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Query: UMLS:C0344307 (analgesia)
 28,200 document(s) hit in 31,850,051 MEDLINE articles (0.00 seconds)

Four experiments were conducted in rats within 2 hr of cesarean delivery to assess antinociception at birth and its possible opioid bases. Morphine antinociception was established in a dose-dependent fashion (0.0625-5.0 mg/kg bw). Analgesia was naloxone (1.0 mg/kg) reversible. In succeeding experiments, antinociception equivalent to that produced by 0.0625-0.125 mg/kg morphine injections was induced by a single 20-microliters bolus of milk (commercial half-and-half) that was delivered over 1-2 s to the middle of the tongue. This, too, was naloxone reversible. Milk-induced antinociception was maintained for at least 4 min. Finally, baseline latencies were progressively reduced during the first 2 hr after delivery to levels (8-10 s) that are typically obtained in older (10-day-old) rats. This decline was not opioid mediated because it was not affected by naloxone. Thus, at birth, delivering milk to the mouth in physiological volumes can exert opioid-mediated antinociceptive effects in rats born by cesarean delivery that had never suckled or experienced any other form of maternal contact.
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PMID:Milk-induced, opioid-mediated antinociception in rats at the time of cesarean delivery. 166 30

A randomized, double-blind study was designed to determine the effects on maternal intraoperative analgesia of adding one of the following opioids to the local anesthetic at the onset of epidural block, before surgery and neonatal delivery: morphine (3 mg), fentanyl (75 micrograms), sufentanil (50 micrograms), buprenorphine (0.3 mg) and oxymorphone (1 mg). The duration of postoperative analgesia, the presence of side effects and the neonatal outcome were also studied. Ninety healthy multiparas, at term, undergoing elective cesarean delivery using lumbar epidural anesthesia with 2% lidocaine were randomized in six equal groups to receive one of the opioids or saline. The predelivery administration of morphine, fentanyl and sufentanil significantly improved the intraoperative analgesia. Patients who received fentanyl, sufentanil, buprenorphine or oxymorphone had more somnolence than the others (p less than 0.01), but this did not interfere with the first mother-infant relationship during surgery. Patients in the buprenorphine group had more vomiting during surgery when compared with the others (p less than 0.01). Morphine provided the longest pain-free interval, followed by oxymorphone, buprenorphine, sufentanil and fentanyl. Postoperatively, the number of patients having pruritus and vomiting was significantly higher in the morphine and buprenorphine groups, respectively (p less than 0.01 versus others). No adverse neonatal effects were noted in any group.
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PMID:Epidural analgesia during and after cesarean delivery. Comparison of five opioids. 167 19

The sites of action of spinally administered opiates are specific receptors (mu kappa delta) located in the spinal dorsal horn. Pharmacokinetics of spinally administered opiates are determined by their lipophilic property. Morphine has a weak octanol-water partition coefficient and remains in the CSF during a long period following the cephalic movements of lumbar CSF to the supraspinal structures. More lipophilic opiates are rapidly eliminated from the CSF. Nevertheless, significant pethidine concentrations are documented in the ventricular CSF, due to vascular absorption of the drug. Pharmacokinetics features of different opiates determine the duration of analgesia and the risk of respiratory depression after spinal injection.
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PMID:[Pharmacology and mechanism of action of opiates administered by the subarachnoid route]. 167 77

This study was designed to determine if morphine administered intrathecally (IT) interacts with serotonergic or noradrenergic nerve terminals in the spinal cord to produce analgesia on the spinally mediated tail-flick test. Male Sprague-Dawley rats were fitted with IT catheters. One week later, animals were spinally pretreated with receptor antagonists selective for opioid, serotonin or alpha-adrenoceptors, and the ability of these agents to alter spinal morphine-induced antinociception was assessed. Morphine dose-dependently elevated tail-flick latency in a naltrexone-reversible manner. The serotonin receptor antagonists spiroxatrine (5-HT1A), pindolol (5-HT1B), ritanserin (5-HT2) and ICS 205-930 (5-HT3) attenuated the spinal analgesic effects of morphine. In contrast, the alpha 1 and alpha 2-adrenoceptor antagonists prazosin and yohimbine, respectively, did not alter morphine-induced elevations in tail-flick latency. These data substantiate earlier reports that spinal morphine-induced antinociception relies on an opioid receptor-mediated component in addition to a local serotonergic component. The finding that the alpha-adrenoceptor antagonists did not alter the antinociceptive effects of IT morphine suggests that spinal norepinephrine does not contribute to the analgesic effects of the opiate.
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PMID:Serotonin contributes to the spinal antinociceptive effects of morphine. 168

The process of nociception, the anatomy of the epidural space, and the placement of the epidural catheter are reviewed, and the pharmacology and pharmacokinetics, analgesic efficacy, and potential adverse effects of epidurally administered narcotics and local anesthetics are discussed, as well as patient monitoring standards and solution preparation guidelines for these agents. The epidural space is located between the dura mater (the outer-most membrane surrounding the spinal cord) and the vertebral canal. The site of catheter placement is determined by the dermatomes corresponding to the site of desired analgesia. The primary factors that differentiate epidural narcotics are related to their pharmacokinetic profiles. Morphine, which is hydrophilic, has a slower onset of action and a longer duration of analgesia than lipophilic compounds such as fentanyl; morphine also results in less segmentalization (the degree to which analgesia is limited to discrete dermatomal segments corresponding to the level of the epidural narcotic injection) than is seen with lipophilic compounds. Studies have shown that epidural narcotics provide superior pain relief compared with systemic narcotics. Common adverse effects associated with therapeutic doses of intraspinal narcotics include itching, nausea and vomiting, urinary retention, and sedation; respiratory depression is uncommon after epidural administration of narcotics. The most bothersome adverse effect encountered with analgesic doses of local anesthetics is paresthesia. Solutions for epidural administration must be sterile and preservative free. Epidural administration of narcotics and local anesthetics seems to provide better pain relief than conventional methods but may be associated with more bothersome adverse effects.
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PMID:Epidural analgesia. 174 84

Morphine and other opioid analgesics may interfere with normal cognition and motor function when the drugs are used for long-term treatment of pain. We used individually tailored steady-state drug infusions to identify the nature and extent of cognitive and motor effects of the mu-receptor-selective opioid morphine in healthy volunteers. The tailored infusions allowed evaluation of cognitive and motor effects at three sequential, constant plasma concentrations of morphine in each subject. Compared with functional assessments obtained in a separate saline infusion day, infusions of morphine to plasma concentrations in the usual therapeutic range for analgesia caused significant impairments of some but not all elements of cognitive and motor function. The time needed to encode and process serially presented verbal information increased and the ability to maintain low consistent levels of force decreased during the morphine infusion. We also assessed verbal recall 3 hours after the morphine and saline infusions. Delayed recall of information presented during the morphine infusion was significantly impaired. Our results demonstrate that morphine can interfere with cognitive and motor performance at plasma drug concentrations within the usual therapeutic range.
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PMID:Concentration-related effects of morphine on cognition and motor control in human subjects. 175 31

We compared patient-controlled analgesia (PCA) and continuous infusion (CI) morphine delivery in a randomized controlled trial in adolescents during oropharyngeal mucositis pain after bone marrow transplantation. Results from 20 patients who completed 7 or more days on study (10 PCA, 10 CI) were evaluated. The group means for age, weight and height were comparable. Daily measures were morphine intake, self-report of pain intensity and side effect scores. Over 10 study days, the mean cumulative morphine dose to subjects in each group was 4.94 mg/kg (PCA) vs. 12.17 mg/kg (CI); the difference is significant (P less than 0.01). No significant differences were found between the groups for patient ratings of pain intensity or side effect scores despite the large difference in mean morphine intake, but the PCA group tended to report less intense sedation and less difficulty concentrating. Adolescents can use PCA effectively and safely for 1-3 weeks. Morphine intake of adolescent patients using PCA morphine intake is significantly lower than that of similar patients receiving staff-controlled CI.
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PMID:Adolescents use patient-controlled analgesia effectively for relief from prolonged oropharyngeal mucositis pain. 175 10

Seventy cancer patients suffering from visceral or somatic pain received continuous epidural methadone (EM) analgesia. Initially, 4 mg of 0.1% methadone was given three times daily. If this dose proved ineffective, it was gradually increased to 8 mg four times daily. With this regimen good pain control was obtained in 56 patients (80%). Patients continued the EM therapy for periods up to 140 days, with an average duration of 27 days. Morphine was substituted for methadone in 14 patients (20%). Four of these patients responded well and continued treatment for an average of 18 days. No serious side effects have been observed with EM. With a proper selection of patients and following strict therapy guidelines, epidural methadone is efficacious in treating cancer pain.
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PMID:Continuous epidural methadone treatment for cancer pain. 180 48

We have studied the ability of clonidine to potentiate morphine analgesia in 28 patients (ASA I) after meniscectomy under general anaesthesia. One hour after surgery, morphine 3 mg (n = 10), clonidine 75 micrograms (n = 8) or morphine 3 mg plus clonidine 75 micrograms (n = 10) was injected extradurally. Morphine alone and in combination with clonidine produced similar and significant analgesia as assessed by verbal analogue pain scores. Pain scores did not decrease significantly in patients given clonidine alone. There were statistically, but not clinically significant decreases in systemic arterial pressure after morphine alone and clonidine alone. No patient developed sensory or motor block. One patient given morphine alone developed retention of urine. It is concluded that, in the dose used in this study, clonidine did not potentiate the analgesia produced by extradural morphine.
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PMID:Extradural clonidine does not potentiate analgesia produced by extradural morphine after meniscectomy. 181 28

Although morphine typically produces analgesia in a variety of species, recent research has identified a biological model in which morphine produces a naloxone-reversible, paradoxical hyperalgesic response to a noxious thermal stimulus in young domestic fowl. The present study examined opioid receptor-mediation of this atypical opiate effect. Patterns of morphine hyperalgesia (1.25 to 5.0 mg/kg IM) were examined on a standard hot-plate test following administration (10 micrograms/5 microliters ICV) of the mu antagonist beta-funaltrexamine, the delta antagonist naltrindole, or the kappa antagonist nor-binaltorphimine in 15-day-old White Leghorn cockerels. Respiration measures were also recorded because they are indicative of opiate effects. Morphine produced a dose-dependent decrease in mean jump latencies (i.e., hyperalgesic effect). Mu receptor antagonism attenuated this morphine-induced hyperalgesic effect. Kappa receptor antagonism attenuated morphine-induced hyperalgesia only at the highest morphine dose (i.e., 5.0 mg/kg) and delta receptor antagonism failed to attenuate morphine-induced hyperalgesia. These results suggest that morphine-induced hyperalgesia, like morphine-induced analgesia, is mediated primarily by mu receptor activation.
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PMID:Effects of selective opiate antagonists on morphine-induced hyperalgesia in domestic fowl. 185 Jan 36


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