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)

The aim of this paper was to study the effect of two benzomorphan derivatives MR2266 and MR2267 with predominant antagonism to kappa-opioid receptors administered intrathecally on the analgesic action of morphine and nalbuphine. Both compounds attenuated the analgesia elicited by examined opioid agonists. Our results support the hypothesis that the spinal opioid receptors take part in analgesic effect of morphine and nalbuphine. It was for the first time described that MR2267, considered as inactive enantiomer of MR2266, is an active opioid antagonist when administered intrathecally.
Pol J Pharmacol
PMID:Antagonistic effect of MR2266 and MR2267 on morphine or nalbuphine analgesia at the spinal levels in rats. 886 73

The purpose of this study is to present several years experiences in using of epidural analgetic blockade in patients with a substantial exacerbation of radicular pain syndrome in the course of discopathy resistant to traditional treatment. The observation of 61 non-surgical patients, who were given epidurally an analgetic (Bupivacainum hydrochloricum or Morphinum hydrochloricum) and a steroid antiphlogistic (Depo-Medrol) simultaneously, using a stationary catheter, confirms the efficacy of the method. Taking advantages of local analgesia in order to break the pain arc, the possibility of sustaining it for an extended period of time, as well as its local antiphlogistic activity, even while using minimal doses of the drugs, show evident therapeutic effects.
Neurol Neurochir Pol
PMID:[Continuous epidural blockade as a method of treatment of low back pain syndrome in the course of disk pathology. Introductory research]. 896 75

It was proposed that the repetitive rapid-rate transcranial magnetic stimulation (TMS) induces the functional and structural changes analogous to those which are evoked during the electroconvulsive treatment. Presently, we compared the effects of 8 daily treatments with TMS (t = 5 min, B = 0.1 T, trise = 200 microseconds, f = 50 Hz) and electroconvulsive shock (ECS) (t = 0.5 s, I = 150 mA, f = 50 Hz) on the behavior of rats in the forced swimming test (24 h after the last treatment), the exploratory activity test (0-10 min), the basal locomotor activity test (11-30 min), and the tail flick test (2 h after the last treatment). We also tested (24 h after the treatment) the reactivity of the cyclic AMP generating system in cerebral cortical slices. Statistical significance of the results was estimated by ANOVA and t-Student test. The immobility time in the forced swimming test was shortened after TMS and ECS to 86 and 75% of control values, respectively (p < 0.05 and p < 0.01). Both ECS and TMS depressed the basal locomotor activity (by 60 and 80%, resp.), and ECS, but not TMS, diminished also the exploratory activity by 70% (p < 0.01) only ECS induces analgesia, prolonging tail-flick latency by 90% (p < 0.01). ECS diminished the accumulation of the noradrenaline-stimulated cyclic AMP in the cortex slices (by 35%; p < 0.05). The effect after TMS was similar but statistically not significant (87% of control values). The data suggest that TMS produces in rats some responses that are regarded as predictive for the antidepressant activity, similar to those produced by ECS, but less side effects.
Psychiatr Pol
PMID:[Behavioral and biochemical effects of magnetic brain stimulation and electroshock in rats]. 897 60

Recent studies suggested that the L-arginine/nitric oxide (NO)/cyclic GMP pathway is involved in the modulation of pain perception. The present experiments were undertaken to find out the role of this pathway in the antinociception induced by oxotremorine administration. Male mice of the CD-1 strain were injected with different doses of the muscarinic agonist oxotremorine (0.005, 0.01, 0.02, 0.03 mg/kg i.p.) 5 min after the administration of saline solution or the inhibitors of NO synthase NG-nitro-L-arginine methyl ester (L-NAME: 10 and 20 mg/kg, i.p.) or NG-nitro-L-arginine (N-ARG: 10 and 20 mg/kg i.p.). Oxotremorine induced a dose- and time-dependent analgesic effect in mice, which was significantly increased by L-NAME and N-ARG administration. Either doses of the NO inhibitors given alone had no effect on the nociceptive threshold. The present results show a role of NO in the antinociception mediated by the muscarinic receptor stimulation and suggest that it exerts an inhibitory action on cholinergic analgesia.
Pol J Pharmacol
PMID:Nitric oxide synthase inhibitors enhance the antinociceptive effects of oxotremorine in mice. 943 49

For many gynecological surgery patients belonging to deep vein thrombosis (DVT) high-risk group the analgesia of choice is regional spinal analgesia. Perioperatively LMWH--Fraxiparine was administered to 426 gynecological surgery patients and to 113 caesarean section patients. The first dose 7500 ICU s.c. was administered 2 hours before operation and consecutive ones every 24 hours for 5 to 7 days. The drug didn't cause any anaesthesia complications like enhanced bleeding after lumbar punction. It was emphasised in the discussion that in choosing this kind of prophylaxis certain conditions should be fulfilled in order to avoid spinal hematoma.
Ginekol Pol 1997 Nov
PMID:[Spinal analgesia and perioperative low molecular weight heparin (LMWH) prophylaxis of thrombosis. Safety aspect]. 977 Aug 48

Osteoporosis seems to be a component of body aging process. Through the years, muscles, ligaments, and fasciae loose their natural elasticity; degenerative changes form in joints; also, mechanical resistance of bones reduces. Involutive changes in central nervous system (CNS) cause disturbances in reciprocal transmission of impulses between CNS and muscles. This changes normal motion pattern, leading, consequently, to lasting stress of ligaments, muscles, joints and bones, what becomes a source of strong nociceptive impulses. One of first symptoms of this is pain, localized particularly in spine region. Pain is another cause of increased, abnormal tension of muscles and, thus, of their stress. Proper treatment of above situation must be necessarily consisted of simultaneous analgesia, correcting of muscle tension and relaxation. Therefore, guideline for the rehabilitation program needs to be supported by thorough clinical, biomechanical, roentgenographic and densitometrical case analysis. Rehabilitation works as prophylactics of formation and fixing of deformities. Therefore, this must be aimed to: pain relief, maintaining of proper patient's stance, rebuilding of normal muscle force, maintaining of normal motion range and increasing of daily motion activity, what would stimulate skeletal system. For practical reasons, forming of dysfunctions in motion system in course of osteoporosis is classified into three stages--I--early, II--advanced osteoporosis and III--late.
Pol Merkur Lekarski 1998 Oct
PMID:[Analgetic treatment and rehabilitation in osteoporosis]. 1010 47

Calcitonin is one of three most important factors involved in the regulation of systemic calcium homeostasis. Since its discovery in 1961 the structure of calcitonin from different species including human was established, synthetized and developed for use in human clinic. Up to now calcitonin is utilized in treatment of hypercalcemia, Paget disease, algodystrophy, primary and secondary osteoporosis and analgesia. Beside comparative studies aiming on selection of the most effective protocol of treatment and utilization, lately calcitonin is extensively studies for its antifracture potency in osteoporosis. One of the substantial therapeutical progress also appeared the utilization of intransal preparation of calcitonin.
Pol Merkur Lekarski 1998 Oct
PMID:[Calcitonin -- 1998]. 1010 52

Converging lines of evidence indicate that N-methyl-D-aspartate (NMDA) receptor antagonists attenuate the development of morphine tolerance tested in antinociception assays in rodents. The present study extends these findings to the effects of clinically available NMDA receptor antagonist, memantine. Male Albino Swiss mice were tested for analgesia using the tail-flick apparatus. Preliminary experiment was designed to find out the optimal dose of morphine and the number of injections that would produce tolerance to its analgesic effects. In the main experiment, during the development of tolerance period (6 days), mice received 10 mg/kg sc b.i.d. morphine injections in the animal room (non-associative tolerance). This treatment resulted in 5.8 fold rightward shift of morphine cumulative dose-response effect from 3.39 mg/kg on day 1 to 16.19 mg/kg on day 8 of the experiment. Memantine pretreatment (5 and 10 mg/kg, but not 2.5 mg/kg), given 30 min prior to each morphine dose during the development of tolerance period, inhibited the rightward shift of morphine cumulative dose-response curve. Thus, pretreatment with memantine at doses of 2.5, 5 and 10 mg/kg resulted in ED50 values of 12.13, 4.74 and 1.95 mg/kg, respectively, corresponding to 3.35, 1.02 and 0.94 fold changes. These data indicate that low affinity, clinically available NMDA receptor antagonist, memantine, may be used to inhibit the development of morphine tolerance.
Pol J Pharmacol
PMID:Clinically available NMDA antagonist, memantine, attenuates tolerance to analgesic effects of morphine in a mouse tail flick test. 1060 36

The few experimental studies suggest that repetitive rapid-rate transcranial magnetic stimulation (TMS) evokes in the brain functional and structural changes similar to those evoked by electroconvulsive therapy (ECT). The aim of the present work was to compare the influence of the repetitive TMS (B = 1.6 T; f = 20 and 30 Hz; t = 5 and 5.5 minutes; N = 9 and 18 days) and that of ECT (I = 150 mA; f = 50 Hz; t = 0.5 s; N = 9 days) on rats' behaviour in the tests of free field, tail flick, motor hyperactivity after administration of apomorphine and in forced swimming. None of the rats subjected to TMS suffered from convulsive attack, which followed every electroconvulsive shock. In the free field test it was detected that neither TMS nor ECT applied individually or repetitively disturbed general motor activity of rats. Repetitive electroconvulsive shocks caused analgesia, prolonging the latency of tail flick by 46% (p < 0.001). Moreover, the tail flick test revealed hyperalgesia in the rats subjected to TMS (24 and 21% of control values respectively; p = 0.05). Motor hyperactivity of rats stimulated with administration of apomorphine was intensified both by TMS (by 58% at maximum in the 30th minute of the experiment; p = 0.001) and, all the more, by ECT (by 92% at maximum at the end of the test; p = 0.01). In the forced swimming test, the greatest decrease of inertia period was observed ECT--up to 50% of control values (p = 0.001). TMS had weaker effects--the decrease amounted to 29% of control values (p = 0.01). The shortening effect depended on the parameters of TSM. The obtained results seem to confirm that TMS, like ECT, evokes in rats certain reactions suggesting its antidepressive action, but causes less undesirable effects.
Psychiatr Pol
PMID:[The behavioral effects of the transcranial magnetic brain stimulation in rat: the comparison with electroshock]. 1085 62

Imipramine and amitriptyline, nonselective monoamine reuptake inhibitors, citalopram, selective serotonin reuptake inhibitor, and maprotiline, selective noradrenaline reuptake inhibitor, were tested after intracerebroventricular (icv) and intrathecal (it) administration in the rat writhing test to establish the role of the spinal and/or supraspinal structures in their effects. All drugs evoked dose-dependent analgesia after icv but not after it microinjections. The changes in the nociceptive behavior of rats pre-treated with antidepressants were not due to the non-specific influences of the drugs on the animals' gross behavior, as revealed by the open field test. The obtained results suggest that an antidepressant-induced analgesia mainly depends on the supraspinal effect with minor, if any, contribution from the spinal mechanisms.
Pol J Pharmacol
PMID:Supraspinally mediated analgesic effect of antidepressant drugs. 1094 10


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