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)

In a randomized crossover study 15 dysmenorrheic women were treated during two consecutive menstrual period, once with the potent prostaglandin-synthesis inhibitor: ibuprofen and once with an identical looking placebo. Each patient was medicated for 12 hours during the first day of her menstrual flow and was subsequently fitted with a cervical cup for the collection of menstrual blood during three hours. In these samples the concentrations of prostaglandin (PG)F and PGE were measured by radioimmunoassay. The patients receiving placebo had high PGF levels 135 +/- 27 ng/ml (Mean +/- S.E.) which were significnatly reduced by Ibuprofen to 24 +/- 5 ng/ml (P less than 0.001). The PGE concentrations decreased from 5 +/- 1 ng/ml to 2 +/- 1 ng/ml (P less than 0.05). Ibuprofen also reduced the menstrual pain significantly (P less than 0.001). These results substantiate the earlier conclusion that a causal relationship exists between effective treatment with PG-synthesis inhibitors and decrease in menstrual blood PG levels, intrauterine pressure and dysmenorrheic pain.
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PMID:Effect of ibuprofen on menstrual blood prostaglandin levels in dysmenorrheic women. 39 21

(1) The isolated rabbit ear was perfused via its artery and the venous outflow superfused a PGE-sensitive rat stomach strip or a PGF-sensitive rat colon. (2) Injection of bradykinin intra-arterially into the ear produced a larger contraction of the rat stomach strip than the application of the same dose of bradykinin directly to the superfused muscle. (3) This difference is explained as a release of PGE-like material by bradykinin since indomethacin (infused i.a. into the ear) reduced the effect of the i.a. applied bradykinin. (4) PGF-like material could not be detected in the venous effluent. (5) ACh released only minimal amounts of PGE-like substance. (6) CONCLUSION: The amount of PGE-like material released by bradykinin is large enough to sensitize the paravascular pain receptors in the rabbit ear for the attack of bradykinin. Therefore, inhibition of PG-synthesis (i.e. by indomethacin) or inhibition of the sensitizing action of E-type PGs (i.e. by polyphloretin phosphate) reduces the pain producing effect of bradykinin. Since ACh releases only minimal amounts of E-type PGs, its effect is reduced only to a minimal extent by indomethacin or polyphloretin phosphate.
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PMID:Release of prostaglandins from the isolated perfused rabbit ear by bradykinin and acetylcholine. 97 Feb 94

Sixty-two patients that had consulted for impotence were evaluated by intracavernal injection of prostaglandin E1 and duplex echo-Doppler. The internal diameter and the mean flow of the cavernosal arteries were determined by echo-Doppler in the flaccid state. Thereafter 20 micrograms of PGE 1 was injected intracavernously and the erectile response was evaluated clinically after 5 to 15 minutes. Another Doppler evaluation was performed during tumescence to study the changes of the internal diameter and the mean flow increase of the cavernal arteries. Twenty-nine patients (46.7%) achieved normal erection after intracavernal PGE 1 and the Doppler study was normal in all but 2 patients (3.2%). The remaining 33 patients (53.1%) failed to achieve normal erection following intracavernal injection of PGE 1. The Doppler study, however, was normal in 7 of these patients (11.2%), which indicates venous leak to be the underlying cause of impotence. There were minor complications (19.3%) presented a small hematoma at the site of injection and 12.9% referred moderate pain at the time of injection) and no patient has a sustained erection for more than 3 hours. The hemodynamic mechanisms and the current concepts relative to the neurologic aspects of erection are discussed. We believe duplex echo-Doppler combined with intracavernal PGE 1 to be a very reliable method in the diagnosis of impotence of a vascular origin. It can distinguish those patients that cannot achieve erection following intracavernal PGE 1 with a normal arterial tree whose impotence can be ascribed to venous leak.
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PMID:[Echo-Doppler duplex combined with intracavernous injection of prostaglandin E1 in the diagnosis of impotence]. 158 15

Two prospective randomized trials were referred. In the first study 50 patients with femorotibial greater saphenous vein in situ bypasses were treated intraarterially with 0.2 ng PGE 1/kg body weight/min and 15,000 i.U. of heparine continuously. The control group of 50 patients also got 15,000 i.U. of heparine and 3 x 0.5 g of Aspirin. We observed 2 (4%) immediate occlusions in the PGE 1 group and 7 (14%) immediate occlusions in the control group. This difference proved to be statistically significant. In the second study 83 patients with three level occlusions (ilio-femoro-tibial) in stage III and IV were treated with a profundaplasty. 42 patients received 60 micrograms PGE 1 in 250 ml saline twice daily. The control group of 41 patients only got twice 250 ml saline over a period of three weeks. In the PGE 1 group 26 patients (61%) showed disappearance of rest pain and healing of necrotic lesions, whereas in the control group this could only be achieved in 15 patients (35%). The difference proved to be statistically significant.
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PMID:[Experiences with adjuvant prostaglandin therapy in vascular surgery interventions]. 178 55

The peripheral cholinergic, central dopamine antagonist drug metoclopramide was assessed as an anesthesia adjunct in a randomized, double-blind trial in 15 women having 2nd trimester abortion by intraamniotic prostaglandin F2a (Pgf2alpha). 7 of the women received 10 mg metoclopramide iv, and 8 received saline, when patient-controlled-analgesia with iv morphine by pump according to a standard protocol was begun. Pain was assessed every 2 hours by a visual analogue scale (0-10), and by number of doses and total amount of morphine used. The metoclopramide group used 54% less morphine (24.1 vs 52.0 mg), used less morphine in 2-hour intervals for the 1st 6 hours, reported less pain on analog scales, and expelled the fetus significantly earlier than did the saline group (7.2 vs 15.3 hours, p0.05). The lower cumulative morphine dose was influenced by the fact that the fetus was aborted earlier in the test group. There were no significant differences in time of placental delivery, or of hospital discharge, dose of antiemetic (droperidol) or of PGE suppositories given to speed the onset of contractions. metoclopramide may act to coordinate the contractions of the uterus and improve expulsive force. It was effective here only for 6 hours, probably related to its half life of 4-5 hours.
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PMID:Metoclopramide: an analgesic adjunct to patient-controlled analgesia. 195 34

Pain induced by a stimulus that is normally not painful is referred to as hyperalgesic pain. Inhibition of arachidonic acid metabolism and/or sympathectomy have been found to be effective treatment for this type of pain. We propose that the lowered pain threshold is induced by arachidonic acid metabolites produced in inflamed tissue or by sympathetic postganglionic neurons after nerve injury. The most extensively studied hyperalgesic mediators are prostaglandin E(2) (PGE(2)) and prostacyclin (PGI(2)), products of the cyclooxygenase pathway of arachidonic acid metabolism, whose production is inhibited by nonsteroidal antiinflammatory analgesics (NSAIAs). Recent studies, however, have demonstrated that products of the NSAIA-resistant lipoxygenase pathway of arachidonic acid metabolism are also hyperalgesic. Their production is inhibited by corticosteroids and current experimental agents.
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PMID:Hyperalgesic pain: a review. 196 69

A total of 119 patients with myocardial infarction hospitalized within 24 hrs from the disease onset were examined. He-Ne laser irradiation of the blood (daily 40 min sessions for 3-5 days) was carried out in 45 patients (Group 1). The rest 74 patients (Group 2) were administered common therapy. A number of biologically active substances were radioimmunoassayed in the blood of 12 Group 1 and 11 Group 2 patients on days 1, 3, and 7 of the disease. The pain syndrome was alleviated in Group 1 patients, in contrast to Group 2 patients, and the frequencies of ventricular arrhythmias, of heart failures, and of the condition recurrences were reduced, as was the mortality rate. Laser therapy resulted in reduction of the activities of the hypophyseoadrenocortical and aldosteron-renin-angiotensin systems. Besides blood levels of dilatants and proaggregants (PGF2 alpha, vasopressin, angiotensin II) reduced in these patients, whereas vasodilating and antiaggregation hormones (PGE, PGI2) levels increased and the PGI2/TxB2 ratio improved.
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PMID:[The use of low-intensity laser irradiation of the blood in myocardial infarction]. 236 94

The use of high epidural anesthesia for cesarean section has generally been accepted as a safe and comfortable means of intra- and post-operative pain relief in recent years. However, the accompanying vasomotor blockade of the lower body and the sometimes impaired cardiac reflex activity restrict the use of concomitant--even local--medication. Described are the deleterious side effects on hemodynamic stability and patient comfort of an intramyometrically administered synthetic prostaglandin E (PGE2)-compound (dinoprostone) given to three female patients under high epidural anesthesia during cesarean section. Differentiation of the various symptoms is made in relation to their epidural or PGE origin or to a combination of the two. A striking therapeutic resistance of the hypotension of a sufficiently volume-expanded patient to even large doses of ephedrine is discussed as representing possible PGE-mediated suppression of peripheral norepinephrine release.
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PMID:[Epidural anesthesia and local administration of high-dose prostaglandin in obstetrics. A dangerous combination]. 277 77

In a double-blind, placebo-controlled study 50 patients with peripheral arterial occlusive disease stage IIb were given daily or intra-arterial infusion of either 1 ampoule of Prostavasin (20 micrograms PGE 1) or 1 ampoule of placebo (646.7 micrograms alpha-cyclodextrin), each dissolved in 50 ml saline, over 60-120 min. Weekends excepted, the therapy was continued for three weeks. Under PGE 1 therapy the maximum ergometric walking distance increased by 146% (mean: from 109 m to 268 m), as opposed to 40% in the placebo group (mean: from 101.5 m to 142 m). Furthermore, significant improvements were seen with regard to painfree walking capacity (PGE 1: + 170%; placebo: + 49%). Free maximum and pain-free walking distances were increased as well (PGE 1: + 131% and 48%; placebo: + 26% and 27%). Haemorrheological parameters, e.g. plasma and whole blood viscosity, haematocrit and erythrocyte aggregation decreased (p less than 0.01) after PGE 1, whereas a significant increase (p less than 0.01) in acral digital temperature, blood flow and ultrasonic Doppler values was seen. No side-effects were observed.
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PMID:[Intra-arterial infusion treatment with prostaglandin E1 in patients with intermittent claudication]. 306 6

Prostaglandin E 1 has been used for the past 15 years in decreased peripheral arterial perfusion with differing degrees of success. The exact mechanism of action has not been clarified so far. Vasodilatation, increased fibrinolytic activity and an improved cellular metabolism were observed in response to PGE 1 in animal experiments both in vivo and in vitro. In the clinical studies performed so far PGE 1 has been used in cases of decreased peripheral arterial perfusion after functional, inflammatory, degenerative or diabetic arteriopathy (stages IIb-IV). Reduction or alleviation of ischaemic rest pain, as well as a faster healing of tissue necrosis was reported after intaarterial administration, especially in non-controlled, but also in controlled studies. Intravenous administration of PGE 1 had a positive influence on clinical symptoms in non-placebo-randomized patients; in the controlled studies, however, the results were not significant. The greatest therapeutic success can be achieved using intermittent intraarterial administration in decreased peripheral arterial perfusion due to functional or inflammatory arteriopathies.
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PMID:[Prostaglandin E1 in decreased arterial perfusion]. 306 8


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