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 (EP,-3) involved in these sensory disorders by use of 7 synthetic prostanoid analogues.2 Sulprostone (EPI EP3) and 16,16-dimethyl PGE2 (EPI = EP2 = EP3) were as potent as PGE2 in inducing allodynia, and more potent than sulprostone. Butaprost (EP2), 1 1-deoxy PGE, (EP2 = EP3), MB 28767 (EP3), and cicaprost (prostaglandin 12 (IP-) receptor) induced allodynia, but with much lower scores. 13,14-Dihydro-I5-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 pg kg-' PGE2: 50 pg-0.5 gg kg-') with two apparent peaks at 0.5 ng kg-' and 0.5 gg kg-'. Sulprostone (EPI EP3) showed a bell-shaped hyperalgesia at lower doses of Spg-Sngkg'1 and 50pg-50ngkg-', respectively. MB28767 (EP3) showed a monophasic hyperalgesic action over a wide range of dosages at 50 pg-S5 jg kg-'. Butaprost (EP2) induced hyperalgesia at doses higher than 50ngkg-'. 5 These results demonstrate that PGE2 may exert allodynia through the EP,-receptor and hyperalgesia through EP2-and EP3-receptors in the mouse spinal cord.

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Muscle relaxation appears to facilitate ProSeal insertion efficacy by enabling higher successful insertion rates, higher sealing pressure, lower leakage volume, and lower subjective difficulty of insertion in anesthetized patients.