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)

A 72 h infusion of prostacyclin or placebo was given into femoral artery as a treatment for ischemic ulcers in 30 patients with peripheral arterial disease. Patients were well matched for age, sex, type and localization of disease, rest pain, number and area of ulcers, calf blood flow and previous sympathectomies. They had no diabetes mellitus, gangrene or marked aorto-iliac involvement. Six weeks after the infusion there was a significant difference in ulcer area between the two groups (p less than 0.02, t unpaired test): mean ulcer area decreased (p less than 0.02, t paired test) in the prostacyclin-treated group, but not in the placebo group (p greater than 0.05, t paired test). Thus, intra-arterial infusion of prostacyclin promotes healing of ischemic ulcers in non-diabetic patients with peripheral arterial disease without gangrene.
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PMID:Prostacyclin for ischemic ulcers in peripheral arterial disease. A random assignment, placebo controlled study. 388 72

A study was carried out in 17 patients with arteriosclerosis obliterans to assess the effectiveness of treatment with pentoxifylline ('Trental') and to investigate its possible mechanism of action. Patients received pentoxifylline on a combined intravenous/oral dosage regimen for 3 weeks and then were maintained on 800 mg orally for a further 2 weeks. The results showed that there was clinical improvement in 16 patients which was evident as a significant increase in the pain-free walking distance and blood flow in ischaemic legs, and the disappearance of rest pain. These changes were seen as soon as 1 week after the start of treatment. At the same time, an increase was observed in platelet sensitivity to the anti-aggregatory action of endogenous PGI2, as well as an activation of fibrinolysis in blood. After 5 weeks of treatment, further improvement was observed; however, platelets were no more hypersensitive to PGI2, and fibrinolytic activity of blood returned to the previous value. In experiments ex vivo, no release of a disaggregatory substance into blood was observed after a single bolus intravenous injection of pentoxifylline in patients with arteriosclerosis obliterans. It is concluded that the beneficial results of pentoxifylline therapy in such patients may be explained partially by a potentiation of the action of endogenous PGI2.
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PMID:Beneficial results of pentoxifylline ('Trental') therapy in arteriosclerosis obliterans: possible mechanism of action. 388 6

Certain polyunsaturated fatty acids, such as arachidonic acid, are metabolized by oxygenation into a large family of biologically active substances, the prostanoids. These include the prostaglandins, thromboxanes, prostacyclins, leukotrienes and also a number of related compounds. Oxygenation can take place at many different positions of arachidonic acid. A cyclo-oxygenase introduces oxygen at C-11 and converts the resulting peroxy compound into a 9, 11-endoperoxide structure. The cyclic peroxides thus formed, PGG2 and PGH2, are highly potent compounds and are the immediate precursors of the prostaglandins, thromboxanes and prostacyclin. Other enzymes, the lipoxygenases, may instead introduce oxygen at C-5, C-8, C-9, C-12 or C-15: further conversions from, for example, the initially formed 5- or 15-hydroperoxy acids may lead to the leukotrienes. The prostanoids display strong and varied biological activities, and have effects on numerous processes in the body. In some pathological conditions the prostanoids play important roles. For example, certain products of the arachidonic acid cascade are considered to be mediators of the inflammatory response: they are formed during the process, contribute to the symptoms of erythema, vascular leakage, fever, pain and chemotaxis, and inhibition of their biosynthesis can be achieved at different levels by the anti-inflammatory drugs.
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PMID:The arachidonic acid cascade. The prostaglandins, thromboxanes and leukotrienes. 609 Mar 12

Intraarterial injection of histamine into the isolated perfused rabbit ear causes a reflex fall in mean arterial blood pressure by stimulation of perivascular pain receptors. This effect is reduced by a low concentration of indomethacin (1 microgram/ml). The histamine H1-receptor antagonist mepyramine (10 micrograms/ml) reduced the effect of histamine. However, it also reduced the effect of acetylcholine. The histamine H2-receptor antagonist cimetidine (3-10 micrograms/ml) did not reduce the effect of histamine. Exogenously applied phospholipase A2 did not stimulate pain receptors on its own but enhanced the algesic effect of histamine, acetylcholine or bradykinin. This enhancement was abolished by indomethacin. Prostacyclin also enhanced the effect of histamine. The results suggest that histamine releases prostaglandins (E-type and prostacyclin) which in turn render the 'pain receptors' more sensitive to histamine. This effect may be of importance in inflammatory pain in that the effect of algogens (including histamine) is enhanced by an increased phospholipase A2-mediated synthesis of prostaglandins. Not only endogenously activated phospholipase A2 is able to split off prostaglandin precursors followed by subsequent generation of prostaglandins but also exogenously administered phospholipase A2 is able to induce the release of pain-enhancing prostaglandins.
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PMID:Dependence of histamine-evoked nociception on prostaglandin release. 612 58

A 96 h infusion of epoprostenol (prostacyclin) or placebo was given as a treatment for rest pain to 28 patients with severe peripheral arterial disease. 24 h after the end of the infusion patients given epoprostenol had significantly less pain and took fewer analgesics tablets than did the controls. In some patients the epoprostenol effect lasted for over 1 month.
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PMID:Epoprostenol (prostacyclin) and severe arterial disease. A double-blind trial. 613 Mar 30

Twenty-one patients with arteriosclerosis obliterans of lower extremities were treated with beta-pyridylcarbinol (Ronicol) for five weeks. The long-term therapy with beta-pyridylcarbinol did not influence platelet aggregability. Activation of the fibrinolytic system was observed. This fibrinolytic effect of Ronicol was abolished in patients treated with aspirin. In most cases a slight clinical improvement was seen, manifested by elongation of pain-free walking distance and increased blood flow in affected limbs. It is concluded that the therapeutic effect of Ronicol in humans may be partly mediated by the release of endogenous prostacyclin.
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PMID:Fibrinolytic activity and the effects of beta-pyridylcarbinol (Ronicol) in patients with arteriosclerosis obliterans. 636 47

A case is reported of a patient with diabetes and rheumatoid arthritis who presented with vasculitic ulceration of the lower leg and foot. The ulceration was associated with severe pain and showed no sign of healing despite conservative treatment and skin grafting. At the time when amputation seemed inevitable an intravenous infusion of prostacyclin was given. There was a rapid and lasting relief of pain and the ulcerated area began to heal spontaneously.
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PMID:Spontaneous healing and relief of pain in a patient with intractable vasculitic ulceration of the lower limb following an intravenous infusion of prostacyclin: a case report. 637 Mar 67

Twelve patients (age 33-77 years, mean age 68.4 years) with peripheral vascular disease (PVD) stage III-IV received continuous intravenous infusions of 5 ng prostacyclin (PGI2)/kg/min and physiological saline for 7 days. The administration was randomized and double-blind with an interval of 7 days between the infusions. During PGI2 infusion systolic blood pressure fell significantly from 147.8 +/- 4.8 mm Hg to 140.6 +/- 4.0 mm Hg (P less than 0.01) and returned to 144.5 +/- 4.9 mm Hg post infusion. Transcutaneous pO2 (tcpO2) measured on the instep of the affected limb increased significantly by 8.9 +/- 3.8 Torr during PGI2 infusion and remained elevated during the subsequent week. A significant reduction of pain was observed from the 5th day of PGI2 infusion, lasting for at least the following observation period. Platelet cAMP increased from 18.8 +/- 1.5 pmol/10(8) platelets to 24.7 +/- 1.6 pmol/10(8) platelets on the 3rd day of PGI2 infusion (P less than 0.01). Spontaneous platelet aggregation was also significantly reduced during PGI2 infusion. However, 7 days after the infusion thromboxane B2 (TXB2) in plasma and spontaneous platelet aggregation significantly increased in comparison with the preinfusion values, indicating a rebound phenomenon. The clinical outcome was favorable in 9 of 12 patients, was unchanged in two patients, while progressing to limb amputation in one patient.
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PMID:Prolonged infusion of prostacyclin in patients with advanced stages of peripheral vascular disease: a placebo-controlled cross-over study. 639 90

1 Cyclo-oxygenase products such as prostaglandins of the E series and prostacyclin produce the hyperalgesia associated with inflammation. 2 These substances may cause pain and incapacity in some inflammatory conditions. 3 Prostaglandin E2 sensitizes the chemical receptors of afferent pain endings to other inflammatory mediators such as bradykinin and histamine. 4 Unstable intermediates formed in the generation of prostaglandins may also play a role in the production of pain. 5 Drugs such as indomethacin and aspirin which are potent inhibitors of prostaglandin biosynthesis may exert their analgesic effect through this mechanism.
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PMID:Arachidonic acid metabolism, pain and hyperalgesia: the mode of action of non-steroid mild analgesics. 700 84

Severe extremity ischemia frequently cannot be relieved by surgical means and failure of current drug therapy may then result in prolonged disability or amputation. Prostaglandins E1 (PGE1) and I2 (prostacyclin, PGI2) are potent vasodilators and inhibitors of platelet aggregation which have been reported to be of value in the treatment of peripheral ischemia. Nineteen patents with severe extremity ischemia and one with vasculitic leg ulceration were treated on 25 occasions by intravascular infusion of PGE1 or PGI2 for 72 to 96 hours. Causes of ischemia were arteriosclerosis, Raynaud's phenomenon (secondary), Buerger's disease, and "trash" foot. Prolonged pain relief and promotion of tissue healing occurred mainly in patents with patent proximal axial arteries. Patency of the superficial femoral artery was associated with a good clinical response in eight of nine cases of foot ischemia, and mean hallux temperature rose 4.6 +/- 2.5 degrees C. In contrast, occlusion of the artery was associated with failure in eight of nine cases, and hallux temperature rose 0.6 degrees +/- 1.3 degrees C. PGE1 or PGI2 administered intravenously may be the treatment of choice for severe ischemia in distal arteriopathy, although the exact mechanisms by which these prostaglandins act are far from clear.
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PMID:Preliminary experience with prostaglandins E1 and I2 in peripheral vascular disease. 700 84


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