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Br J Anaesth 2002 May;88(5):745-6
Publication Types:
PMID: 12067027, UI: 22061777
Other Formats:
Br J Anaesth 2002 May;88(5):743; discussion 744
PMID: 12067025, UI: 22061773
Br J Anaesth 2002 May;88(5):743-4; discussion 744
PMID: 12067024, UI: 22061774
Br J Anaesth 2002 May;88(5):714-6
University Department of Anaesthesia, Critical Care and Pain Management, Leicester Royal Infirmary, UK.
BACKGROUND: The aim of this prospective, double-blind, randomized, placebo-controlled clinical trial was to investigate the opioid-sparing effects of rectal diclofenac following total abdominal hysterectomy. METHODS: Forty ASA I-II patients, aged 20-60 yr, were randomized to receive identical-looking suppositories of either diclofenac 75 mg or placebo, twice daily. All patients were given a standardized anaesthetic, with intravenous morphine via a patient-controlled analgesia device and either diclofenac or placebo for postoperative analgesia. RESULTS: The median 24 h morphine consumption (interquartile range) was significantly higher (P=0.02) in the placebo group [59 (45-85) mg] than in the diclofenac group [31 (14-65) mg]. In comparison with the placebo group, there were significant reductions in total pain score in the diclofenac group at rest (P=0.04) and on movement (P<0.01). Total (SD) sedation score was significantly lower (P=0.04) in the diclofenac group [90 (73) mm] than in the placebo group [148 (89) mm]. Total (interquartile range) nausea score was significantly lower (P<0.01) in the diclofenac group [14 (0-53) mm] than in the placebo group [64 (30-109) mm]. There was no significant difference between the two groups of patients in episodes of vomiting or number of rescue antiemetics. CONCLUSIONS: Rectal diclofenac reduces morphine consumption, improves postoperative analgesia, and reduces the incidence of adverse effects such as sedation and nausea.
PMID: 12067012, UI: 22061761
Br J Anaesth 2002 May;88(5):685-91
Monash University Department of Anaesthesia, Monash Medical Centre, Clayton, Victoria, Australia.
BACKGROUND: Ketamine has been found to exert antinociceptive effects in animals and to be analgesic at subanaesthetic doses in humans. This study was designed to investigate the involvement of spinal cord mechanisms in the potentiation of opioid analgesia by parenteral non-spinal administration of ketamine. METHODS: Thresholds for nociception were measured in an acute pain model in rats that allowed identification of antinociceptive effects due to drug action in the spinal cord. Dose-response curves for the antinociceptive effects of ketamine alone and ketamine in conjunction with the mu opioid fentanyl were constructed. RESULTS: Intraperitoneal ketamine up to 3.75 mg kg(-1) caused no sedative or antinociceptive effects and intrathecal ketamine caused dose-dependent, spinally mediated antinociceptive effects. Injections of ketamine doses that caused no antinociceptive effects when given alone (intrathecal 25 microg and intraperitoneal 3.75 mg/kg) significantly increased spinally mediated antinociception produced by intrathecal fentanyl injections when assessed using noxious heat (tail-flick test) but not when assessed by noxious electrical current (electrical current threshold test). CONCLUSIONS: We conclude that ketamine can potentiate the effects of fentanyl by an interaction at the level of the spinal cord even when ketamine is given via a non-spinal route of administration.
PMID: 12067007, UI: 22061756
Br J Anaesth 2002 May;88(5):679-84
BACKGROUND: Intrathecal administration of 5-hydroxytryptamine (5-HT) is antinociceptive to noxious heat and electrical stimuli. The contributions of different receptor subtypes to the antinociceptive effects of 5-HT are controversial. The main reasons for this are the poor receptor subtype selectivity of some agonist drugs and the difficulty of restricting drug action to the spinal cord in some experimental paradigms. This study investigated the roles of different 5-HT receptor subtypes involved in the spinal cord control of the nociception produced by these two nociceptive testing paradigms. METHODS: Tail-flick latency and electric current threshold for nociception were measured in an acute pain model that allowed the study of the antinociceptive effects of intrathecally administered drugs that were due to actions of these drugs at spinal cord receptors. Experiments were performed in male Wistar rats with chronically implanted lumbar subarachnoid catheters. Dose-response curves for spinally mediated antinociceptive effects of agonists selective for 5-HT receptor subtypes were constructed. RESULTS: The 5-HT1 agonist 1-(3-chlorophenyl)-piperazine dihydrochloride caused a dose-dependent antinociceptive effect, measured by both nociceptive tests. However, 8-hydroxy-DPAT (selective 5-HT1A agonist) produced antinociception assessed by electric current but not tail flick. A 5-HT1A-selective antagonist, 4-[3-(benzotriazol-1-yl)propyl]-1-(2-methoxyphenyl)-piperazine, reversed the antinociception in the electrical test produced by both of these agonists but the tail-flick latency effects after intrathecal 1-(3-chlorophenyl)-piperazine were not suppressed by this antagonist. CONCLUSIONS: We conclude that 5-HT1A receptors in the spinal cord are involved in the nociceptive mechanisms assessed by noxious electrical stimuli. Other 5-HT1 receptors (non 5-HT1A receptors) are involved in the spinally mediated antinociception assessed by thermal noxious stimuli.
PMID: 12067006, UI: 22061755
Lancet 2002 Jun 29;359(9325):2275
PMID: 12103311, UI: 22100139
Lancet 2002 Jun 8;359(9322):2006
PMID: 12076562, UI: 22072495
Other Formats: Links:
N Engl J Med 2002 Jul 4;347(1):55-7
PMID: 12097542, UI: 22092567
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