced a pronounced behavioral "5-HT syndrome" in these rats with medial plus lateral lesions but not in controls. Pain sensitivity, as measured by the hot plate test, was not changed by any lesion, even when tryptophan hydroxylase was partly inhibited with alpha-propyldopacetamide (100 mg/kg). Morphine analgesia and acquisition of a one-way avoidance response also were unchanged. Apomorphine (2 mg/kg)-induced locomotor activity and stereotyped behavior, as measured in an Animex activity meter, were not significantly different from control values in the 5,7-DHT groups. It was concluded that the medial 5-JT BUNDLE INNERVATES BOTH THE HYPOTHALAMUS AND THE CORTEX CEREBRI AND THE LATERAL 5-HT bundle mainly the cortex. These ascending 5-HT neurons are involved in maintaining open field ambulation. No wupport was obtained for the view that they are involved in pain mechanisms, in morphine-induced analgesia, in apomorphine-induced motor behavior, or in one-way avoidance learning.
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PMID:Behavioral effects of 5, 7-dihydroxytryptamine lesions of ascending 5-hydroxytryptamine pathways. 94 13

Electrodes were implanted in mesencephalic, pontine, and bulbar reticular formation, and in spinal trigeminal nucleus and tract of rats. Central and peripheral aversive response thresholds were studied under normal conditions and with morphine. Peripherally elicited aversive reactions were assessed with tail-flick, hot-plate, and footshock responses. Centrally elicited aversive reaction thresholds were in all cases based on unconditioned behavioral distress signs (non-stereotyped, escape-like movements, vocalization, freezing, excretion, etc.) and confirmed in some cases with avoidance learning. Morphine (10 mg/kg) elevated the unconditioned aversive reaction threshold for brain stimulation in the trigeminal complex and for peripheral aversive stimulation, but failed to affect the thresholds for reticular brain stimulation. The failure to affect reticular thresholds was independent of stimulation frequency. Thresholds for 5 and 200 Hz sinusoidal stimulation were both unaffected as were previously reported thresholds with 333 Hz pulsatile stimulation. Trigeminal nucleus and tract stimulation were affected in similar degrees. The data were discussed as supporting descending inhibitory models of opiate analgesia.
Pain 1976 Dec
PMID:Differential effect of morphine on trigeminal nucleus versus reticular aversive stimulation: independence of negative effects from stimulation parameters. 102 23


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