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)

The algesic effects of intravascularly injected solutions of sorbitol and ionic and nonionic contrast media (CM) with high and low osmolality were tested in the perfused isolated rabbit ear connected to the body by the great auricular nerve. The threshold for the pain reflex effect was found to be at an osmolality of between 600 and 700 mosm/kg H2O, that is, at about twice the osmolality of blood. This result is consistent with results obtained to date in investigations in the non-anesthetized rat and in diagnostic examinations with CM in humans. The effects of both sorbitol and the ionic CM at a given osmolality were dose dependent only after low doses and not after a high dose. There were no pain reactions after injection of ionic and nonionic CM with a low osmolality. Release of prostacyclin was observed in preliminary tests after injection of ionic substances with high osmolality, but not after injection of CM with low osmolality.
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PMID:Experimental evaluation of radiographic contrast media in perivascular pain receptors in the perfused isolated rabbit ear. 256 7

Eighteen patients suffering from true menstrual migraine and 12 control subjects were studied. We evaluated in different phases of the menstrual cycle and during the migraine crisis the peripheral plasma concentrations of 6-keto-PGF1 alpha (the stable metabolite of PGI2), thromboxane B2 (the stable metabolite of thromboxane A2), PGF2 alpha and PGE2. The mean values of 6-keto-PGF1 alpha in menstrual migraine sufferers are lower than in normal women throughout the whole cycle. The difference between the trends observed in the two groups is statistically significant (p less than 0.05). The plasma levels of TXB2 and of PGF2 alpha are similar in the two groups investigated, both in basal conditions and during the attack. The plasma concentrations of PGE2 are slightly lower in migraineurs in basal conditions than in normals. However, during the crisis they increase significantly (p less than 0.05). In conclusion, among all the parameters considered, PGE2 seems to play the most important role during the pain phase of the attack. The results of the present study suggest that a deficit of PGI2, one of the most important protecting agents against ischemia, might be a typical feature of menstrual migraine and might cause in these patients a vascular hypersensitivity to different ischemic stimuli.
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PMID:Relevance of prostaglandins in true menstrual migraine. 271 74

Metabolites of arachidonic acid have important regulatory functions within several areas of concern to the otolaryngologist. Prostaglandins, composing one group, are involved in smooth-muscle contraction, regulation of renal glomerular blood flow, and in the modulation of immune and allergic responses, inflammation, fever, pain, and tumor growth. A second group, the leukotrienes, may be even more important than prostaglandins in allergy and inflammation. The elusive slow-reacting substance of anaphylaxis belongs in this group. Two other metabolites, thromboxane and prostacyclin, seem to be critical in hemostasis and the metastatic spread of tumors.
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PMID:Prostaglandins and other metabolites of arachidonic acid. An overview for the otolaryngologist. 298 36

The effect of a prostacyclin infusion was studied in 5 men with persistent pain associated with Peyronie's disease. Marked side effects were associated with the infusion, which was of limited benefit.
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PMID:Prostacyclin in the treatment of painful Peyronie's disease. 304 83

This review covers eicosanoid metabolism in human uterine tissues, in normal menstrual cycles, menorrhagia, and IUD contraception. Since measuring tissue level of prostaglandins (PGs) leads to artifacts, recent studies have involved tissue culture, superfusion and histochemistry, to analyze arachidonic acid metabolism, in endometrium, its tissues, and myometrium. First, it was established that Pgf2alpha and PGE2 are the primary PGs elaborated by human endometrium. The enzyme that produces Pgf2alpha, cyclooxygenase, is located primarily in the glandular endothelium. Pgf2alpha is under estrogen receptor control. Progesterone reduces Pgf2alpha and antiprogestogens increase it. In normal menstrual cycles, both PGs are highest in late luteal phase. In women with menorrhagia, defined as menstrual blood loss over 90 ml, the Pgf2alpha:PGE2 ratio is abnormally low, a reasonable finding since Pgf2alpha is vasoconstrictive, and PGE2 is a vasodilator. Another vasodilator PG, prostacyclin or PGI2, may be abnormally high in women with excessive bleeding. Some experiments on endometrium and myometrium, cultured apart and together, suggest that there may be flow of substrates of the PG pathways such that less Pgf2alpha is available in this condition. Using radiolabelled arachidonic acid, researchers concluded that the Pgf2alpha pathway may be saturated because of substrate being incorporated into excess triglycerides, leading to alternative PG release. Another theory proposes that PG antagonist drugs which block menstrual pain may also lower synthesis of leukotrienes, an eicosanoid that causes vasoconstriction as well as inflammation and pain. There have been no studies comparable to the tissue culture work cited above concerning IUDs. Some explorations of leukocyte PG metabolism and the effects of copper are relevant to the conclusions about PGE2 as a vasodilator. There could also be an alteration of locally produced thromboxanes and prostacyclins on blood clotting in IUD wearers.
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PMID:The role of prostaglandins and allied substances in uterine haemostasis. 331 24

Platelet activation, with subsequent formation of thromboxane A2 (TxA2), is thought to play a role in the development of arterial occlusion. In patients with severe atherosclerosis of the lower limbs, characterized by leg ulcers and rest pain, the basal formation of TxA2 and prostacyclin (PGI2) is increased. Corresponding data in patients with more moderate atherosclerosis of the lower limbs have not been reported. Since the capacity to physical exercise is not blunted in such patients proper evaluation of their TxA2-PGI2 synthesis should comprise not only assessment of the basal formation, but also TxA2/PGI2 biosynthesis during conditions of elevated cardiovascular activity. To address this, we analysed these eicosanoids in patients with a history of intermittent claudication. Urinary dinor-metabolites of TxB2 and PGI2 (Tx-M and PGI-M, respectively) were estimated by gas chromatography/negative ion-chemical ionization mass spectrometry in samples collected prior to, during and immediately after 20 min of severe treadmill exertion. The basal excretion of Tx-M was 105 +/- 26 pg/mg creatinine. It was not changed during exercise, but increased to 176 +/- 48 pg/mg creatinine (P less than 0.05) during the recovery. The basal excretion of PGI-M was 142 +/- 25 pg/mg creatinine. The PGI-M response to exercise varied from no change at all to a 30-fold increase, without any obvious correlation to experienced leg pain, walking distance or other recorded variables. During the recovery period the outflow of PGI-M was significantly higher than at rest (482 +/- 145 pg/mg creatinine; P less than 0.01). We conclude that in patients with intermittent claudication due to atherosclerosis (1) platelet activation does not occur during the course of the exercise, and (2) vascular prostacyclin formation can be dissociated from of TxA2 synthesis. The observed increase in PGI-M in some of the patients is suggested to reflect tissue ischaemia induced by the lack of adequate hyperaemia during exercise.
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PMID:Excretion of thromboxane A2 and prostacyclin metabolites during treadmill exercise in patients with intermittent claudication. 340 85

The efficacy of prostacyclin (PGI2) treatment was assessed in 26 patients with surgically unreconstructible atherosclerotic arterial occlusive disease of the lower extremity manifested by nonhealing ulcers and rest pain. Patients were randomized to receive a 72-hour intravenous infusion of PGI2 (6 ng/kg/min, n = 13) or placebo (n = 13). Ulcer size was measured by photographic planimetry, and rest pain was graded by blinded objective scoring at monthly intervals for 6 months. Ulcer size increased 64% in PGI2-treated patients and 22% in placebo-treated patients by 1 month after infusion. Rest pain decreased slightly in both PGI2 and placebo groups. At the conclusion of the study, 54% of placebo-treated patients and 31% of PGI2-treated patients had a positive treatment response, indicated by at least a 20% decrease in ulcer size and a 33% decrease in rest pain. PGI2 infusion did not improve the high-placebo response rate seen in these patients with severely ischemic extremities. These results emphasize the importance of placebo-controlled studies, even in patients with unreconstructible arterial disease.
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PMID:Prostacyclin treatment of ischemic ulcers and rest pain in unreconstructible peripheral arterial occlusive disease. 352 9

Prostacyclin was infused into the uterus of non-pregnant women either during early menstruation or in the secretory phase of the cycle. A dose of 5 micrograms/min produced little systemic effect and caused a significant decrease in uterine activity on Days 1 and 2 of the menses whereas 0.5 microgram/min did not. However, when dysmenorrhoeic pain and increased uterine activity were produced by infusion of PGF2 alpha during the secretory phase, PGI2 neither decreased the activity nor the pain. This indicates that PGI2 does not cause uterine relaxation by blocking the action of PGF2 alpha.
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PMID:The effect of intrauterine administration of prostacyclin on the contractility of the non-pregnant uterus in vivo. 353 3

Intraperitoneal injection of zymosan (1 mg in 0.5 ml saline) in mice induces a transient writhing response accompanied by the synthesis of small amounts of prostaglandin E2(PGE2, less than 2 ng) and larger amounts of PGI2 (200 ng per mouse), measured as its non-enzymatic breakdown product, 6-keto-PGF1 alpha. Although both centrally-acting analgesics (morphine, clonidine) and prostaglandin biosynthesis inhibitors (aspirin, indomethacin, ibuprofen) blocked the writhing response to intraperitoneal injection of zymosan, only the latter reduced prostaglandin levels in the peritoneal cavity. The writhing response correlated equally well with PGE2 levels and 6-keto-PGF1 alpha levels when data from mice treated with centrally-acting analgesics were excluded. However, intraperitoneal injection of PGI2, but not PGE2, reversed the analgesia induced by indomethacin in zymosan-injected mice. Centrally-acting agents, but not ibuprofen, blocked the ability of PGI2 to reverse the analgesic activity of indomethacin. PGI2 (2 micrograms per mouse), injected intraperitoneally in otherwise untreated mice, induced writhing. These data indicate that PGI2 is the prostaglandin involved in mediation of the writhing response to zymosan and that prostaglandin biosynthesis inhibitors, but not centrally-acting analgesics, exert their analgesic activity by reducing the peritoneal level of PGI2. It is possible that PGI2 may have the ability to stimulate pain receptors directly in the mouse peritoneal cavity, in addition to its previously recognized ability to sensitize pain receptors to other pain-producing stimuli.
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PMID:The role of prostaglandins in the nociceptive response induced by intraperitoneal injection of zymosan in mice. 359 81

A mode of interaction of bradykinin with prostaglandins (PGs) in pain were compared with that in acute inflammation. When pain production was measured as an increase in reflex hypertensive response of the lightly anesthetized dogs after intrasplenic injection of bradykinin, the response was dependent to the doses (0.3-5 nmol) of bradykinin and that by the small doses (0.1-1 nmol) was blocked by intrasplenic infusion of indomethacin (0.54 mumol/min). The response to the threshold dose of bradykinin (0.3 nmol), which was suppressed during the indomethacin infusion, was potentiated by simultaneous injection of exogenous PGs. Order of the potency was PGI2 greater than PGH2 greater than PGE2 = TXA2 much greater than PGD2. Thus, it is clear that bradykinin induced pain through the generation of one of prostaglandins. On the other hand, the activity of bradykinin in plasma leakage was potentiated by simultaneous injection of PGE2, when tested in rabbit skin. In rat carrageenin-induced pleurisy, plasma prekallikrein was activated and high molecular weight (HMW) kininogen, not low molecular weight (LMW) kininogen, was consumed in the pleural cavity in the entire course of the pleurisy. Bradykinin played a role in plasma exudation in the pleurisy, because the plasma leakage was markedly inhibited in the rats, in which prekallikrein and HMW kininogen in plasma were depleted by intravenous bromelain. PGE2 was found in the pleural exudate, but the contribution of PGE2 itself to the plasma exudation seems to be only 10%. On the basis of the bradykinin release in the pleural cavity, once the PGE2 release was superimposed, the maximal plasma leakage was observed, indicating that PGE2 was released independently from bradykinin, and potentiated the plasma leakage by bradykinin.
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PMID:Different modes of interaction of bradykinin with prostaglandins in pain and acute inflammation. 381 4


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