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Query: UMLS:C0030193 (pain)
 261,466 document(s) hit in 31,850,051 MEDLINE articles (0.00 seconds)

Prostaglandin E1 (PGE1), prostaglandin E2 (PGE2) and arachidonic acid have been demonstrated to potentiate the peritoneal writhing response in the mouse induced by benzoquinone. The resultant dose-response relationships were bell shaped with a maximum activity of 10 ng/kg i.p. of potentiating agent. Floctafenine, indometacin and acetylsalicylic acid (ASA) blocked the potentiation induced by arachidonic acid but not that induced by PGE2. This suggests that it is prostaglandin that causes the potentiation and that the mechanism of action of ASA-like drugs against hyperalgesia associated with inflammation is blockade of prostaglandin synthesis. Morphine reduced the potentiation by PGE2 and arachidonic acid but the bell shaped hyperalgesia was still evident using both agonists. These results indicate that morphine does not inhibit prostaglandin synthetase but may modify the effect of prostaglandin. This method may be useful to distinguish between ASA-like and morphine-like analgesic compounds using a pain response in vivo.
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PMID:Hyperalgesia after treatment of mice with prostaglandins and arachidonic acid and its antagonism by anti-inflammatory-analgesic compounds. 31 5

Effect of tolmetin sodium on the pain-like responses caused by various nociceptive stimuli was examined in experimental animals. Tolmetin sodium showed a potent inhibitory activity on the acetic acid-induced writhing in mice and rats, and its potency, (ED50 = 23.4 and 3.01 mg/kg, p.o.) was about 2.4--10.3 times that of ibuprofen and aspirin. The hypertension induced by intraarterial injection of bradykinin toward the spleen of dogs was inhibited by tolmetin sodium (ED50 = 80 mg/kg, i.v.), but the hypertension by a simultaneous injection of bradykinin and PGE1 was not inhibited by tolmetin sodium and sulpyrine, though pentazocine inhibited both hypertensions. The pain-like response caused by pressing mechanically the inflamed paws or joints of rats induced by kaolin-carrageenin or adjuvant was inhibited by tolmetin sodium (30--100 or 20--40 mg/kg, p.o., respectively), and the potency was approximately equal that of ibuprofen and phenylbutazone. Tolmetin sodium produced a significant inhibition of the pain-like response induced by electrical stimulation of tooth pulp of dogs, but showed no effect when the methods of Haffner and D'Amour-Smith were applied to mice. Anti-writhing action of tolmetin sodium was not antagonized by naloxone. From these results, it was concluded that tolmetin sodium has a potent inhibitory activity on the pain-like responses induced by the chemical nociceptive stimuli and by the mechanical pressure stimulus of the inflamed tissue, especially on the writhing. The analgesic activity probably involves a peripheral mechanism.
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PMID:[Analgesic activity of a non-steroidal anti-inflammatory agent, tolmetin sodium in experimental animals (author's transl)]. 53 31

1 The isolated perfused ear of the rabbit connected to the body only by its nerve, was used to investigate the influence of prostaglandin F2alpha on the algesic effect of bradykinin and acetylcholine. 2 Bradykinin and acetylcholine, following intra-arterial injection into the isolated perfused ear elicited a dose-related reflex fall in blood pressure due to stimulation of paravascular pain receptors (= algesic effect). 3 Infusion of prostaglandin F2alpha (0.1 to 1 ng/ml) into the rabbit ear reduced the algesic effect of bradykinin but not that of acetylcholine. 4 The onset of the reflex fall in blood pressure by bradykinin but not that by acetylcholine was delayed by infusion of prostaglandin F2alpha into the ear. 5 Infusion of prostaglandin E1 into the rabbit ear led to an enhancement of the algesic effect of bradykinin and acetylcholine. Enhancement of both effects was abolished by infusion of prostaglandin F2alpha. 6 During inhibition of the endogenous synthesis of prostaglandins (mainly E-type) by indomethacin, a low concentration of prostaglandin F2alpha no longer reduced the algesic effect of bradykinin. However, a high concentration of F2alpha continued to enhance the effect of bradykinin and acetylcholine. 7 Prostaglandin F2alpha influenced neither the brief reduction in venous outflow produced by bradykinin nor the brief increase in venous outflow caused by acetylcholine. 8 The results suggest that prostaglandin F2alpha does not directly reduce the effect of bradykinin but inhibits the enhancement of its algesic effect produced by prostaglandin E that is released endogenously by bradykinin. That the algesic effect of acetylcholine is not reduced by prostaglandin F2alpha is in keeping with its releasing very little endogenous prostaglandin E.
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PMID:Prostaglandin F2alpha reduces the algesic effect of bradykinin by antagonizing the pain enhancing action of endogenously released prostaglandin E. 84 80

Application of bradykinin to the exposed ventricular surface of the dog heart elicits a reflex cardiovascular response which includes a rise in blood pressure, tachycardia, renal vasoconstriction and muscular vasodilation. The reflex response depends on the dose of bradykinin and is increased by concomitant application of prostaglandin E1 or E2 and reduced by indomethacin. Temporary occlusion of the coronary artery supplying the area of the ventricle under study also sensitized the heart to topical application of bradykinin. Bradykinin and prostaglandins are released by the heart during ischaemia. We suggest, therefore, that bradykinin and prostaglandins acting in concert are the natural stimulus for excitation of the sensory receptors signalling the pain of myocardial ischaemia. We also suggest that the nervous reflex which arises from activation of sympathetic sensory nerve endings is the mechanism subserving the cardiovascular events which accompany anginal attacks.
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PMID:An excitatory nociceptive cardiac reflex elicited by bradykinin and potentiated by prostaglandins and myocardial ischaemia. 95 16

(1) The method of the isolated perfused rabbit ear connected to the body by its nerve only was used to investigate the influence of the prostaglandin-antagonist polyphloretin phosphate (PPP) on the algesic effect of bradykinin (B) and acetylcholine (ACh). (2) Intra-arterial injections of B and ACh into the ear elicit a reflex fall in systemic blood pressure of the anaesthetized animal. PPP reduces this effects of B in proportion to the dose. The effect of ACh is reduced only to a small extent and only under higher concentrations of PPP than those necessary for inhibiting the effect of B. (3) Prostaglandin E1 (PGE1), when infused i.a. into the ear, enhances the effect of B and ACh by a sensitizing action on the perivascular pain receptors. PPP reduces or totally abolishes the PGE1-induced enhancement of the effect of B and ACh. (4) It is concluded that PPP reduces the effect of B mainly by inhibiting directly the pain enhancing action of the endogenously released PGs of the E-type. The effect of ACh is reduced only in the high concentration of PPP to a small extent probably by inhibiting the ACh-action rather than the sensitizing action of the only minimal released amounts of PGs. The PG-antagonizing action of PPP is further proven by the fact that during an additional infusion of PGE1 the enhanced effects of both B as well as ACh are reduced or abolished by PPP.
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PMID:Polyphloretin phosphate reduces the algesic action of bradykinin by interfering with E-type prostaglandins. 97 Feb 95

The effect of prostaglandin E1 on regional cerebral blood flow (rCBF) was studied with the intra-arterial 133Xe method in ten awake patients under local anesthesia. Measurements were taken from 16 areas of a hemisphere in seven patients, from 35 areas of a hemisphere in two patients and from 256 areas of a hemisphere in one patient. The prostaglandin was dissolved from the crystalline state without the aid of alcohol. It was given intracarotidly as a constant infusion at a rate of 5 ng per kilogram per minute for five minutes before the measurement and continued during the measurement. In every patient a mild increase in blood flow during the prostaglandin infusion was seen. The flow increase took place in all parts of the hemisphere. It averaged 11.2% (p less than 0.01). During the infusion, the skin supplied by the internal carotid artery and the conjunctiva on the infused side became red and sometimes swollen. A slight pressure was noted by most patients, but none had pain. No side effects of the infusion were noted.
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PMID:Effect of intracarotid prostaglandin E1 on regional cerebral blood flow in man. 100 30

A method has been developed to measure the analgesic action of aspirin-like drugs in knee joints of anaesthetized dogs. Bradykinin, injected into the joint cavity, induced a reflex rise in blood pressure which was dose-dependent; this was used as a measure of nociceptive activity. The joint cavity became more sensitive to bradykinin as the experiment proceeded, or when a low concentration of prostaglandin E1 or E2 was infused locally. The increase in sensitivity with time was prevented by local injection of aspirin or indomethacin, but that induced by exogenous prostaglandin infusion was not. Injections of carrageenin into dog knee joints increased the prostaglandin E2 content of synovial fluid by up to 160 ng per joint; indomethacin prevented this increase. These experiments support our previous conclusion that local biosynthesis of a prostaglandin (induced by mild trauma) sensitizes pain receptors to mechanical or chemical stimuli. Aspirin-like drugs are analgesic because they prevent prostaglandin biosynthesis, thereby preventing this sensitization.
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PMID:Inhibition of prostaglandin biosynthesis as the mechanism of analgesia of aspirin-like drugs in the dog knee joint. 114 92

The intracavernous injection of vasoactive drugs is a valuable diagnostic aid and an important tool for the treatment of erectile failure. A comparative study with intracavernous injection of prostaglandin E1 (PGE1) and papaverine was performed in 60 patients with impotence. We evaluated the efficiency and side effects of both agents. The overall positive response rate was 85.0% in the PGE1 group and 65.0% in the papaverine group which suggests PGE1 has a stronger vascular effect. The mean onset of maximal erection was after 9.6 minutes in the PGE1 group and after 6.5 minutes in the papaverine group. The mean maintenance of erection was for 53.2 minutes in the PGE1 group and for 38.6 minutes in the papaverine group. There were no systemic side effects of either agent. Three instances of injection pain and 2 of burning sensation in the penis were noted in the PGE1 group, while in the papaverine group, there were 21 reports of injection pain, 4 of prolonged erection and 2 of burning sensation in the penis. These results suggest that PGE1 is a more desirable vasoactive alternative for the diagnosis of impotence.
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PMID:A comparative study with intracavernous injection of prostaglandin E1 versus papaverine for the diagnostic assessment of erectile impotence. 129 38

From February to July in 1989, 47 patients came to our O.P.D. with the chief complaint of impotence. The average age was 48.3 +/- 10.7 y/o. We applied intracoporeal injection of prostaglandin PGE1 (20 mg); and evaluated its penile blood flow effect by color duplex scanning (Acuson 128). The erectile responses of the test showed that: 6 patients (12.8%) had normal response: and 16 patients (34%) had imperfect response. Altogether, the total positive response rate was 46.8%, and 25 patients (53.2%) showed impaired response. The onset of response was 9.1 +/- 3.6 minutes and the duration of erection was 59.2 +/- 24.7 minutes. The percentage of diameter change of both deep arteries after injection was Rt: 58.1 +/- 41.5%; left: 52.3 +/- 35.6%. The peak velocity of right cavernosal arterial flow after intracoporeal injection was 35.5 +/- 15.9 cm/sec; and that of the left side was 33.2 +/- 16.9 cm/sec. There was no correlation between the increment of peak velocity of the deep arterial flow and the erection grade. The same phenomenon was also found between the increased change in the diameter of the deep artery and the erection grade. 16 patients (34.1%) experienced tolerable pain during the procedure. Two patients (4.3%) experienced dizzines and discomfort due to venous leakage. No priapism was found. This study suggests PGE1 may be an excellent potential alternative to other vasoactive drug with less complication in the diagnosis and treatment of impotence. But the cost and stability were its shortcoming.(ABSTRACT TRUNCATED AT 250 WORDS)
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PMID:[Effects of PGE1 on penile blood flow]. 135 14

We performed a double-blind, crossover study using objective measurements to compare maximum rigidity and duration of erections with papaverine hydrochloride in combination with phentolamine mesylate and/or prostaglandin E1. The rationale for the protocol was to combine a smooth muscle relaxant (papaverine) with either or both vasodilating agents (phentolamine and prostaglandin E1) commonly used for injection therapy. The 7 volunteer patients with organic impotence documented by abnormal nocturnal penile tumescence testing were injected with 0.5 to 1.0 ml. papaverine (30 mg./ml.) in combination with phentolamine (0.5 mg./ml.) and/or prostaglandin E1 (5 micrograms./ml.). Each patient received 2 injections on each of 2 testing dates; injection 2 was given after tumescence resulting from injection 1 had subsided completely. The medications were given in a randomized, counterbalanced order following double-blind procedures. Patients evaluated the erections subjectively. In addition, the RigiScan device was used to measure maximum rigidity and duration of erections. All patients observed increased duration of erections with both combinations containing prostaglandin E1. Analysis of RigiScan measurements showed no statistically significant differences for maximum rigidity (p greater than 0.1) but significantly greater duration of erections with papaverine plus prostaglandin E1, and papaverine plus phentolamine plus prostaglandin E1 compared to papaverine plus phentolamine (p less than 0.001). There was no statistical difference in rigidity or duration of erections between papaverine plus prostaglandin E1 and papaverine plus phentolamine plus prostaglandin E1. No patient reported significant penile pain with any of the injections. We conclude that the combination of papaverine and prostaglandin E1 produces erections of longer duration than papaverine plus phentolamine and that no additional benefit is gained by adding phentolamine to a combination of papaverine and prostaglandin E1. Further studies are in progress to define optimal dose response curves for papaverine and prostaglandin E1 as individual agents and in combination.
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PMID:Objective double-blind evaluation of erectile function with intracorporeal papaverine in combination with phentolamine and/or prostaglandin E1. 140 32


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