We evaluated the efficacy of the 60% lidocaine tape in alleviating pain associated with intravenous propofol administration in 71 gynecological patients. Thirty-eight women had the tape applied for 2.5 h before venipuncture, with the remaining patients acting as the control. A 20 gauge cannula was inserted into the cephalic vein. Propofol at room temperature was injected at a rate of 1200 ml.hr-1. The statistical significance of differences was established with the Mann-Whitney's U test and the chi 2 test. The median level of pain intensity resulting from venipuncture among the patients treated with the tape was smaller than that in the control group (16.5, vs 34, P = 0.006). Thereafter, cannulation was successfully achieved with reduced or no pain (VAS at cannulation < or = 25, n = 39), and only 16% of the treatment group complained of pain on injection as compared with 53.8% of the control group (P = 0.02). Moreover, the pain intensity was decreased with lidocaine tape (P = 0.006). The cost of the lidocaine tape is covered by medical insurance for reducing pain on venipuncture. Thus, as the tape also alleviates the pain on injection of propofol through its anesthetic action, it can be a safe, easy and cost-effective method as "it kills two pains with one tape".

Adult↗

PubMed1996

[The relief of postoperative pain by suppositories of buprenorphine or NSAID].

We evaluated the effects of suppositories of buprenorphine (BN) or NSAID (supp.) preoperatively administered for postoperative pain relief in patients who underwent elective gynecological surgeries. Fifty six patients were randomized into four groups: group B; 0.4 mg BN supp., group B+I; 0.4 mg BN supp. and 50 mg indomethacine (IND) supp., group B+D; 0.4 mg BN supp. and 50 mg diclofenac supp., group C; no supp. given as control. They were administered rectally after induction of general anesthesia. In all the supp. groups the patients had good pain relief during the first 24 hrs after the administration of supp. Group B+I seemed to have better pain relief, but, there was no statistical significance among the 3 groups. Nausea and vomiting were observed more frequently in group B and in control group C than in NSAIDs combined groups. The difference in the incidence rates was not significant. In conclusion, the simultaneous administration of BN and IND supp. was considered to be useful for postoperative pain relief without producing major side effects.

Adult↗

PubMed1995

Effect of NMDA receptor antagonists on prostaglandin E2-induced hyperalgesia in conscious mice.

Intrathecal (i.t.) injection of prostaglandin E2 (PGE2) to conscious mice produced a hyperalgesic action over a wide range of dosages with two apparent peaks at 100 pg and 10 ng per mouse, which may be mediated through EP3 and EP2 subtypes of the PGE receptor. In the present study, the effects of NMDA receptor antagonists on hyperalgesia induced by PGE2 were evaluated by the hot plate test at 30 min after i.t. injection. Hyperalgesia induced by a higher dose of PGE2 (10 ng/mouse) was relieved by D-AP5 (a competitive antagonist), 7-Cl-KynA (a glycine site antagonist), and ketamine and MK801 (non-competitive channel blockers). Intrathecal injection of butaprost (10 ng/mouse), an EP2 agonist, induced hyperalgesia, and this hyperalgesia was blocked by D-AP5, 7-Cl-KynA, ketamine, and MK801, similar to that induced by 10 ng of PGE2. On the other hand, hyperalgesia induced by a lower dose of PGE2 (100 pg/mouse) was blocked by D-AP5 and 7-Cl-KynA, but not by ketamine and MK801. Intrathecal injection of sulprostone (100 pg/mouse), an EP1 and EP3 agonist, induced hyperalgesia, and this hyperalgesia was blocked by D-AP5 and 7-Cl-KynA, but not by ketamine and MK801, similar to that induced by 100 pg of PGE2. These results first demonstrate that the NMDA receptor is involved in the PGE2-induced hyperalgesia and suggest that the hyperalgesic action by lower and higher doses of PGE2 may be mediated through EP3 and EP2 subtypes, respectively.

Alprostadil↗

PubMed1994

Characterization of EP-receptor subtypes involved in allodynia and hyperalgesia induced by intrathecal administration of prostaglandin E2 to mice.

1. Intrathecal (i.t.) administration of prostaglandin E2 (PGE2) to conscious mice induced allodynia, a state of discomfort and pain evoked by innocuous tactile stimuli, and hyperalgesia as assessed by the hot plate test. We characterized prostaglandin E receptor subtypes (EP1-3) involved in these sensory disorders by use of 7 synthetic prostanoid analogues. 2. Sulprostone (EP1 < EP3) induced allodynia over a wide range of dosages from 50 pg to 5 micrograms kg-1. The maximal allodynic effect was observed at 5 min after i.t. injection, and the response gradually decreased over the experimental period of 50 min. This sulprostone-induced allodynia showed a time course similar to that induced by PGE2. 3. 17-Phenyl-omega-trinor PGE2 (EP1 > EP3) and 16,16-dimethyl PGE2 (EP1 = EP2 = EP3) were as potent as PGE2 in inducing allodynia, and more potent than sulprostone. Butaprost (EP2), 11-deoxy PGE1 (EP2 = EP3), MB 28767 (EP3), and cicaprost (prostaglandin I2 (IP-) receptor) induced allodynia, but with much lower scores. 13,14-Dihydro-15-keto PGE2, a metabolite of PGE2, did not induce allodynia. 4. 16,16-Dimethyl PGE2 as well as PGE2 induced hyperalgesia over a wide range of dosages (16,16-dimethyl PGE2: 5 pg-0.5 micrograms kg-1 PGE2: 50 pg-0.5 micrograms kg-1) with two apparent peaks at 0.5 ng kg-1 and 0.5 micrograms kg-1. Sulprostone (EP1 < EP3) and 17-phenyl-omega-trinor PGE2 (EP1 > EP3) showed a bell-shaped hyperalgesia at lower doses of 5 pg-5 ng kg-1 and 50 pg-50 ng kg-1, respectively. MB28767 (EP3)showed a monophasic hyperalgesic action over a wide range of dosages at 50 pg-S5 Microg kg-1. Butaprost(EP2) induced hyperalgesia at doses higher than 50 ng kg-1.5. These results demonstrate that PGE2 may exert allodynia through the EP1-receptor and hyperalgesia through EP2- and EP3-receptors in the mouse spinal cord.

Animals↗

PubMed1990

Nociceptive effects induced by intrathecal administration of prostaglandin D2, E2, or F2 alpha to conscious mice.

The effects of intrathecal administration of prostaglandins on pain responses in conscious mice were evaluated by using hot plate and acetic acid writhing tests. Prostaglandin D2 (0.5-3 ng/mouse) had a hyperalgesic action on the response to a hot plate during a 3-60 min period after injection. Prostaglandin E2 showed a hyperalgesic effect at doses of 1 pg to 10 ng/mouse, but the effect lasted shorter (3-30 min) than that of prostaglandin D2. Similar results were obtained by acetic acid writhing tests. The hyperalgesic effect of prostaglandin D2 was blocked by simultaneous injection of a substance P antagonist (greater than or equal to 100 ng) but not by AH6809, a prostanoid EP1-receptor antagonist. Conversely, prostaglandin E2-induced hyperalgesia was blocked by AH6809 (greater than or equal to 500 ng) but not by the substance P antagonist. Prostaglandin F2 alpha had little effect on pain responses. These results demonstrate that both prostaglandin D2 and prostaglandin E2 exert hyperalgesia in the spinal cord, but in different ways.

Animals↗