Gene/Protein Disease Symptom Drug Enzyme Compound
Pivot Concepts:   Target Concepts:
Query: UMLS:C0344307 (analgesia)
 28,200 document(s) hit in 31,850,051 MEDLINE articles (0.00 seconds)

1. Thirty-eight pregnant women, 2 to 33 days overdue with a menstrual period, were treated with a single intrauterine injection of PGE2. 2. Abortion occurred in 7 of 12 patients (58.3%) treated with PGE2 100 mug and in 22 of 26 patients (84.6%) given PGE2 500 mug. 3. The only side effect was uterine pain requiring analgesia in four of the former and 15 of the latter. Four patients required curettage to control bleeding.
Adv Prostaglandin Thromboxane Res 1976
PMID:Intrauterine prostaglandin E2 as an postconceptional abortifacient. 98 69

Flunixin (FLX) and ketoprofen (KET) are potent nonsteroidal anti-inflammatory drugs (NSAIDs) used to alleviate pain and decrease inflammation. These drugs block access of arachidonic acid to its binding site on the cyclooxygenase enzyme, thus preventing conversion to thromboxane A2 and subsequent degradation to thromboxane B2 (TBX). Consequently, plasma TBX may be used to estimate duration of NSAID action. Sixteen adult mallard ducks (Anas platyrhynchos) were randomly assigned to three treatment groups: control (n = 4), FLX 5 mg/kg (n = 6), or KET 5 mg/kg (n = 6). Blood samples were taken 1 hr prior to and just before (0 hr) injection and 0.25, 0.5, 1, 2, 4, 6, 12, 24, 36, and 48 hr after injection. Plasma samples were analyzed for corticosterone and TBX. The feces were tested for the presence of hemoglobin and the ducks were euthanized for complete necropsy at the end of the study. Samples of muscle, kidney, liver, proventriculus, and intestine were taken for histologic analysis. Thromboxane was suppressed significantly in all birds following administration of either FLX or KET for 4 hr and decreased for approximately 12 hr compared with baseline samples (-1 and 0 hr). In the control group, TBX gradually declined over time. None of the ducks showed evidence of gastrointestinal bleeding, but the FLX group had muscle necrosis present at injection sites. FLX and KET likely exert pharmacological effects for at least 12 h. Although degree of TBX inhibition cannot be correlated absolutely with degree of analgesia or anti-inflammatory effects, it is possible that these effects are present during this time. This work suggests that FLX and KET can potentially be used as anti-inflammatory and analgesic agents in waterfowl. However, because of muscle necrosis at the injection site, we do not recommend parenteral use of FLX in ducks.
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PMID:Pharmacodynamics of flunixin and ketoprofen in mallard ducks (Anas platyrhynchos). 1279 Apr 25

Antagonist at specific prostaglandin receptors might provide analgesia with a more favourable toxicity profile compared with cyclooxygenase inhibitors. We analyzed nociceptive responses in prostaglandin D, E, F, prostacyclin and thromboxane receptor knockout mice and mice deficient of cyclooxygenase 1 or 2 to evaluate the contribution of individual prostaglandin receptors for heat, mechanical and formalin-evoked pain. None of the knockouts was uniformly protected from all of these pain stimuli but COX-1 and EP4 receptor knockouts presented with reduced heat pain and EP3 receptor and COX-2 knockout mice had reduced licking responses in the 2nd phase of the formalin assay. This was accompanied with reduced c-Fos immunoreactivity in the spinal cord dorsal horn in EP3 knockouts. Oppositely, heat pain sensitivity was increased in FP, EP1 and EP1+3 double mutant mice possibly due to a loss of FP or EP1 receptor mediated central control of thermal pain sensitivity. Deficiency of either EP2 or DP1 was associated with increased formalin-evoked flinching responses and c-Fos IR in dorsal horn neurons suggesting facilitated spinal cord pain reflex circuity. Thromboxane and prostacyclin receptor knockout mice showed normal pain behavior in all tests. The results suggest a differential, pain-stimulus and site-specific contribution of specific PG-receptors for the processing of the nociceptive stimuli, a differential modulation of nociceptive responses by COX-1 and COX-2 derived prostaglandins and compensatory and/or developmental adaptations in mice lacking specific PG receptors.
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PMID:Comparison of nociceptive behavior in prostaglandin E, F, D, prostacyclin and thromboxane receptor knockout mice. 1893 93