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Morphine Analgesia (morphine + analgesia)

Distribution by Scientific Domains

Life Sciences	60%
Medical Sciences	40%

Selected Abstracts

Blocking the R-type (Cav2.3) Ca2+ channel enhanced morphine analgesia and reduced morphine tolerance

EUROPEAN JOURNAL OF NEUROSCIENCE, Issue 12 2004
Kazuaki Yokoyama
Abstract Morphine is the drug of choice to treat intractable pain, although prolonged administration often causes undesirable side-effects including analgesic tolerance. It is speculated that voltage-dependent Ca2+ channels (VDCCs) play a key role in morphine analgesia and tolerance. To examine the subtype specificity of VDCCs in these processes, we analysed mice lacking N-type (Cav2.2) or R-type (Cav2.3) VDCCs. Systemic morphine administration or exposure to warm water swim-stress, known to induce endogenous opioid release, resulted in greater analgesia in Cav2.3,/, mice than in controls. Moreover, Cav2.3,/, mice showed resistance to morphine tolerance. In contrast, Cav2.2,/, mice showed similar levels of analgesia and tolerance to control mice. Intracerebroventricular (i.c.v.) but not intrathecal (i.t.) administration of morphine reproduced the result of systemic morphine in Cav2.3,/, mice. Furthermore, i.c.v. administration of an R-type channel blocker potentiated morphine analgesia in wild-type mice. Thus, the inhibition of R-type Ca2+ current could lead to high-efficiency opioid therapy without tolerance. [source]

The effects of local perfusion of DAMGO on extracellular GABA and glutamate concentrations in the rostral ventromedial medulla

JOURNAL OF NEUROCHEMISTRY, Issue 3 2008
Raf Jan-Filip Schepers
Abstract Electrophysiological data suggest an involvement of rostral ventromedial medulla (RVM) GABA and glutamate (GLU) neurons in morphine analgesia. Direct evidence that extracellular concentrations of GABA or GLU are altered in response to mu opioid receptor (MOP-R) activation is, however, lacking. We used in vivo microdialysis to investigate this issue. Basal GABA overflow increased in response to intra-RVM perfusion of KCl (60 mmol/L). Reverse microdialysis of the MOP-R agonist d -Ala(2),NMePhe(4),Gly-ol(5)]enkephalin (DAMGO) (20,500 ,mol/L) produced a concentration-dependent decrease of RVM GABA overflow. Behavioral testing revealed that concentrations that decreased GABA levels increased thermal withdrawal thresholds. A lower agonist concentration that did not increase GABA failed to alter thermal thresholds. DAMGO did not alter GLU concentrations. However, KCl also failed to modify GLU release. Since rapid, transporter-mediated uptake may mask the detection of changes in GLU release, the selective excitatory amino acid transporter inhibitor pyrrolidine-2,4-dicarboxylic acid (tPDC, 0.6 mmol/L) was added to the perfusion medium for subsequent studies. tPDC increased GLU concentrations, confirming transport inhibition. KCl increased GLU dialysate levels in the presence of tPDC, demonstrating that transport inhibition permits detection of depolarization-evoked GLU overflow. In the presence of tPDC, DAMGO increased GLU overflow in a concentration-dependent manner. These data demonstrate that MOP-R activation decreases GABA and increases GLU release in the RVM. We hypothesize that the opposing effects of MOP-R on GLU and GABA transmission contribute to opiate antinociception. [source]

Interpleural analgesia for attenuation of postoperative pain after hepatic resection,

ANAESTHESIA, Issue 7 2010
L. Weinberg
Summary We performed a prospective randomised trial to evaluate the analgesic efficacy of interpleural analgesia in patients undergoing hepatic resection. The control group (n = 25) received multimodal analgesia with intravenous morphine patient-controlled analgesia; in addition, the interventional group (n = 25) received interpleural analgesia with a 20-ml loading dose of levo bupivacaine 0.5% followed by a continuous infusion of levobupivacaine 0.125%. Outcome measures included pain intensity on movement using a visual analogue scale over 24 h, cumulative morphine and rescue analgesia requirements, patient satisfaction, hospital stay and all adverse events. Patients in the interpleural group were less sedated and none required treatment for respiratory depression compared to 6 (24%) in the control group (p< 0.01). Patients in the interpleural group also had lower pain scores during movement in the first 24 h. Patients' satisfaction, opioid requirements and duration of hospital stay were similar. We conclude that continuous interpleural analgesia augments intravenous morphine analgesia, decreases postoperative sedation and reduces respiratory depression after hepatic resection. [source]

Impact of ageing on the antinociceptive effect of reference analgesics in the Lou/c rat

BRITISH JOURNAL OF PHARMACOLOGY, Issue 6 2002
Didier Jourdan
Research on the evolution of experimental pain perception and on the achievement of analgesia with ageing has led so far to contradictory results. This study investigated in the rat the impact of ageing on the antinociceptive effect of reference analgesics, acetaminophen (50, 100, 200, 400 mg kg,1 po), aspirin (50, 100, 200, 400 mg kg,1 sc), clomipramine (5, 10, 20, 40 mg kg,1 sc) and morphine (1.25, 2.5, 5, 10 mg kg,1 sc). Lou/c rats were chosen because they provide a model of healthy ageing and they do not develop obesity with age. Three groups of 40 rats each (mature (4 months), middle-aged (18 months) and old (26 months)), were treated with each drug at 14 days interval. Two tests were used: a thermal test (tail immersion in 48°C water and measurement of reaction latency) and a mechanical test (paw pressure and measurement of struggle threshold). Results confirm the increased mechanical sensitivity to pain and no change in thermal sensitivity for old rats compared to mature and middle-aged animals. They show a marked decrease in the effect of morphine with age and no age-related effect for acetaminophen, aspirin or clomipramine. Plasma levels of morphine and metabolites are not different in the three age groups. It is likely that the influence of age on morphine analgesia is linked mainly to pharmacodynamic rather than pharmacokinetic changes. British Journal of Pharmacology (2002) 137, 813,820. doi:10.1038/sj.bjp.0704944 [source]