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)

Muscle energy metabolism was studied by chemical analysis of biopsy samples from: 1) trigger points in the trapezius muscle from 15 patients with primary fibromyalgia (PF), 2) nonpainful, anterior tibial muscle from 6 patients with PF, and 3) the trapezius muscle from 8 healthy controls. We found a decrease in the levels of adenosine triphosphate, adenosine diphosphate, and phosphoryl creatine, and an increase in the levels of adenosine monophosphate and creatine, in the trapezius muscles from the patients. These findings support the notion that the pain in patients with PF is of muscular origin.
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PMID:Reduced high-energy phosphate levels in the painful muscles of patients with primary fibromyalgia. 374 98

Eleven men with claudication and ten control subjects had calf muscle metabolism studied at rest and during exercise and the subsequent recovery period by 31P nuclear magnetic resonance (n.m.r.) spectroscopy. The muscle of patients with severe claudication had a significantly greater depletion of phosphocreatine and fall in pH during exercise and a slower recovery of phosphocreatine and pH after exercise. The muscle of patients with both mild and severe disease had slower rates of ADP recovery after exercise than that of control subjects. Surgical correction of the associated arterial stenosis abolished claudication and led to correction of the metabolic abnormalities in two patients. Claudication pain was not related to intracellular pH or concentration of phosphorus-containing metabolites. Energy production via oxidative metabolism is impaired but glycolysis may be increased in the calf muscle of patients with intermittent claudication.
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PMID:Muscle metabolism in patients with peripheral vascular disease investigated by 31P nuclear magnetic resonance spectroscopy. 375 32

Six patients are described in whom gangrene of one or more toes occurred as the presenting feature of essential thrombocythaemia. Spontaneous platelet aggregation was observed in platelet-rich plasma from four patients and platelet aggregation after the addition of adenosine diphosphate and collagen was highly abnormal in samples from all six. All of the patients described dramatic relief of pain within six hours of ingestion of aspirin and this coincided with disappearance of the spontaneous platelet aggregation and collagen-induced platelet aggregation. Treatment with phosphorus-32 corrected the platelet count and there were no further recurrences of peripheral vascular disease. Platelet function tests performed at the time all gave normal results. It is concluded that essential thrombocythaemia is an important and treatable cause of peripheral vascular disease.
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PMID:Essential thrombocythaemia and peripheral gangrene. 447 3

Adenosine triphosphate (ATP), adenosine diphosphate (ADP), adenosine monophosphate (AMP), adenosine, adenine and inosine were injected intradermally into the backs of human volunteers. ATP, ADP and AMP evoked weal and flare responses in the skin in a dose dependent manner. The rank order of potency was ATP greater than ADP greater than AMP; other metabolites were apparently inactive. The potency of ATP was approximately 0.002 times that of histamine. In the forearm, cross tachyphylaxis was demonstrated between ATP and histamine weals; also the flare due to injected ATP spread beyond a band which was applied to prevent diffusion, indicating that the flare is neurogenic. Injections of ATP and high doses of ADP produced a sensation of persistent pain, unlike histamine which produced transient pain or itch on some occasions, and saline which was without effect. The possible involvement of histamine, mast cells and prostaglandins in the response was examined. The inhibitory actions of systemic pretreatment with diphenhydramine suggests that the erythema and wealing responses to ATP are at least partly due to ATP-evoked histamine release. Indomethacin, doxantrazole and cimetidine did not alter the ATP reaction.
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PMID:Adenosine triphosphate-evoked vascular changes in human skin: mechanism of action. 617 40

1. In peripheral arterial insufficiency, leg blood flow during exercise is reduced. The aim of this study was to investigate the metabolic response in different muscle types during exercise at reduced versus normal exercise blood flow. 2. A modified rat hindlimb perfusion model was used. Muscle metabolites and distribution of labelled microspheres were analysed in the soleus and the gastrocnemius muscles during exercise induced by sciatic nerve stimulation. 3. Blood flow distribution between the soleus and the gastrocnemius muscles (per unit weight) was 1.7:1 at rest, and this ratio did not change significantly during exercise at reduced flow. 4. There was a more pronounced decrease in the [phosphocreatine], the [glycogen] and the [ATP]/[ADP] ratio as well as a more pronounced increase in the [lactate] and the [lactate]/[Pyruvate] ratio in the gastrocnemius muscle during exercise at reduced blood flow as compared with values obtained at normal exercise flow. In the soleus muscle the difference between the two conditions was confined to an increased [lactate]/[pyruvate] ratio. 5. The results show that a muscle composed mainly of fast-twitch fibres with a high glycolytic and low oxidative capacity is much more susceptible to a reduced exercise flow than a muscle composed of slow-twitch, oxidative fibres. It is suggested that claudicating pain is related to these metabolic changes and it is concluded that pain most probably originates in type II fibers.
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PMID:Metabolic response in different muscle types to reduced blood flow during exercise in perfused rat hindlimb. 709 39

The "adenosine" and "non-adenosine" mechanisms of adenine nucleotide (ATP, ADP, AMP KP) metabolism were studied in 58 patients with myocardial infarction. Predominant activation of the "adenosine" mechanism of metabolism was revealed in patients with acute myocardial infarction with a marked pain syndrome in the first 24 hours of the disease. In the painless form of myocardial infarction the "nonadenosine" nucleotide metabolism is activated while the "adenosine" type is inhibited. The determination and comparison of indices reflecting the condition of the "adenosine" and "nonadenosine" mechanisms of metabolism provide the possibility for evaluating the severity of the pathological process and, on this basis, elaborating a differentiated approach to the treatment of the patient.
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PMID:[Adenine nucleotide metabolic characteristics in different forms of myocardial infarct]. 726 40

The effect of the non-steroidal analgesic diflunisal on platelet aggregation and clinical haemorrhage at a dosage 250 mg twice or 3-times daily, sufficient to relieve musculo-skeletal pain and other painful conditions, was studied in 15 patients and 5 normal subjects. Platelet aggregation was carried out with ADP and collagen before and during treatment with diflunisal. The results indicated that diflunisal is an effective analgesic with no significant adverse effect on platelet function or clinical bleeding.
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PMID:Platelet aggregation in patients treated with diflunisal. 736 51

Three patients (two of them siblings) presented with easy fatiguability and prominent postexercise pain. Muscle biopsy showed that large areas of about one third of the type II fibers were completely devoid of mitochondria. The remaining mitochondria were unusually large in size, but otherwise normal ultrastructurally. In two patients, 31P in vivo MRS showed low phosphocreatine (PCr), high ADP, low phosphorylation potential at rest and slow ADP and PCr recovery after aerobic exercise. This appears to be a pathologically unique form of metabolic myopathy. The cause of the focal mitochondrial depletion is not known. It should be distinguished from the mtDNA depletion syndrome in which muscle mitochondria are not reduced, but proliferate.
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PMID:Familial myopathy with conspicuous depletion of mitochondria in muscle fibers: a morphologically distinct disease. 776 93

Ketorolac, ketoprofen and nefopam are often used in the treatment of postoperative pain. While nefopam is a non-narcotic, non-opioid central analgesic agent, ketorolac and ketoprofen are non-steroidal anti-inflammatory drugs, which, due to their prostaglandin-synthetase inhibiting activity, have antiplatelet effects. In this study we investigated the effect of ketorolac, ketoprofen and nefopam on platelet function by performing bleeding time and in vitro platelet aggregation in 30 healthy volunteers (10 for each treatment) before and 3 h after drug administration. Nefopam did not affect bleeding time and platelet aggregation, while ketorolac and ketoprofen significantly prolonged bleeding time without significantly inhibiting platelet aggregation in response to adenosine diphosphate. The prolongation of bleeding time observed after ketorolac and ketoprofen may have clinical relevance and suggests that nefopam could be more safely administered for the treatment of postoperative pain, especially in patients with haemostatic defects or after high bleeding risk surgery.
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PMID:Effect of ketorolac, ketoprofen and nefopam on platelet function. 786 17

A double-blind, placebo-controlled randomized study with BAY U3405, a specific thromboxane A2 (TX A2) receptor blocker, was performed in patients suffering from severe stade II limb arteriopathy. BAY U3405 or placebo was administered in 16 patients at 20 mg four times a day (from day 1 to day 3). Hemostatic studies were done before therapy, and on day 2 and day 3 under therapy. On day 3, BAY U3405 was shown to induce a highly statistically significant decrease of the velocity and the intensity of the aggregations mediated by arachidonic acid (56 +/- 37% for the velocity, 58 +/- 26% for the intensity) or by U46619 endoperoxide analogue (36 +/- 35% for the velocity, 37 +/- 27% for the intensity). Similar results were already observed on day 2. By contrast, such a decrease was not noticed with ADP mediated platelet aggregation. Furthermore, plasma levels of betathromboglobulin and platelet factor 4 remained unchanged. Peripheral hemodynamic parameters were also studied. The peripheral blood flow was measured using a Doppler ultrasound; the pain free walking distance and the total walking ability distance were determined under standardized conditions on a treadmill. These last two parameters show a trend to improvement which nevertheless was not statistically significant. All together these results encourage further in vivo studies using BAY U3405 or related compounds on a long-term administration.
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PMID:Ex vivo inhibition of platelet aggregation in patients with severe limb arteriopathy treated with BAY U3405, a specific TX A2 receptor antagonist. 790 69


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