Gene/Protein Disease Symptom Drug Enzyme Compound
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Query: UMLS:C0344307 (analgesia)
 28,200 document(s) hit in 31,850,051 MEDLINE articles (0.00 seconds)

For spinal anesthesia of only one lower extremity, effect factors, assumed to influence the level of anesthesia including the degree of head-down position of the patients during injection, the volume of the drug and the rate of its injection, are studied using 0.2% hypobaric tetracaine solution in water. Seventy-two patients having the surgery of one lower extremity were divided into 7 groups according to the difference in the degree of head-down position (0, 2 and 5 degrees), in the volume (3, 5 and 7 ml) and the rate (0.2, 0.1 and 0.05 ml.s-1) of injection of tetracaine solution. Patients, in lateral position with the operative side up during injection and 20 minutes after injection, were checked for the level of hypesthesia and analgesia on both operative side and non-operative side. Except 2 groups of the patients who were in horizontal position during injection or who are injected with 7 ml of tetracaine solution all at once, the upper level of analgesia in the operative side is well controlled at T10, although in some patients the additional injection of small amount of tetracaine solution was needed. In these patients, the analgesic level in the non-operative side is restricted within S level, and HR and BP changes were very slight. The rate of injection had no effect on the analgesic level on both operative side and non-operative side.
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PMID:[Spinal anesthesia of only one lower extremity with hypobaric tetracaine]. 258 17

Neonatal administration of monosodium glutamate (MSG: 2-4 mg/g, SC) selectively destroys circumventricular organs, especially the arcuate nucleus and median eminence of the hypothalamus, and also attenuates both nonopioid (continuous cold-water swim: CCWS) and opioid (morphine) analgesia when rats are tested as adults. The present study evaluated whether administration of MSG (1-6 g/kg, SC) or its equiosmotic control (2.37 M NaCl) to adult rats altered either basal nociception on the tail-flick and jump tests or analgesia following morphine (5 mg/kg, SC) or CCWS (2 degrees C for 3.5 min). MSG treatment dose-dependently produced small but significant increases in basal nociceptive thresholds in adult rats. Morphine analgesia was significantly reduced on both tests following pretreatment with MSG (30-32%) and hypertonic NaCl (17-25%). In contrast, MSG (55-247%), but not NaCl pretreatment potentiated both nonopioid CCWS analgesia on both tests and CCWS hypothermia. These data are discussed in terms of differential neonatal and adult MSG effects, dissociations between opioid and nonopioid pain-inhibition, and the role of MSG in altering adaptive mechanisms to environmental stressors.
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PMID:Dissociation of opioid and nonopioid analgesic responses following adult monosodium glutamate pretreatment. 260 62

Acute exposure to continuous (CCWS) or intermittent (ICWS) cold-water swims elicits non-opioid and opioid forms of analgesia respectively. Intrathecal administration of methysergide blocks ICWS, but not CCWS analgesia. The present study evaluated the role of serotonin (5-HT) receptor subtypes in the mediation of CCWS and ICWS analgesia on the tail-flick and jump tests following administration of methysergide, a non-specific 5-HT antagonist and pirenpirone and ketanserin, two 5-HT2 receptor subtype antagonists. Systemic methysergide was more effective in reducing CCWS analgesia (50-58%, 0.1-1.0 mg/kg) than ICWS analgesia (21%, 5 mg/kg) on both pain tests. Systemic pirenpirone (0.04-0.2 mg/kg) and ketanserin (1-5 mg/kg) were also more effective in reducing CCWS analgesia (43-57%) on both tests than ICWS analgesia (pirenpirone: 0.4 mg/kg, 34%; ketanserin: 5 mg/kg, 21%) on the tail-flick test. Indeed, both 5-HT2 receptor antagonists potentiated ICWS analgesia on the jump test. While serotonin antagonist effects upon hypothermia could not account for CCWS analgesia effects, similar potentiations in ICWS analgesia and hypothermia were observed following pirenpirone and ketanserin. Finally, both 5-HT2 receptor antagonists differentially reduced CCWS hypothermia and potentiated ICWS hypothermia. These data suggest differential serotonergic modulation of the two forms of swim analgesia with opioid-mediated ICWS analgesia acting through spinal 5-HT1 receptors and non-opioid-mediated CCWS analgesia acting through supraspinal 5-HT2 receptors.
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PMID:Reduction in opioid and non-opioid forms of swim analgesia by 5-HT2 receptor antagonists. 260 92

Spontaneous or induced diabetes, as well as glucose loading, reduce opiate antinociception, presumably through induction of hyperglycemia. While peripheral administration of alloxan is a potent pancreatic beta-cell toxin, intracerebroventricular (ICV) alloxan reduces glucoprivic feeding in the absence of hyperglycemia, presumably through interactions with specific brain glucoreceptors. Our laboratory demonstrated that opioid-mediated 2-deoxy-D-glucose (2DG) antinociception is significantly reduced by central pretreatment with alloxan, and that this deficit is reversed by coadministration with 3M-D-glucose. The present study compared ICV and intravenous (IV) routes of alloxan (200 micrograms) upon morphine (1-10 mg/kg, SC) analgesia on the tail-flick and jump tests in rats, and evaluated these effects in terms of concomitant changes induced by ICV alloxan upon nonopioid-mediated continuous cold-water swim (CCWS: 2 degrees C for 3.5 min) antinociception. Two weeks following central, but not peripheral pretreatment with alloxan, morphine (2.5 and 5.0 mg/kg, SC) antinociception was markedly (30-56%) reduced on both nociceptive tests. In contrast, central pretreatment with alloxan respectively reduced (30 min) and subsequently potentiated (60 and 90 min) CCWS antinociception on the jump test. Alterations in antinociception by central alloxan occurred in the absence of changes in basal nociceptive thresholds, hypothermia or hyperglycemia. These data suggest that central alloxan may be acting upon either specific, but unidentified brain glucoreceptors and/or a glucoprivic control mechanism.
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PMID:Differential actions of central alloxan upon opioid and nonopioid antinociception in rats. 262 9

Parity (number of parturitions) affects the endogenous opioid system. Multiparous lactating rats are less sensitive to the effects of morphine (MOR) on maternal behavior (MB) and analgesia than primiparous lactating rats. In order to determine whether these changes in opiate sensitivity persist beyond the lactational state, the present study compared the sensitivity of ovariectomized nulliparous and nonlactating primiparous rats to MOR's effects on MB (Experiment 1), analgesia (Experiment 2) and prolactin release (Experiment 3) in addition to stress-induced analgesia (Experiment 2). In Experiments 1 and 2 primiparous rats were allowed to give birth and remain with their litter (culled to 6 pups) until weaning. At that time the pups were removed and the dams and age-matched nulliparous rats were ovariectomized. Four weeks later animals were exposed to foster pups daily in order to induce MB (Experiment 1). On day 5 or 6 of full MB the primiparous and nulliparous rats received either saline or one of four doses of MOR (0.625, 1.25, 2.5, or 5.0 mg/kg, SC) and 60 min later MB was assessed. MOR, at the 2.5 mg/kg dose, disrupted MB in a significantly greater percentage of nulliparous as compared to primiparous animals (100% vs. 55%, respectively). In Experiment 2, nulliparous and nonlactating primiparous animals received 2.5 mg/kg of MOR four weeks after ovariectomy. Analgesia was assessed on a tail-flick apparatus 30, 60, 90, 120 and 150 min postinjection. One week later the same animals were exposed to cold-water swims (CWS, 2 degrees C, 3.5 min) and tail-flick latencies were again recorded.(ABSTRACT TRUNCATED AT 250 WORDS)
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PMID:Long-term effects of parity on opioid and nonopioid behavioral and endocrine responses. 262 57

I.c.v. injection of 1 nmol N-ethylmaleimide (NEM) into mice interfered with opioid-induced supraspinal analgesia, as assessed in the warm water tail-flick test. This effect of NEM was long-lasting (more than 3 days), non-competitive and differentially inhibited by the opioids studied. The analgesia induced by [D-Ala2,D-Leu5]enkephalin (DADLE), [D-Ala2,Met5]enkephalinamide (DAME) and [D-Pen2,D-Pen5]enkephalin (DPDPE) was greatly reduced in NEM-treated mice. The antinociception elicited by [D-Ala2,N-MePhe4,Gly-ol5]enkephalin (DAGO) was also impaired although to a lesser extent. In contrast, the activity of morphine and etorphine remained unchanged. NEM-sensitive opioids coadministered with morphine antagonized the analgesia elicited by the alkaloid in NEM-treated mice. The administration of naltrexone or DADLE, DAGO, [D-Ala2,N-MePhe4,Met-(O)5-ol]enkephalin (FK-33824) and morphine in doses equivalent to the ED90 doses for inducing analgesia, a few minutes before NEM prevented it from interfering with DADLE-elicited supraspinal analgesia when evaluated 24 h later. In contrast, the selective delta antagonist, ICI 174864, did not protect the DADLE-induced analgesia against the effect of NEM. We suggest that NEM produced its effect by acting upon a site that appears to be distal to the receptor binding site, presumably located on the guanine nucleotide binding regulatory proteins, Gi/Go. Therefore, these transducer proteins might play a key role in the effects displayed by opioids when acting via the mu receptor-Gi/Go complexes.
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PMID:Intracerebroventricular N-ethylmaleimide differentially reduces supraspinal opioid analgesia in mice. 267 63

When a danger stimulus (a passing shadow) is presented to the crab Chasmagnathus granulatus, an escape response is elicited that habituates after repeated stimulation. Results from previous work suggest that this habituation might be mediated by endogenous opiates and, thus, that after an habituation session an analgesic effect on the response to a painful stimulus should be found. The purpose here was to test this contention. Each crab was lodged in an actometer where two 2-trial sessions with electrical shock stimulation were given (SS1, SS2), the intersession interval being 60 or 105 min, and the response activity recorded. In some experiments, repeated shadow stimulation was inserted during the interval, and the response activity also recorded. In Expt. 1, shadow sessions of 15 and 30 trials were tested and a significant decrease of the reactivity to the shock was only shown with 30 trials. In Expt. 2, crabs were immediately injected after SS1 with distilled water (d.w.) or naloxone (NX) (3.2 micrograms/g), and a shadow session of 30 trials was given to half of the d.w. animals and to half of the NX ones. NX injected crabs showed an increased responsiveness to the danger stimulus during the shadow session but no inhibitory effect on pain reactivity to the subsequent painful stimulus. Issues concerning dependence of the analgesia on danger stimulus iteration and on stimulus controllability, as well as the opioid nature of the analgesia, are discussed.
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PMID:Danger stimulus-induced analgesia in the crab Chasmagnathus granulatus. 272 Mar 82

We report the intraarterial injection of a flunitrazepam tablet dissolved in water in a patient with intravenous drugs addiction. Several ecchymotic lesions were present at different sites of the arm. In order to achieve analgesia and the sympathetic blockade of the arm, we performed an axillary perivascular block of the brachial plexus by means of the intermittent injection through a catheter of 0.25% bupivacaine with a 1:200,000 epinephrine solution. In addition, an anticoagulant treatment with heparin was started as prophylaxis of the thrombosis of the vessel. There was a satisfactory clinical course even though a distal phalange had to be amputated on the 18th day. We propose the continuous perivascular block as the method of choice of this type of medical problem.
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PMID:[Use of axillary perivascular blockage of the brachial plexus with a catheter as treatment in accidental intra-arterial injection of drugs]. 276 12

Repeated exposure of a rat to a nociceptive testing environment ('habituation') enhances its sensitivity to noxious thermal stimuli20 and reduces the antinociceptive effect of a subsequent acute dose of morphine ('behavioural tolerance'). The present study quantitatively characterises the effects of habituation upon morphine antinociception using hot-plate (50 and 55 degrees C) and reflex withdrawal tests (dipping the tail and hindpaws into water at 49 degrees C). Dose-response relationships were modeled with the empirical function; E = Eo + (EMAX*DN)/(ED50N + DN) where E is the time-integrated response, EMAX is the response attributable to morphine, Eo is the baseline response, D is the dose and N is a steepness parameter. Habituation reduced EMAX in both hot-plate tests and also reduced Eo on the 50 degrees C hot-plate. In both reflex tests, habituation reduced Eo to that of spinal animals and EMAX to a value intermediate between that of intact and spinal animals. Neither the ED50 nor the value of N was altered by habituation. Acute spinal novice and habituated animals had similar dose-response curves and parameters. Sham spinalisation had no significant effect on any of the parameters. It is concluded that habituation to the nociceptive testing environment substantially reduces the bulbospinal contribution to morphine analgesia but has no effect upon the spinal component.
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PMID:Behavioural tolerance to morphine analgesia is supraspinally mediated: a quantitative analysis of dose-response relationships. 276 89

The effect of gonadal steroids on the response to analgesia testing was determined in castrated male and female rats and castrated male and female rats treated with testosterone propionate (TP) and estradiol benzoate (EB), respectively. The time to respond to a noxious somatic stimulus in the form of heat was assessed using the tail withdrawal test (tail withdrawal from hot water) and hot plate test (the time to paw lick or jump). In male rats, castration resulted in a significant reduction of the reaction time for tail withdrawal. This effect was reversed by treatment with TP. The time to paw lick or jump in male rats was also diminished by castration. Treatment with TP resulted in a partial reversal of the effect of castration on this response. In castrated female rats, the time required for tail withdrawal was decreased by castration and increased by treatment with EB. The reaction time to the hot plate in female rats was diminished by castration and further reduced by EB administration. These data indicate that gonadal steroids influence the response to a noxious heat stimulus in male and female rats and that the effect may vary according to sex and the way in which the stimulus is applied.
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PMID:The response to analgesia testing is affected by gonadal steroids in the rat. 277 Apr 10


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