Gene/Protein Disease Symptom Drug Enzyme Compound
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Query: UMLS:C0030193 (pain)
 261,466 document(s) hit in 31,850,051 MEDLINE articles (0.00 seconds)

Twenty patients with confirmed gallbladder disease were treated with intravenous indomethacin during 24 separate attacks of biliary pain. In all cases the pain was promptly relieved and there were no important side-effects. Indomethacin, and inhibitor of prostaglandin synthesis, may reduce intraluminal pressure in the gallbladder, and relieve pain.
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PMID:Inhibition of prostaglandin synthesis as a treatment for biliary pain. 8 68

Primary dysmenorrhea is a difficult entity to treat, and therapy is usually directed at relieving symptoms. There is some indication that this disorder is caused by an increase in prostaglandin F2alpha. Therefore, logically the treatment may include antiprostaglandin agents. We have studied 32 women with the diagnosis of primary dysmenorrhea in a randomized double-blind fashion using a placebo and indomethacin. Both agents were taken three times a day over four cycles, and therapy was begun two days before the usual onset of pelvic pain. Only two of 16 patients in the placebo group were significantly improved in the four-month treatment cycles while all 16 in the treatment group showed some improvement, 11 having cessation of pain. In the six months following the study period, all patients were given indomethacin. The original treatment group did not change significantly. However, all in the placebo group when switched to indomethacin had some relief, 12 of the 16 showing complete cessation of pain. Gastric irritation was the main side effect and was present in 18% of the treatment group and 12% in the placebo group. Indomethacin appears to effectively relieve primary dysmenorrhea and does not appear to be associated with a high incidence of side effects.
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PMID:Primary dysmenorrhea treated with indomethacin. 37 24

The isolated perfused rabbit heart has the capacity to rapidly synthesize, release, and inactivate prostaglandins (PGs) which can readily modulate coronary resistance and cardiac performance. Prostaglandin synthetase converts arachidonic acid to prostaglandin-like substance in one passage across the heart. There is little evidence of functional prostaglandin dehydrogenase activity. Arachidonic acid and bradykinin produce a concentration-dependent decrease in coronary resistance directly associated with PG-like substance biosynthesis and release. An inhibitor of bradykinin destruction, the nonapeptide SQ-20881, markedly enhanced both the coronary vasodilation and PG-like substance release produced by cardiac injection of bradykinin. Indomethacin inhibited both the myocardial prostaglandin biosynthesis and the decrease in coronary resistance induced by bradykinin and arachidonic acid. In addition to direct effects on coronary vascular smooth muscle, prostaglandins produced in the heart apparently exert a modulating influence on efferent autonomic and on afferent cardiovascular and pain reflexes.
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PMID:The synthesis and function of prostaglandins in the heart. 78 41

The efficacy of indomethacin 100 mg, diazepam 10 mg, and placebo in producing sleep, relieving night pain, and reducing the severity of morning stiffness, was compared in 18 patients in hospital with active classical or definite rheumatoid arthritis.There was no statistically significant difference in the preference of patients or sleep score among the three forms of treatment. Both indomethacin and diazepam were more effective than placebo in relieving night pain. Indomethacin decreased, but diazepam increased, morning stiffness in comparison to placebo. Neither active therapy produced significant side-effects.
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PMID:Night medication in rheumatoid arthritis. 78 18

In isolated perfused rabbit hearts, bradykinin produced a concentration-dependent decrease in coronary resistance directly associated with biosynthesis and release of prostaglandin-E-like substance. An inhibitor of bradykinin destruction (the nonapeptide SQ-20881) markedly enhanced both the coronary vasodilation and release of prostaglandin-E-like substance produced by cardiac injection of bradykinin. Indomethacin inhibited both the myocardial prostaglandin biosynthesis and the decrease in coronary resistance induced by bradykinin. The demonstration that bradykinin is a potent stimulator of prostaglandin biosynthesis in the heart has implications as to the cause of the afferent cardiovascular reflexes and pain in myocardial infarction and angina pectoris.
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PMID:Mechanism and modification of bradykinin-induced coronary vasodilation. 105 12

Symptomatic pericarditis occurs in the course of maintenance hemodialysis and often requires pericardiectomy in addition to other conventional measures. Three of 11 such patients were treated with frequent dialysis and general supportive treatment. Two of these required pericardiocentesis. The other eight received indomethacin; this was followed by prompt defervescence and abatement of pain within 6 to 24 hours. Only one patient required pericardiocentesis. On every occasion when treatment was discontinued during the first week, symptoms recurred. After three weeks to four months, the drug dosage could be tapered and discontinued. The pericardial aspirate was hemorrhagic in all three patients who required pericardiocentesis. Indomethacin appears to be effective in the treatment of the pericarditis associated with dialysis and precludes the need for invasive procedures.
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PMID:Indomethacin treatment of pericarditis in chronic hemodialysis patients. 113 Sep 25

The local motor response to bradykinin and the bacterial chemotactic peptide, formyl-methionyl-leucyl-phenylalanine (FMLP) was investigated in the guinea-pig isolated renal pelvis and ureter in relation to possible activation of capsaicin-sensitive primary afferent nerves and release of sensory neuropeptides. Both bradykinin (1 nM-10 microM) and FMLP (10 nM-10 microM) produced a concentration-dependent positive inotropic effect in the isolated renal pelvis which was unaffected by in vitro capsaicin desensitization. The response to bradykinin was antagonized by HOE 140, a bradykinin receptor antagonist, while it was unaffected by MEN 10,376, a tachykinin receptor antagonist, hCGRP(8-37) a calcitonin gene-related peptide (CGRP) receptor antagonist and N-t-BOC-Phe-DLeu-Phe-DLeu-Phe (BPLPLP), an FMLP antagonist. The response to FMLP was blocked by BPLPLP while it was unaffected by HOE 140, MEN 10,376 or hCGRP(8-37). Indomethacin (10 microM) enhanced the response to both bradykinin and FMLP. Bradykinin transiently activated rhythmic contractions in the isolated ureter. The response to bradykinin was blocked by HOE 140 and was unaffected by in vitro capsaicin desensitization, indomethacin, MEN 10,376 or BPLPLP. FMLP had no motor effect on the resting ureter but when rhythmic background contractions were evoked by the addition of 100 nM endothelin 1, it produced a transient suppression of ureteral motility. This inhibitory effect was unchanged by in vitro capsaicin desensitization or HOE 140 while it was abolished by indomethacin or BPLPLP pretreatment. Both bradykinin and FMLP evoked the release of CGRP-like immunoreactivity in the renal pelvis. The effect of bradykinin but not that of FMLP was abolished by indomethacin. By contrast neither bradykinin nor FMLP did evoke a significant CGRP-LI release in the ureter. It is concluded that bradykinin and FMLP affect pyeloureteral motility through specific and independent pathways. The local motor responses produced by these chemical stimulants are independent from the release of sensory neuropeptides from capsaicin-sensitive primary afferent neurons. Direct neurochemical evidence was obtained for activation of capsaicin-sensitive primary afferents in the renal pelvis: such a mechanism could be involved in the genesis of ureteral pain whenever bradykinin or FMLP come into contact with sensory nerves in the pyeloureteral wall.
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PMID:Local motor responses to bradykinin and bacterial chemotactic peptide formyl-methionyl-leucyl-phenylalanine (FMLP) in the guinea-pig isolated renal pelvis and ureter. 133 50

In a bid to minimise dosage and possible side-effects when relieving post episiotomy pain, the NSAID Indomethacin was studied in combination with a systemic haemostat Ethamsylate which has been shown to selectively inhibit some prostaglandins. Comparative groups also took Indomethacin alone and placebo in a double blind non-crossover comparison. Efficacy was judged in terms of side-effects and assessments of pain intensity, pain relief and global assessment of pain. There was some evidence of a beneficial interaction between Indomethacin and Ethamsylate when adjustments were made for the patient's age and initial pain score. Side-effects were most common in the combination therapy group.
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PMID:Indomethacin and ethamsylate alone and in combination for the relief of post episiotomy pain. 142 73

Six orthopaedic clinics in Sweden made a comparison of the effects and side effects of Piroxicam (20 mg) and Indomethacin (100 mg) suppositories in 261 patients with painful coxarthrosis on the waiting list for total hip replacement (THR). The study was designed as a single blind study over 4 weeks. Amount of pain and range of motion was registered before the trial and compared with findings after 4 weeks, including reported side effects. Both drugs gave satisfactory pain relief without any appreciable variation on weightbearing or at rest. On the other hand, the trial showed a significant difference (p = 0.0033, Student's-test) between the two drugs as regards the frequency of side effects from the lower gastrointestinal tract, where piroxicam had a lower rate compared with indomethacin. No serious complications occurred; 16 patients dropped out, 8 in each group.
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PMID:Piroxicam and indomethacin suppositories for painful coxarthrosis. 158 14

It was aimed to assess if intrathecal (i.t.) injections of acetylsalicylic acid and salicylic acid depress C fibre-evoked activity in the sensory part of the nociceptive system. In rats under urethane anaesthesia, activity was elicited in single neurones in the dorsomedial part of the ventral nucleus (VDM) of the thalamus and in ascending axons of the spinal cord by supramaximal electrical stimulation of the sural nerve. Acetylsalicylic acid and salicylic acid injected i.t. significantly reduced the activity evoked in thalamic neurones. The maximum depression amounted to about 50% of the activity evoked in the controls and was produced by acetylsalicylic acid at a dose of 50 micrograms (0.28 mumol)/rat and by salicylic acid at a dose of 37.5 micrograms (0.27 mumol)/rat. Indomethacin injected i.t. also reduced C fibre-evoked activity in the thalamus in a dose-dependent fashion, 100 micrograms producing a 50% depression. Salicylic acid (37.5 micrograms/rat, i.e.) depressed C fibre-evoked activity in ascending axons but had no effect on A beta fibre-evoked activity. It is concluded that i.t. injection of acetylsalicylic acid selectively inhibits nociceptive impulse transmission in the spinal cord by an action of the salicylic acid moiety. It is possible that prostaglandins are involved in the central action of salicylic acid.
Pain 1992 May
PMID:Intrathecal injection of acetylsalicylic acid, salicylic acid and indomethacin depresses C fibre-evoked activity in the rat thalamus and spinal cord. 1183 30


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