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PubMed1985

[The modes of anti-inflammatory and analgesic actions of aspirin and salicylic acid].

The modes of anti-inflammatory and analgesic actions of aspirin and salicylic acid were investigated using some experimental animal models. Anti-inflammatory potencies of aspirin were almost equal to those of sodium salicylate in the carrageenin hind paw edema, the cotton pellet granuloma and the adjuvant arthritis tests in rats. On the other hand, in the ultra-violet ray erythema and the arachidonic acid erythema tests in guinea pigs, aspirin was more potent than sodium salicylate. Aspirin and sodium salicylate exhibited almost the same inhibitions of the rat hind paw edema induced by a mixture of carrageenin and prostaglandin E1. These results suggest that inhibition of cyclo-oxygenase by aspirin does not play any important roles for the prevention of the vascular permeability increment and the granulation in the inflamed tissue. Aspirin may exert its antiinflammatory activity mainly as salicylic acid which is not an inhibitor of prostaglandins biosynthesis in vitro. Aspirin showed about 5 times more potent analgesic action than sodium salicylate in the lameness test using adjuvant arthritic rats. Analgesic potency of aspirin was decreased to the level of sodium salicylate by injection of prostaglandin E2 into the inflamed rat paw in the adjuvant-induced lameness test. On the other hand, analgesic potency of sodium salicylate was not decreased by the same treatment. It is concluded that aspirin has two analgesic effects on the inflammatory pain, one is inhibition of prostaglandins biosynthesis by acetylation of cyclo-oxygenase and the other is an action due to salicylic acid, but the action of salicylic acid was not totally explained by the inhibition of prostaglandins synthetase.

Animals↗
PubMedDate not supplied

Analgesic effects of breast-feeding or pacifier use with maternal holding in term infants.

OBJECTIVES: First, to compare analgesic effects of breast-feeding versus pacifier use in newborn infants undergoing blood collection via heel sticks. Second, to compare analgesic effects of pacifier use with maternal holding versus nonmaternal holding. DESIGN: A prospective, randomized, controlled trial. SETTING: Normal newborn nursery at academic teaching hospital. PARTICIPANTS: Full-term breast-feeding infants scheduled for routine newborn screening blood test via heel stick (n = 96). Interventions.-Infants randomized to 3 groups for analgesia: 1) breast-feeding, 2) pacifier use while held by mothers, 3) pacifier use while held by research assistants (nonmothers). OUTCOME MEASURES: Primary outcome was crying (percent of infants who cried during the procedure and mean percent of procedure time that infants cried). Secondary outcomes were physiologic measures. RESULTS: Fewer breast-feeding infants cried than infants using a pacifier while held by nonmothers both during the procedure (69% vs 100%, P < .01) and after the procedure (28% vs 60%, P = .03). Those infants crying during the procedure cried for less time if held by their mothers either breast-feeding (33%, P < .01) or using a pacifier (45%, P = .03) than those using a pacifier while being held by nonmothers (66%). CONCLUSION: Breast-feeding is more analgesic than pacifier use with nonmaternal holding. Maternal holding with either breast-feeding or pacifier use is more analgesic than nonmaternal holding with pacifier use, suggesting that maternal holding itself has an analgesic effect. Breast-feeding and maternal holding should be considered as pain-control measures for the neonate during heel-stick procedures.

Analgesia↗
PubMed1988

Analgesic effect and bioavailability of oral ketogan given as tablets or mixture to patients with chronic pain of malignant origin.

Thirteen cancer patients with moderate to severe chronic pain of malignant origin on treatment with Ketogan tablets were included in an open non-randomized cross-over study comparing the analgesic effect, side effects and serum concentrations of Ketogan tablets and mixture. The patients were six days in hospital and were dosed two days with tablets, two days with mixture and finally another two days with tablets. Recordings of pain and side effects and collection of blood samples prior to dosing and hourly thereafter until remedication were performed on the second day of each dosing period in a morning dose interval. The analgesic effect judged by visual analog score (VAS) and pain intensity differences (PID), the areas under the serum concentration time curves, and the average serum concentrations for the three groups were compared. It was not possible do detect any differences among the three groups concerning the analgesic effect, duration of analgesic effect, the serum concentrations and the side effects. The mean plasma half-life of ketobemidone was 2.74 h +/- 0.90 (SD) and the mean relative bioavailability of the mixture was slightly above 100%. Linear regression analysis revealed a significant correlation between ketobemidone serum concentrations and analgesic effect, VAS, for tablet one and for the mixture but not for tablet two, possibly due to the fixed dosing schedule and to the positive effect of hospitalization on the pain.

Administration, Oral↗
PubMed2002

Peripheral analgesic sites of action of anti-inflammatory drugs.

Inflammatory signs and symptoms of redness, swelling, heat and pain are due to the effects of inflammatory mediators released during the inflammatory response. Depending on the type of injurious stimuli and the tissue involved, the array of mediators may differ but eicosanoids are involved in the genesis of inflammatory pain. They are responsible for the hypersensitisation of the nociceptors (allodynialhyperalgesia). The basic mechanism of analgesic action of nonsteroidal anti-inflammatory drugs results from the inhibition of prostaglandin synthesis (prostacyclin or PGE2), thus preventing nociceptor threshold lowering. Because there is a temporal hierarchy in the release of inflammatory mediators, there are several targets for the action of peripheral acting analgesics before and after the inhibition of prostaglandin synthesis. Blockade of the release and inhibition of inducible cyclooxygenase explain the analgesic action of glucocorticoids. Nimesulide also has an inhibitory action on the cascade of hypersensitising cytokines. Some analgesics, such as dipyrone, flurbiprofen or diclofenac, act directly upon ongoing inflammatory hypersensitisation. Those analgesics restore the nociceptor by stimulating the arginine/NO/cGMP/K(ATP) channel pathway.

Analgesia↗
PubMed2002

[Psychophysiological features of analgesics abuse headache].

Sixty patients with abuse headache (AHA) (58 women and 2 men, mean age 44.5 years) and 10 age- and sex-matched controls have been studied. AHA diagnostic criteria were as follows: daily or almost daily headache, daily or every other day use of analgesics, primary headache (migraine or headache of tension--HAT) in anamnesis, uneffectiveness of medication. Clinico-neurological analysis, headache diary, Beck depression scale, Spilberger Trait/State Inventory, "Pain lifetime anamnesis", autonomic dystonia questionnaire, evaluation of night-time sleep score subjective characteristics and nociceptive flexor reflex (R-111) (NFR) determination were used. The results obtained confirmed the literature data that analgesics abuse in migraine resulted in AHA 2 times more often than in HAT. The causes were mainly psychogenic: mood improvement, night-time sleep normalization and post-stress cephalgia intensification. An influence of such factors as age and menopause was not found. Headache was of mixed character with features of both migraine and HAT and was not dependent on cephalgia type in anamnesis. Quantity of analgesics taken by the patients ranged from 40 to 120 tablets a month and influenced, in general, a speed of primary HA to AHA transformation. For AHA formation, systematic analgesics intake was more significant comparing to its absolute quantity. Pronounced psycho-autonomic disorders and night-time sleep disturbances in AHA were revealed. In analgesics abuse, pain and NFR thresholds were significantly higher as compared to controls. However, pain to reflex thresholds ratio proved to be reduced that indicated a relative deficiency of antinociceptive system which is necessary for pain syndrome reduction.

Adult↗
PubMed2003

[Comparison of analgesic effects of intravenous flurbprofen and suppository indomethacin after laparoscopic cholecystectomy].

BACKGROUND: Epidural analgesia may not be necessary after laparoscopic cholecystectomy, but analgesics, such as non-steroidal anti-inflammatory drugs, may often be required postoperatively. There have been only a few studies comparing different NSAIDs in this situation. METHODS: After laparoscopic cholecystectomy under general anesthesia using intravenous propofol, nitrous oxide and fentanyl 3 micrograms.kg-1, 40 patients were randomly allocated to receive either intravenous flurbprofen 50 mg or suppository indomethacin 50 mg. Visual analogue scales of postoperative pain at 0, 10, 20, 30 and 60 min after surgery (at rest and at coughing), use of rescue analgesics, and the presence or absence of complications were recorded. RESULTS: Pain score at rest was markedly reduced (> 15% reduction from the baseline value) in 13 of 20 patients after injection of flurbiprofen and in five patients after indomethacin during the initial 60 min after surgery (P < 0.05), whereas there was no significant difference between the two groups for the pain score during coughing. There was no difference in the need of rescue analgesics within the initial 60 min, but the flurbiprofen group required significantly more rescue analgesics than the indomethacin group during 1-24 h after surgery (P < 0.005). The incidence of complications was low in both groups. CONCLUSIONS: Compared with suppository indomethacin, intravenous flurbiprofen is more effective in acute postoperative pain but the duration of its analgesic effect is shorter.

Acute Disease↗
PubMed2003

Analgesic effect of caffeine and clomipramine: a possible interaction between adenosine and serotonin systems.

The goals of this study were to determine whether the nonselective adenosine receptor antagonist caffeine exerts an analgesic effect and to investigate the time-dependent influence of the selective serotonin reuptake inhibitor clomipramine on the action of caffeine. Results suggest a possible interaction between serotonin and adenosine systems, which may contribute to the analgesic action of drugs. Therefore, the hot-plate and formalin tests were employed in order to measure the response to painful thermic and chemical stimuli. Results have shown that caffeine (1.67, 16.7 and 67 mg kg(-1), i.p.) exerts a direct dose-dependent analgesic action. When caffeine (1.67 and 16.7 mg kg(-1)) was combined with clomipramine (3 mg kg(-1) i.p.), an enhanced analgesic effect was obtained. However, the same combinations were ineffective in a subacute model. In this model, clomipramine was administered for 14 days and the respective dose of caffeine was added on the last day. Therefore, it can be concluded that the serotonin system interacts with the analgesic action of caffeine and that a long-term use of clomipramine probably triggers subsensitivity of adenosine receptors.

Adenosine↗
PubMed1992

Development of tolerance to the analgesic activity of mu agonists after continuous infusion of morphine, meperidine or fentanyl in rats.

We investigated the role of intrinsic activity in the ability of mu-opioid agonists to produce tolerance to the analgesic effects of other mu agonists. Dose-response curves were generated for each test drug before and 24 hr after 1 week s.c. agonist infusions, using a tail-flick procedure in male rats. Morphine tolerance was dose-dependent over a range of doses, 0.3 to 1.4 mg/kg/hr, infused for 7 days by osmotic pump; 0.8 mg/kg/hr (1/4 acute ED50/hr) shifted the morphine dose-response curve roughly 2-fold to the right. Morphine, fentanyl or meperidine were then infused for 1 week to induce tolerance; doses were based on equipotent acute s.c. doses (1/4 ED50/hr). Drugs tested for analgesic activity, using a cumulative dosing procedure, included morphine, fentanyl, meperidine, methadone, buprenorphine, etorphine and levorphanol. The relative potency (RP) was calculated for each animal by dividing the preinfusion analgesic ED50 by the postinfusion ED50. The potency of morphine, fentanyl, meperidine and levorphanol decreased after a 7-day infusion of 0.8 mg/kg/hr morphine (RP = 0.44-0.70), but the potency of etorphine (RP = 0.85) and methadone (RP = 0.78) were not significantly changed. Chronic infusions of 6.25 mg/kg/hr meperidine produced more tolerance than did morphine (RP = 0.11-0.51). No significant change in analgesic potency was seen in six of the seven test drugs after infusions of 0.01 mg/kg/hr fentanyl (RP = 0.81-1.27). Buprenorphine did not produce an analgesic response in rats that received infusions of any of the three mu agonists. The RP of drugs with low intrinsic activity was lower than the RP of high efficacy drugs.(ABSTRACT TRUNCATED AT 250 WORDS)

Analgesia↗
PubMed1991

Increased analgesic potency of mu agonists after continuous naloxone infusion in rats.

Chronic opioid antagonist administration increases opioid binding sites and potentiates behavioral responses to morphine. The present study was designed to examine in rats the temporal and dosage parameters of naloxone-induced potentiation of morphine analgesia and the effect of continuous infusion of naloxone on the analgesic potency of other mu agonists. Cumulative dose-response curves were generated in a tail-flick procedure for each drug tested. Naloxone-filled osmotic pumps were then implanted s.c. for 1 week after which the rats were retested with the agonist. The potency ratio of morphine (ED50 before naloxone/ED50 after naloxone) showed orderly increases over a range of naloxone doses (0.03-1.0 mg/kg/hr) and increased, then decreased, over a range of time points (6-72 hr) after removal of the osmotic pumps. The relative potency of morphine was 2.1 at 24 hr after a 7-day infusion of 0.3 mg/kg/hr of naloxone. These parameters were then used in tests of other mu agonists. Five drugs produced maximum increases in tail-flick latencies before naloxone. Of these, naloxone increased the analgesic potency of fentanyl, methadone and levorphanol (relative potencies ranged from 1.7-2.1) but not of etorphine and propoxyphene. The naloxone infusion increased the maximum analgesic effect of meperidine, profadol and pentazocine, but had no effect on the analgesic activity of buprenorphine, butorphanol, ethylketocyclazocine and nalbuphine. Our results demonstrate that 7-day naloxone infusion increases the analgesic potency of some, but not all, opioids with mu agonist activity.

Analgesia↗
PubMed1991

[Involvement of solitary tract nucleus in analgesic effect produced by paraventricular nucleus stimulation].

This study was undertaken to evaluate the analgesic effect of paraventricular nucleus (PVN) stimulation with tail stimulation-vocalization test. The mechanism of this analgesia was analysed with nuclear lesion and microinjection technique. The main results were as follows: (1) Electrical stimulation of the PVN could significantly enhance the pain threshold and increase the content of AVP in brainstem measured by radioimmunoassay. (2) Solitary tract nucleus (STN) lesion could eliminate the analgesic effect induced by PVN stimulation. (3) Intranuclear microinjection of AVP-antagonist and AVP-antiserum into the STN could block the analgesic effect of PVN stimulation. (4) Intranuclear microinjection of AVP into the STN could mimick the analgesic effect similar to that of PVN stimulation. These results suggest that electrical stimulation of the PVN could produce an analgesic effect. This effect might be mediated by the activation of VP-ergic neurons in PVN and upon releasing VP from the descending fibers, the activities of neurons in the STN are influenced.

Animals↗
PubMed1991

[Analgesic effects of epidural morphine, fentanyl and lidocaine].

The analgesic effects of epidurally administered morphine 5 mg (group M, n = 15), fentanyl 100 micrograms (group F, n = 15), 2% lidocaine 60 mg (group L, n = 15) and normal saline (group S, n = 10) were investigated in 55 patients scheduled for abdominal surgery. Each drug was prepared in 3 ml solution and was injected though an epidural catheter introduced 3 cm cephalad into the epidural space at T10-11. Analgesic effects were assessed by changes in the dull pain sensation induced by electrical stimulation at 3 Hz through a pair of stainless needles which were placed subcutaneously at T7 and T10 dermatomes. In group M, analgesic effects at T10 were demonstrated in 12 of 15 subjects and the onset of analgesia was more rapid at T10 than at T7. The mean onset time of analgesia was 7.8 +/- 3.6 (mean +/- SD) min. There were 5 subjects in group F and 6 in group L who showed more rapid onset of analgesic effects at T10 than at T7, respectively. There were 2 subjects in group F and 5 in group L, with more rapid onset of analgesia at T7 than at T10. There were several subjects in group F and L with simultaneous onset of analgesia at T7 and T10. In group L, the mean distribution of analgesic area, confirmed with pinprick, was 5.2 +/- 1.9 (mean +/- SD) dermatomal segments. Hypercapnea, associated with somnolence, was frequently seen in group F. None of the subjects in group M, L or S showed such incidents. These results suggest that the main site of action of epidural morphine is located in the spinal cord while that of epidural fentanyl in the brain.

Adult↗
PubMed1979

Analgesic anesthesia with fentanyl (F) and sufentanil (SF) in coronary surgery. A double blind study.

The study includes 54 unselected coronary patients. Fifty underwent one or several aortocoronary bypass associated with left ventricular resection (3 times), mitral valve replacement (twice), aortic valve replacement (twice). Four patients underwent left ventricular resection alone. The operations were performed under analgesic anesthesia with sufentanil (SF) or fentanyl (F) with a double blind protocol. The ratio of concentrations of the two analgesics was SF/F = 1/10. Flunitrazepam induced and maintained sleep. After having reached by increments the total dose of 1.5 mg F/M2 or 0.15 mg SF/M2, droperidol was then added in small amounts of 3.75 mg/M2, alternating with the analgesic both being given as needed to maintain blood pressure between 100 and 120 mm Hg, in order to potentiate the level of analgesia reached and prevent vasoconstriction. Under this setting tachycardia (heart rate greater than 100 beats/min. and less than 120 beaths/min.) was observed before ECC in only 7.4% of cases with both analgesics and brief episodes of hypertension (mean maximum systolic blood pressure 140.7 +/- 20.3 mm Hg seen with SF exclusively). There was neither postoperative hypertension (except with 6 out of the 7 known hypertensive patients) nor low cardiac output, nor arbythmia. No patients remained in intensive care unit more than 24 hour. No difference attribuable to the used analgesic was detectable in the early and late follow-up in both series. On an average, the patients were discharged on postoperative day 10 in a valid condition.

Adult↗
PubMed1984

[Characterization of the effect of analgesics on the assessment of experimental pain in man. Pethidine and tramadol in a double-blind comparison].

The effect of the opioid analgesics tramadol and pethidine on experimentally induced pain was investigated in a double blind study with healthy volunteers. Using a constant current shocker, compensating the changes of the skin resistance, a constantly increasing pain stimulus was produced. Detection-, pain-, and tolerance-thresholds were assessed before and three times after intravenous injection of either pethidine (1 mg/kg bodyweight), tramadol (2 mg/kg bodyweight) or placebo (NaCl). While the two analgesics caused an increase of all three thresholds the placebo did not cause any threshold changes. The rise of the detection threshold after application of tramadol and pethidine suggests a sedation effect. However, in relation to the analgesic effect this sedation effect is stronger with tramadol than with pethidine. With the dosage used in this experiment, there is no difference in the analgesic effect of tramadol and pethidine. Compensating for intra- and interindividual changes in skin resistance, the pain stimulation method used in this study provides a good quantification of the effects of analgesics.

Adult↗
PubMed1984

[Types of bronchial reaction to analgesics].

Bronchial reaction of asthma bronchiale patients (n = 102) to analgesics was tested by oral exposure to acetylsalicylic acid. 73 patients produced no changed bronchial response to the exposure test. Ventilation parameters improved in 12 patients. In cases in which analgesics intolerance had been recordable from case histories (n = 17), acetylsalicylic acid doses were carefully increased in a stepwise approach to identify the threshold dose required for inset of bronchoconstriction. The average triggering threshold dose was found to be 200 mg. In patients with normal analgesics tolerance products of arachidonic acid metabolism seem to have no effect on bronchial tonus. The observed dilating effect of analgesics may, possibly, be associated with elimination of a cyclooxygenase metabolite with relevance to bronchoconstriction. Inducer of analgesics intolerance is the shift of arachidonic acid metabolism in favour of the route of lipoxygenase. Of importance is possibly a free proteolytic activity (inhibitor deficiency) with increased basic release of arachidonic acid.

Aspirin↗
PubMedDate not supplied

Analgesic activity of double endorphins in vivo.

The effects of double endorphins DALA2, DYNO2, CASO2 on pain threshold in the rats were compared with those of DALA (D-Ala2-Met5-enkephalinamide). Marked differences in the analgesic potency of the investigated peptides were noted. The most potent analgesic effect was exerted by DALA2. DYNO2 was weaker than DALA and DALA2 due to lack of glycine residue in position 3, probably responsible for the receptor affinity and analgesic activity in vivo. The weak analgesic activity of CASO2 in vivo corresponds with the weak opiate agonistic action of this peptide in vitro [see 7]. All investigated peptides induced changes in animal behaviour when injected i.c.v. The results indicated that among peptides in the novel group of double endorphins, DALA2 is of special interest because of a potent and long lasting analgesic action.

Analgesia↗
PubMed1982

Declining incidence of analgesic nephropathy in Canada.

Surveys of nephrologists in Canada indicate that the incidence of analgesic nephropathy has decreased by about 50% in less than a decade in association with the removal of phenacetin from the market and restrictions on the availability analgesic mixtures containing acetaminophen and acetylsalicylic acid. The number of patients presenting with end-stage renal disease attributed to analgesics has shown a similar drop. These decreases have occurred in spite of increased consumption of acetaminophen as a single analgesic. Analgesic nephropathy should not be expected to disappear, however, since there is evidence that the drugs still in use have the potential to cause renal damage.

Canada↗
PubMed1981

Chronic renal failure and end-stage renal disease in northwest North Carolina. Importance of analgesic-associated nephropathy.

A retrospective study was undertaken to determine the extent to which analgesic-associated nephropathy (AAN) causes chronic renal failure (CRF) and end-stage renal disease (ESRD). Of 363 cases of CRF diagnosed between 1974 and 1976, 48 were caused by AAN; 14 of 140 cases of ESRD were caused by AAN. Of the 14 patients with ESRD from AAN, 12 initially had ESRD and two progressed to ESRD while continuing consumption of analgesics. The remaining 34 patients who had AAN with CRF discontinued using analgesics and have not progressed to ESRD. Thus, 34 of 36 patients with AAN-CRF who initially did not have ESRD discontinued use of analgesics and have not progressed to ESRD. We conclude that AAN causes a large percentage of CRF and ESRD in our patient population. Early recognition of this entity can prevent progression to ESRD if analgesic consumption is discontinued.

Female↗
PubMed1976

Prenatal administration of morphine to the rat: tolerance to the analgesic effect of morphine in the offspring.

The analgesic activity of morphine was assessed by the hot-plate technique in the offspring of female CFE rats that had received morphine twice daily on days 5 to 12 of pregnancy. A dose of 5.0 mg/kg of morphine was administered for the first 3 injections; 10 mg/kg was used for each of the remaining 13. Morphine dose-response curves were determined in the offspring at 5 weeks of age. The analgesic effect of morphine in the offspring of morphine-treated females (morphine offspring) was attenuated by as much as 50% compared to the offspring of saline-treated females (saline offspring). This same relationship between the morphine and saline offspring was also observed in offspring rendered tolerant to the analgesic effect of morphine. A diminished analgesia in the morphine offspring compared to the saline offspring was also observed after the injection of graded doeses of levorphanol in both nontolerant and morphine-tolerant offspring. The analgesic effect of a single dose of morphine was also attenuated in 3-, 5- and 11-week-old morphine offspring. No differences were found in either brain or plasma concentration of morphine between the morphine and saline offspring. The long-term effect of prenatal morphine administration could not be explained on the basis of maternal influences since cross-fostering procedures failed to abolish it. It is concluded that the administration of moderate doses of morphine to gestating rats can induce a long-lasting tolerance to the analgesic effect of morphine in the offspring.

Aging↗