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)

Morphine analgesia can be reduced by prior exposure to food and flavored fluids. The early onset of reduced morphine-induced analgesia (RMA) was studied in 82 male Wistar rats after allowing them access to either a dextrose-saccharin solution or unflavored tap water for 6 or 3 h (Experiment 1, n = 40) or for 3 h, 90, or 45 min (Experiment 2, n = 42). Morphine (4 mg/kg) was injected subcutaneously at the end of the drinking period, and after 25 min a series of tail flick tests was conducted. Morphine produced strong analgesia in all rats that drank unflavored tap water; however, in rats that drank the flavored solution, the analgesic effect of morphine was significantly attenuated following exposures of 6 or 3 h, but not following exposures of 90 or 45 min. Similar quantities of flavored fluid were consumed by groups at all exposure durations; thus, RMA was determined by duration of exposure and not amount consumed. No analgesia attributable to flavor consumption per se was observed. The results suggest that RMA is mediated by endogenous opioid activity in the gustatory and analgesic systems by a mechanism akin to tolerance that requires about 3 h to operate.
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PMID:Early onset of reduced morphine analgesia by ingestion of sweet solutions. 843 57

Since clonidine potentiates the analgesia by morphine, the current study was performed to investigate whether oral clonidine premedication would enhance the postoperative analgesia by intrathecal morphine. Twenty-six patients, aged 37-60 yr, schedule for abdominal total hysterectomy under spinal anesthesia, were studied. Patients were randomly allocated to one of two groups; the clonidine group (n = 13) received oral clonidine approximately 5 micrograms/kg, and the control group (n = 13) received no clonidine. All patients received hyperbaric tetracaine 12 mg dissolved in 10% dextrose and morphine 0.2 mg for spinal anesthesia. We measured duration of analgesia (time to the first request for supplemental analgesics) and motor block. We also recorded the total number of injections of supplemental analgesics, and intensity of postoperative visual analog pain scores, nausea, and pruritus for 48 h after intrathecal administration. Duration of analgesia in the clonidine group was longer than the control group (2017 +/- 263 vs 1190 +/- 199 min, mean +/- SEM; P < 0.05). Although there was no difference in the total number of injections of supplemental analgesics (1.1 +/- 0.4 and 2.2 +/- 0.3 in the clonidine and control groups, respectively), the number of patients not requiring supplemental analgesics during the entire study period was larger in the clonidine group than the control group (six patients versus one patient; P < 0.05). There were no differences at any observation point between groups in visual analog pain scores, or the incidence of nausea and pruritus. Oral clonidine preanesthetic medication enhances the postoperative analgesia of intrathecal morphine plus tetracaine without increasing the intensity of side effects from morphine.
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PMID:Oral clonidine premedication enhances the quality of postoperative analgesia by intrathecal morphine. 863 90

MOR-1 encodes a mu receptor. In an effort to establish the relationship of this cloned opioid receptor with ingestive behavior and analgesia in rats, the present study examined the actions of four antisense oligodeoxynucleotides aimed at exons 1 (AS1), 2 (AS2), 3 (AS3) and 4 (AS4) of the MOR-1 clone, as well as a mismatch antisense sequence (MS1). Rats were administered intracerebroventricular injections (10 micrograms/2 microliters) of each of the oligodeoxynucleotides on days 1, 3 and 5. Body weight and spontaneous food and water intake were monitored daily. In addition, 2-deoxy-D-glucose (2DG)-induced hyperphagia, central Angiotensin II (ANG-II) induced hyperdipsia and central morphine analgesia were examined 24 h following the last antisense injection. AS1, AS2, AS3 and AS4 each significantly reduced body weight (7-17 g), food intake (8-13 g) and water intake (11-23 ml), while the vehicle or MS1 conditions significantly increased weight (9-20 g) and produced smaller reductions (2-4 g) in food intake. None of the AS probes altered the magnitude of either 2DG-induced hyperphagia or ANG-II-induced hyperdipsia. Central morphine analgesia was reduced by pretreatment with AS1 and AS4, but not AS2, AS3 or MS1. The sensitivity of general feeding to all four exons suggest that the receptor responsible for this action is encoded by the MOR-1 clone. The differences between feeding and morphine analgesia raise the possibility that these two actions are mediated through different mu receptor subtypes. Our results also demonstrate the viability of the in vivo antisense technique in modulating opioid-mediated ingestive responses.
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PMID:Antisense oligodeoxynucleotides against the MOR-1 clone alter weight and ingestive responses in rats. 878 66

This study compared the quality of analgesia and incidence of adverse effects with two doses of intrathecal morphine in patients undergoing elective Caesarean section. Fifty patients were randomly allocated to receive either morphine 0.1 mg or 0.2 mg in addition to a standard intrathecal dose of 2.5 ml bupivacaine 0.5% in 8% dextrose. The quality of analgesia was assessed using visual analogue scores and the incidence of nausea, vomiting and itching were recorded during the first 24 h postoperatively. There was no statistically significant difference in the quality of analgesia nor in the incidence and severity of itching between the two groups. Fewer patients in the 0.1 mg morphine group experienced postoperative nausea and vomiting (7 versus 14, p < 0.05). We conclude that the use of 0.1 mg morphine intrathecally produces comparable analgesia to 0.2 mg after Caesarean section with significantly less nausea and vomiting.
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PMID:Intrathecal administration of morphine for elective Caesarean section. A comparison between 0.1 mg and 0.2 mg. 912 72

A randomized, single-blind trial of two spinal anesthetic solutions for outpatient laparoscopy was conducted to compare intraoperative conditions and postoperative recovery. Thirty women (ASA physical status I and II) were assigned to one of two groups. Group I patients received a small-dose hypobaric solution of 1% lidocaine 25 mg made up to 3 mL by the addition of fentanyl 25 micrograms. Group II patients received a conventional-dose hyperbaric solution of 5% lidocaine 75 mg (in 7.5% dextrose) made up to 3 mL by the addition of 1.5 mL 10% dextrose. All patients received 500 mL of crystalloid preloading. Spinal anesthesia was performed at L2-3 or L3-4 with a 27-gauge Quincke point needle. Surgery commenced when the level of sensory anesthesia reached T-6. Intraoperative hypotension requiring treatment with ephedrine occurred in 54% of Group II patients but not in any Group I patients. Median (range) time for full motor recovery was 50 (0-95) min in Group I patients compared to 90 (50-120) min in Group II patients (P = 0.0005). Sensory recovery also occurred faster in Group I patients (100 +/- 22 min) compared with Group II patients (140 +/- 27 min, P = 0.0001). Postoperative headache occurred in 38% of all patients and 70% of these were postural in nature. Oral analgesia was the only treatment required. Spinal anesthesia did not result in a significant incidence of postoperative backache. On follow-up, 96% said they found spinal needle insertion acceptable, 93% found surgery comfortable, and 90% said they would request spinal anesthesia for laparoscopy in future. Overall, this study found spinal anesthesia for outpatient laparoscopy to have high patient acceptance and a comparable complication rate to other studies. The small-dose hypobaric lidocaine-fentanyl technique has advantages over conventional-dose hyperbaric lidocaine of no hypotension and faster recovery.
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PMID:Small-dose hypobaric lidocaine-fentanyl spinal anesthesia for short duration outpatient laparoscopy. I. A randomized comparison with conventional dose hyperbaric lidocaine. 898

Dextrose-free anesthetic medications are commonly used to provide subarachnoid anesthesia and analgesia. Hypobaricity has been proposed as a mechanism to explain postural effects on the extent of sensory block produced by these drugs. Densities of dextrose-free solutions of local anesthetics and opioids, and commonly used anesthetic/opioid mixtures were determined at 37.00 degrees C for comparison with the density of human cerebrospinal fluid (CSF). Measurements accurate to 0.00001 g/mL were performed using a mechanical oscillation resonance frequency density meter. All undiluted solutions tested are hypobaric relative to human lumbar CSF with the exception of lidocaine 1.5% and 2.0% with epinephrine 1:200,000. All mixtures of local anesthetics and opioids tested are hypobaric. We observed good agreement between measured densities and calculated weighted average densities of anesthetic mixtures. While the influence of baricity on the clinical effects of dextrose-free intrathecal anesthetics remains controversial, attempts to attribute postural effects to the baricity of these drugs requires establishment of accurate density values. These density data may facilitate elucidation of the mechanisms underlying the behavior of dextrose-free intrathecal anesthetics.
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PMID:Densities of dextrose-free intrathecal local anesthetics, opioids, and combinations measured at 37 degrees C. 898 7

The symptoms and signs of sickle cell disease are exacerbated in times of crisis, characterized by tissue infarction or worsening anaemia. Prompt medical intervention is required in these distressing situations to provide relief and comfort to the patient. Effective analgesia is crucial in treating the painful crisis of sickle cell disease. The haemoglobinopathy may cause hyposthenuria with reduced ability to excrete the sodium load in normal saline. A 5% dextrose solution or 5% dextrose in 25% normal saline is therefore recommended for intravenous hydration. As the leading cause of morbidity and mortality in sickle cell disease, infections call for vigorous antibiotic therapy. Oxygen administration should be reserved for hypoxic patients, and blood transfusion given only when really indicated. Acute chest syndrome and cerebrovascular accidents are life-threatening complications of sickle cell disease whereas priapism can cause important long-term sequelae; all deserve urgent attention. In the long term, comprehensive care is cost-effective in reducing the frequency and adverse effects of sickle cell crisis.
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PMID:The management of crisis in sickle cell disease. 945 21

The extract of Viticis Fructus appeared to have an analgesic effect, and was subjected to activity-guided separation using acetic acid-induced writhing in mice. The active fraction gave new compounds, vitexfolin A (1A), B and C, 10-O-vanilloylaucubin (3), dihydrodehydrodiconiferylalcohol-beta-D- (2'-O-p-hydroxybenzoyl)glucoside (4), and vanilloyl-beta-D-(2'O-p-hydroxybenzoyl)glucoside, together with agnuside (2) and erythro- and threoguaiacylglycerols. Compounds 1A and 2-4 showed significant writhing inhibition following oral administration at doses of 15, 50, 25, and 50 mg/kg, respectively. The effect on pressure pain threshold was tested using compounds 1A and 2 at a dose of 50 mg/kg, and only the former produced the analgesia. The analgesic effect of some related iridoid glucosides is also discussed.
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PMID:Pharmacologically active components of viticis fructus (Vitex rotundifolia). II. The components having analgesic effects. 957 42

The objective of this study was to determine hemodynamic effects and pharmacokinetic profiles of fentanyl with continuous infusion in 1- to 3-day-old newborn piglets. The piglets (n = 6) were administered a loading dose of fentanyl at 30 microg/kg i.v. over 15 min followed by a continuous i.v. infusion at 10 microg/kg/h for 6 h. The control group (n = 8) received equivalent volume bolus and infusion of 5% dextrose. Blood samples were obtained serially from systemic circulation and sagittal sinus vein for measurement of plasma fentanyl, pH and blood gases. Plasma fentanyl achieved steady state levels by 30 min of infusion both in the systemic (202.7 +/- 39.1 ng/ml) and sagittal sinus vein (136.7 +/- 20.7 ng/ml). Fentanyl caused a transient increase in respiratory rate at 2 h. Heart rate was significantly elevated at 30 min and 6 h during infusion but systemic and sagittal sinus vein blood pressure remained unchanged. Systemic and sagittal sinus vein PO2 were significantly decreased from 2 through 6 h of infusion. Compared to the control group, there was a 56% (p < 0.01) decrease in sagittal sinus vein O2 content at 30 min of infusion, an effect which lasted up to 6 h (47%, p < 0.01). Fractional O2 extraction by the brain increased significantly at 30 min (26%, p < 0.01) and remained elevated throughout the infusion time (22%, p < 0.05 at 6 h). Brain fractional O2 extraction increased as a function of brain fractional fentanyl extraction (r2 = 0.40, p < 0.001). Mean clearance was estimated as 56.2 +/- 13.7 ml/kg/h (range 43.5-76.9 ml/kg/h), mean volume of distribution at steady state was 1.29 +/- 0.6 liters/kg (range 0.78-2.15 liters/kg) and the mean half-life was 15.7 +/- 5.7 h (range 9.4-22.5 h). These data suggest that increased systemic oxygen may be necessary to maintain normal cerebral oxygen extraction during fentanyl anesthesia/analgesia.
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PMID:Pharmacodynamic effects and pharmacokinetic profile of continuous infusion fentanyl in newborn piglets. 965 68

We have investigated the effect of infusion of nimodipine on the spread of spinal anaesthesia in 50 patients undergoing transurethral procedures. Patients were allocated randomly to receive during operation continuous infusion of nimodipine 10 ml h-1 (group N, n = 25) or normal saline (group C, n = 25) in a double-blind manner. All patients received hyperbaric lidocaine 100 mg (5% in 8% dextrose) intrathecally and were then placed in the lithotomy position. Twenty minutes after intrathecal injection the level of spinal anaesthesia was tested with a pressure palpator and a baseline was established. Assessments were repeated 5, 10 and 15 min thereafter. Five minutes after establishing baseline, mean regression of sensory analgesia did not differ between groups. Analgesia had regressed by 1.3 (SD 1.4) and 1.0 (1.9) cm, respectively. After 10 min, sensory block in group N regressed by 1.7 (1.7) cm and in group C by 1.5 (1.6) cm. After 15 min these values were 1.1 (1.7) cm and 2.2 (1.9) cm, respectively (P < 0.035). Similar results were found after normalizing the changes by dividing the change by patient height.
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PMID:Effect of nimodipine on regression of spinal analgesia. 986 Nov 19


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