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

The action of the adenyl compounds adenosine triphosphate (ATP), adenosine diphosphate (ADP), adenosine monophosphate (AMP) and adenosine was studied on the human blister base preparation. All 4 adenyl compounds produced pain which was slow in onset and not maintained. The threshold concentration for pain was of the order of 1-3 micron. The slopes of log concentration:pain intensity plots were relatively shallow and for moderate to severe pain a 100-fold increase of the threshold concentration was required. The adenyl compounds resembled 5-hydroxytryptamine and bradykinin with respect to onset and duration of action but were less potent. On the other hand, for threshold effects they were more potent than acetylcholine or potassium. Evidence was found for an interaction of adenyl compounds with 5-hydroxytryptamine but not with potassium, acetylcholine or bradykinin. Cyclic adenosine 3',5'-monophosphate or the chelation of extracellular calcium or magnesium were shown not to be involved in the algogenic action of adenyl compounds and the action of adenyl compounds on the rabbit isolated jejunum too was found to be unrelated to their algogenic action on the human blister base preparation.
Pain 1977 Aug
PMID:Observations on the algogenic actions of adenosine compounds on the human blister base preparation. 19 25

Three young family members with recurrent arterial thrombosis underwent investigation for lipid or coagulation abnormalities. Lipoprotein electrophoresis, cholesterol, triglyceride levels, and routine coagulation studies were unremarkable. By contrast, testing of platelet function showed enhanced platelet aggregability to epinephrine and collagen in two of the subjects. In addition, release of 14C-serotonin by adenosine diphosphate and epinephrine was increased over control values in these same two patients. The third subject demonstrated decreased platelet aggregation and lowered 14C-serotonin release, but was symptomatic with rest pain at the time of testing. The ongoing in vivo thrombosis in the third subject may account for hypocoagulable platelets by in vitro testing. These abnormally sensitive platelets identified by platelet function testing may be associated with a familial "hypercoagulability" syndrome. Definition of the hemostatic abnormality in these individuals provided a rational basis for pharmacological therapy with antiplatelet drugs, which appeared to be successful.
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PMID:Platelet function abnormalities in a family with recurrent arterial thrombosis. 62 88

Lysates of human erythrocytes produce pain when applied to a human blister base. The algogenic material is not potassium, acetylcholine, bradykinin, 5-hydroxytryptamine, histamine or a prostaglandin, and is dialysable. 2. Fractionation of dialysates of freshly lysed erythrocytes by Sephadex gel filtration coupled with assays on the human blister base preparation showed that the algogenic material was a mixture of the adenyl compounds adenosine triphosphate (ATP), adenosine diphosphate (ADP) and adenosine monophosphate (AMP). 3. On the human blister base preparation ATP, ADP and AMP had comparable activity and produced threshold pain in a concentration of 2 muM. 4. The rabbit isolated jejunum preparation was found useful in these studies since ATP, ADP and AMP produced a relaxation which was proportional to their concentration in test samples obtained from dialysates. Of more limited usefulness was the rat isolated stomach strip preparation on which ATP and ADP produced contractions which also were proportional to their concentrations in text samples. 5. The possible role of adenyl compounds in the production of pain in vivo is discussed.
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PMID:Identification of algogenic substances in human erythrocytes. 99 34

Twenty patients with obliterative atherosclerosis in the lower extremities arteries (Fontaine's stage II) were treated with nitrendipine (Bayotensin) given in the dose of 20 mg daily for 6 weeks. This therapy with nitrendipine produced improvement manifested by the prolongation of the distance of intermittent claudication, shortening of pain duration, increase in blood flow in the ischemic extremity, and increase in pressure index. At the same time, nitrendipine decreased ADP-produced platelet aggregation and activated fibrinolytic system. Clinical trials have shown that nitrendipine is effective in the obliterative atherosclerosis in the lower extremities.
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PMID:[Use of nitrendipine in treating patients with obliterative atherosclerosis of arteries in the lower extremities]. 166 21

Twenty-five patients (seven male, 18 female) were diagnosed as having the loin pain and haematuria syndrome. Presenting symptoms were either loin pain alone or pain associated with macroscopic or microscopic haematuria, and were longstanding, having been present for mean of 9.3 years in males, and 10 years in females. Ten patients described symptoms of passing gravel or renal stones but these were only demonstrated radiologically in two patients. Investigation of all patients showed anatomically normal renal tracts, normal renal function, and no significant proteinuria. Phase-contrast microscopy during episodes of haematuria revealed dysmorphic red cells in all 10 patients studied. Renal biopsies were performed in 20 patients and showed no glomerular pathology, but arteriolar and arterial hyalinosis was seen in 13 of 20 (65 per cent), fibro-elastosis in larger vessels in eight of 20 (40 per cent) and red blood cells in tubules in 13 of 20 (65 per cent) patients. The histological appearance in vessels was similar to that seen in cyclosporin A nephrotoxicity and would be consistent with the hypothesis that regional vasospasm occurs in the cortical circulation. Haematological studies in 22 patients, when compared with age and sex matched controls, showed the presence of circulating platelet aggregates, elevation of plasma beta-thromboglobulin (p less than 0.001), and increased platelet aggregation in response to serotonin and ADP (p less than 0.05 and p less than 0.03, respectively). Plasma concentrations of D dimer (p less than 0.02) and C-reactive protein (p less than 0.03) were also significantly elevated in the patient group. There was no deterioration of renal function during a mean observation period of 3.7 years and no patients developed proteinuria. Treatment was largely supportive; seven patients with intractable loin pain underwent surgical denervation with the relief of pain in four.
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PMID:Haemostatic changes in the loin pain and haematuria syndrome: secondary to renal vasospasm? 223 80

Normal subjects performed voluntary, isometric exercise 1 s contraction, 1 s rest for 10 min) of the first dorsal interosseous (FDI) muscle with a target force of 25, 50 and 100% of the maximal voluntary contraction (MVC) force. 31P NMR spectra were collected continuously before, during and after exercise. Data were also taken from the resting muscles 2-28 h after the studies at 50% MVC. Calculations were made of the intracellular pH and concentrations of PCr, Pi, ATP, ADP and H2PO4-. The 25% MVC contractions did not affect the MVC, but those at 50 and 100% MVC reduced the force by 20% and 60%, respectively (p less than 0.005). During the highest force contractions, the MVC declined from the first minute but the target forces of 25 and 50% were maintained throughout. All protocols caused significant changes in pH, PCr, Pi, ADP and H2PO4-. Exercise at 50% MVC caused greater metabolic changes than that at 25%, but there was no overall difference in the pH and phosphorus metabolites between the two higher forces. In parallel studies, electrical stimulation of the muscle indicated that during the voluntary contractions with a target force of 100% MVC in the magnet: (a), additional muscles were being used to generate the recorded force; and (b), the subjects were not fully activating the FDI. There was no obvious causal relationship between any one metabolite and the decline of force. Resting muscle showed an increase in the Pi peak 2-28 h after exercise at 50% MVC force, despite the muscles being of full strength and pain free.
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PMID:A 31P study of fatigue and metabolism in human skeletal muscle with voluntary, intermittent contractions at different forces. 228 60

The effects of injecting ATP, ADP, AMP, adenosine and adenine intrathecally on the pain response induced by the injection of substance P (10 ng/mouse) intrathecally were studied. All the compounds except adenine inhibited the pain response in a dose-related manner. The ED50 values of ATP, ADP, AMP and adenosine were 2.10, 0.93, 0.88 and 0.48 micrograms/mouse, respectively. Pretreatment with theophylline at a dose of 100 mg/kg p.o. markedly diminished all the antinociceptive effects. The effect of adenosine was not affected by s.c. injection of naloxone. These results suggest the existence of adenosine receptors which modulate spinal nociceptive sensory processing, independently of the endogenous opiate system.
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PMID:Spinal antinociceptive effects of adenosine compounds in mice. 244 Jul 5

Thirty patients with ischaemic peripheral vascular disease and intermittent claudication were randomly allocated to receive either placebo or taprostene, a chemically stable prostacyclin analogue, intravenously at a rate of 25 ng/kg/min for 6 hours daily on 5 consecutive days. Taprostene produced a significant (p less than 0.05) increase in absolute walking time compared to placebo on one day after infusion and at 1, 4 and 8 weeks (14% vs 2.8%) later. Taprostene also produced a significant (p less than 0.05) increase in the pain-free walking time compared to placebo in the follow-up period (8 weeks after infusion: 23% vs 3.8%). During the infusion period systolic and diastolic blood pressure decreased (p less than 0.05) and heart rate was accelerated (p less than 0.05) in the taprostene treated group whereas no change was monitored in the placebo group. The ankle/brachial Doppler index was unaffected by taprostene. The platelet half-life was significantly (p less than 0.05) prolonged following taprostene-infusion (72.6 +/- 9.35 vs 77.9 +/- 7.44 hours). However, no change on platelet half-life was found in the placebo group (p less than 0.05). Various measures of platelet function parameters followed in vitro (ADP-induced aggregation, platelet sensitivity to PGI2, PGE1, PGD1 and taprostene, concentrations of platelet factor 4 and beta-thromboglobulin) showed no change with taprostene. Measures of circulating platelet aggregates and endothelial cells count showed no changes during the 2 months follow-up period too. It is assumed that taprostene may be of clinical benefit in patients with ischaemic peripheral vascular disease. However, future investigations have to be carried out to assess the optimal dose regime.
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PMID:Effects of taprostene, a chemically stable prostacyclin analogue, in patients with ischaemic peripheral vascular disease: a placebo controlled double-blind trial. 251 30

Platelet activation at sites of enmeshed sickled red cells in the microcirculation may contribute to platelet plug formation and microinfarction in sickle cell anemia. To test this hypothesis platelets from 116 sickle cell anemia patients free of crisis, 32 patients with crisis, 16 convalescents within 1 week of crisis, and 180 normal controls were studied. Platelets store 90% of their ADP in dense secretory granules. During activation ADP is secreted and permanently lost from the cell. This leads to a decrease in cellular ADP concentration and a sharp rise in the ATP/ADP ratio. ATP and ADP were ethanol-extracted from platelet-rich plasma, measured in the luciferase-luciferin assay and expressed in nmoles per 10(8) cells. No adenine nucleotide differences were found in platelets from patients free of crisis compared with normal controls. The ADP concentration of platelets from patients in crisis was significantly lowered, indicating that in vivo platelet secretion of ADP had occurred. Total and released ADP was decreased from 2.69 to 1.66, and from 1.90 to 1.21 respectively, and the total ATP/ADP ratio was increased from 1.85 to 2.84 (P less than 0.001). ADP stores in platelets from convalescents were significantly different from sickle controls (P less than 0.001) but were less abnormal than ADP stores in platelets from crisis patients (P less than 0.01), indicating recovery. Total and released ADP was decreased to 1.97 and 1.31 respectively, and the ATP/ADP ratio was increased to 2.38. Platelets from patients in crisis were able to release their remaining granular ADP in response to thrombin as effectively as normal platelets. Thus significant platelet activation with ADP release occurs during acute sickle pain crisis. This might contribute to platelet plug formation and microvascular obstruction.
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PMID:Platelet activation during pain crisis in sickle cell anemia patients. 274 22

There is little information available concerning the alterations in skeletal muscle energy metabolism which occur in response to chronic arterial occlusive disease. In addition, the effect of arterial reconstruction on skeletal muscle energy metabolism in patients with peripheral vascular disease has not been defined. Needle biopsies were obtained from the quadriceps femoris muscle of 7 patients with aortoiliac disease and 15 patients with femoropopliteal disease and from the gastrocnemius muscle of 9 patients with femoropopliteal disease. Muscle samples were analyzed for ATP, ADP, AMP, phosphocreatine, creatine, and lactate. Eleven patients were rebiopsied after vascular reconstruction. Patients with rest pain had decreased total adenine nucleotides, energy charge potential, and ATP/ADP ratios as compared to those of controls. ATP levels were significantly decreased in muscle samples obtained distal to the arterial occlusion (i.e., quadriceps/aortoiliac, gastrocnemius/femoropopliteal) in patients with rest pain (compared with controls). ATP levels did not differ significantly from those of controls in muscle samples obtained from patients with claudication. However, energy charge potential was significantly decreased in all patients with claudication regardless of biopsy site and location of arterial occlusive disease. Normalization of muscle energy metabolism was not demonstrated following arterial reconstruction. We conclude that resting skeletal muscle energy metabolism is abnormal in patients with chronic arterial insufficiency and that progression of disease toward more severe ischemia is associated with more marked derangement. Whether the possible beneficial effects of revascularization on muscle energy metabolism are masked by the concurrent effect of injury in the early postoperative period remains to be clarified.
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PMID:Muscle high energy phosphates in chronic peripheral vascular disease. 334 25


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