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)

This study was designed to investigate the antinociceptive effects of one of the most prescribed benzodiazepines (BZ) -i.e., alprazolam. Groups of CD-1, SWISS, BALB/c and C57BL mice were treated with alprazolam. Analgesia was assayed, using the radiant heat tailflick assay. Alprazolam given i.p. elicited analgesia in a dose-dependent manner only in the BALB/c mice (ED50 1.1 mg/kg). No analgesia was observed in CD-1 or C57BL mice. The sensitivity of SWISS mice was intermediate, but still very low. Intrathecally administered alprazolam elicited analgesia in BALB/c, Swiss and CD-1 mice with ED50 values of 10, 22.8 and 34.6 micrograms, respectively. No analgesia was observed in C57BL mice. Intracerebroventricular injections did not induce analgesia in any of the strains. In other sets of experiments with BALB/c mice, we found a supra-additivity increase in analgesia when a subthreshold dose of alprazolam was given with morphine (mu-subtype agonist). This interaction was antagonized by naloxone and less so by flumazenil. No effect was found when alprazolam was co-administered with other specific opioid agonists (delta and kappa). Our results demonstrate that injections of alprazolam can produce analgesia in different genetic subjects and can modify morphine-induced antinociception. The fact that the interaction between morphine and alprazolam analgesia was sensitive to naloxone but less to flumazenil indicates that the analgesic effects of alprazolam are mediated primarily by an opioid mechanism of action but less by benzodiazepines.
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PMID:Strain differences in mice antinociception: relationship between alprazolam and opioid receptor subtypes. 888 80

Alprazolam is a triazolobenzodiazepine, with a potent anxiolytic action and a short half-life. Alprazolam analgesia was measured, using the radiant heat tailflick assay in mice, which was administered alone or in combination with opioids. Intrathecally administered alprazolam produced a dose-response increase in the tailflick latency with an ED50 of 34 microg (19.4-72.5, 95% CL). There were almost no effects after intracerebroventricular injections. Naloxone almost completely abolished the analgesia response mediated by alprazolam. This sensitivity to naloxone indicates that at least some of the analgesic effects of alprazolam are mediated by an opioid mechanism of action. When administered together with various antagonists of opioid receptor subtypes, we found that the mu antagonists, but not the delta and kappa1 subtypes inhibited alprazolam analgesia significantly. No effect was found when alprazolam was coadministrated with kappa3 opioid agonists. In addition, we found a supra-additivity (synergistic) increase in analgesia when alprazolam was given with morphine. Competition binding assays show the highest affinity of alprazolam to the mu1 subtype. In summary, we conclude that alprazolam mediates its analgesic effect, most probably via an mu opiate mechanism of action.
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PMID:Antinociceptive interaction between alprazolam and opioids. 899 36

Animal research has shown that anxiety may inhibit pain through the release of endogenous opioids. On the other hand, anxiety is often believed to exacerbate pain in clinical situations, and anxiety reduction has been shown to attenuate the affective component of pain. In the present study phobic anxiety was induced by confronting forty-eight spider phobic subjects with a spider, after which they received two mildly painful electrical stimuli at two different current levels. The benzodiazepine alprazolam (1 mg) was administered to investigate the influence on pain of a reduction in anxiety, while the role of endogenous opioids was studied by administering the opioid antagonist naltrexone (50 mg). Alprazolam resulted in lower anxiety and pain ratings during pain stimulation, supporting the idea that (presumably pain-related) anxiety may increase the experience of pain. Naltrexone did not influence pain and anxiety ratings, nor was there a significant interaction between the two pharmacological manipulations. These findings confirm previous evidence that phobic fear does not necessarily induce an endogenous opioid-mediated analgesia.
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PMID:No interactive effects of naltrexone and benzodiazepines on pain during phobic fear. 992 60

Estimation of the quality of the epidural anaesthesia of the patients sedated with Alprazolam and Midazolam in premedication before arthroscopy or arthrotomy of the knee was the goal of our study. Forty six (34 men and 12 women) ASA physical status 1-2 patients were divided into groups depending on the drugs orally applied in premedication (Alprazolam 0.5 mg, n = 29 or Midazolam 15 mg, n = 17) and of the kind of analgesia. The patients subjected to arthroscopy were treated with a single-shot epidural analgesia (n = 38), while those subjected to arthrotomy--with a continuous epidural analgesia (n = 8). 2% Lignocain with addition of Epinephrine and Fentanyl was used in the perioperative analgesia, while 0.25% Bupivacain with addition of Morphine was used in the postoperative period when continuous epidural analgesia was applied. The ISAS, VAS and Ramsey scales were used and the data were analysed with the Kormogolov test. The perioperative sedation in arthroscopy and arthrotomy of the knee is good without any significant differences associated with a kind of the drugs applied. The single-shot epidural anaesthesia is inadequate only during a prolonged arthroscopy of the knee. The postoperative continuous epidural analgesia, expressed in the VAS scale, was inadequate. A level of general satisfaction of the patients of the sedation and analgesia, expressed in the points of the ISAS scale, was satisfactorily good.
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PMID:[Perioperative sedation and analgesia for complications from arthroscopy and arthrotomy of the knee joint]. 1281 76

Stress can be viewed as a cause of adverse circumstance that induces a wide range of biochemical and behavioral changes. Oxidative stress is a major contributor to the genesis of neurodegenerative and neuropsychiatric problems. In the present study, we investigated the protective effect of alprazolam in acute immobilization-induced various behavioral and biochemical alteration in mice. Mice were immobilized for a period of 6 h. Alprazolam (0.25 and 0.5 mg/kg, i.p.) was administered 30 min before subjecting the animals to acute stress and several behavioral (mirror chamber, actophotometer, tail flick test) and biochemical tests (malondialdehyde level, glutathione, catalase, nitrite and protein) were performed. Acute immobilization stress for a period of 6 h caused severe anxiety, analgesia and decreased locomotor activity in mice. Biochemical analyses revealed an increase in malondialdehyde, nitrite level and depleted glutathione and catalase activity in stressed brain. Pretreatment with alprazolam (0.25 and 0.5 mg/kg, i.p.) significantly reversed immobilization stress-induced anxiety, analgesia and impaired locomotor activity. Biochemically, alprazolam pretreatment decreased malondialdehyde, nitrite activity and restored reduced glutathione level and catalase activity. These results suggest that alprazolam has a neuroprotective effect and can be used in the treatment and management of stress and related disorders.
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PMID:Protective effect of alprazolam in acute immobilization stress-induced certain behavioral and biochemical alterations in mice. 1765 28