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 behaviour of muscular metabolism was investigated in 10 patients with peripheral arterial occlusive disease stage II at rest and after maximum ergometric calf exercise. The intracellular concentrations of phosphocreatine, inorganic phosphate and adenosine triphosphate as well as muscle pH were measured by means of 31P magnetic resonance spectroscopy and compared with those from a control group. In addition, arteriovenous differences in concentrations of lactate, pyruvate, ammonia, hypoxanthine and alanine in the femoral blood were determined. The fall in intracellular phosphocreatine concentration during exercise was significantly greater in the calf muscles of patients with arterial occlusion than in controls and correlated linearly with the increase in femoral arteriovenous differences in lactate, ammonia and alanine. A significant fall in intracellular pH occurred during muscular activity only in the patient group, but not in the identically exercised control group. The fall in pH correlated closely with the rise in arteriovenous lactate difference in the femoral blood. The intramuscular ATP concentration remained constant throughout the exercise procedure. The behaviour of both the directly and indirectly measured metabolites permits the deduction of activation of the creatine kinase reaction, glycolysis, myokinase reaction and the purine nucleotide cycle during exercise-induced hypoxia in the presence of arterial occlusive disease. The anaerobic production of energy is sufficient to maintain the ATP concentration even during claudication pain.(ABSTRACT TRUNCATED AT 250 WORDS)
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PMID:Assessment of muscular metabolism in peripheral arterial occlusive disease using 31P nuclear magnetic resonance spectroscopy. Comparison with metabolite concentrations in femoral blood. 279 50

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

The analgesic, anti-inflammatory and gastrointestinal effects of rimazolium, morphine and prostaglandin synthesis inhibitors were compared in a battery of tests. Rimazolium, morphine and indomethacin all inhibited carrageenin-induced inflammation; however, the onset of action was different. The first (histamine-serotonin) phase was inhibited by rimazolium, the second (kinin) phase by morphine and the third (prostaglandin) by indomethacin. The chemoluminescence of leucocytes was inhibited by morphine and indomethacin but was unaffected by rimazolium. Prostaglandin-mediated pain (ACh, ATP, acetic acid writhing) was inhibited by all three types of compound; however, pain reaction where prostaglandins (PGs) are not involved (MgSO4 writhing) was inhibited by rimazolium and morphine, but not (or only slightly) by PG synthesis inhibitors. Gastric lesions produced by indomethacin were depressed by rimazolium and aggravated by morphine. These results suggest different mechanisms of anti-inflammatory and analgesic action of rimazolium, morphine and PG synthesis inhibitors.
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PMID:Analysis of the analgesic and anti-inflammatory effects of rimazolium, a pyrido-pyrimidine derivative, compared with that of prostaglandin synthesis inhibitors and morphine. 387 53

The role of lipid peroxidation (LPO) in the damages of the enzymic system of Ca2+ transport in sarcoplasmic reticulum (SR) membranes of skeletal and cardiac muscles under conditions of vitamin E deficiency, ischemia and limb reoxygenation as well as in emotional-pain stress was investigated. It was shown that these processes are associated with activation of endogenous LPO in SR membranes "in vivo" and with simultaneous inhibition of Ca2+ transport, (i. e. decrease of the Ca2+/ATP ratio) and inactivation of Ca-ATPase. The degree of damage of the Ca2+ transport system was correlated with the concentration of LPO products accumulated in SR membranes "in vivo and during LPO induction by the Fe2+ + ascorbate system 'in vitro". Injection of natural and synthetic free radical scavengers (e. g. 4-methyl-2.6-ditretbutylphenol, alpha-tocopherol) to experimental animals resulted in practically complete suppression of LPO activation "in vivo" and in partial protection of the Ca2+-transporting capacity of SR membranes. A comparison of experimental results allowed to estimate the role of LPO in SR damage under pathological conditions. Model experiments with "contraction-relaxation" cycles including isolated components of muscle fibers (SR fragments and myofibrils) demonstrated that LPO induction in SR membranes by the Fe2+ + ascorbate system results in complete elimination of the relaxation step in myofibrils due to the loss of the SR affinity to decrease the concentration of Ca2+ in the incubation medium. This effect can be removed by free radical scavengers. The role of LPO in pathological changes of muscle contractility is discussed.
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PMID:[Modification of an enzymic system of Ca2+ transport in sarcoplasmic reticulum during lipid peroxidation. In vivo damages in the development of pathological changes]. 622 70

The prostaglandin synthesis inhibitors studied were highly potent analgesics against ATP and ACh-induced writhing, but slightly effective or ineffective against MgSO4-induced pain. Morphine also proved to be more effective against ATP and ACh than against MgSO4-induced writhing. ATP and ACh-induced writhing syndrome could be inhibited by the prostaglandin receptor antagonist- Sc-19220. However, Sc-19220 failed to inhibit writhing elicited by MgSO4. The concentration of malondialdehyde was significantly higher in the peritoneal fluid following intraperitoneal injection of ATP and ACh, but was unaltered when MgSO4 was applied as a challenge substance. These results suggest that the prostaglandin system might be involved in the ATP- and ACh- but not in MgSO4-induced pain reaction.
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PMID:The use of the writhing test in mice for screening different types of analgesics. 672 21

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

Changes in rat bladder function following the exposure to physical stress were studied in vitro. Rats were divided into two stress groups and two control groups and maintained for 6 months under specific conditions. The stress groups, consisting of animals subjected to water or pain stress and control groups were kept in cages floored with wooden chips or wire net. The body weight of the stressed groups was significantly lower than that of the controls. Gastric ulcer occurred in none of the groups. The detrusor response of the water group to acetylcholine was significantly greater than that of the two control groups. In the pain group, the contractile response was induced by norepinephrine. In the other three groups, however, norepinephrine evoked a relaxation of muscle strips. The contractile response of the bladder to both serotonin (5-hydroxytryptamine) and ATP (adenosine 5'-triphosphate) did not differ between the four groups.
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PMID:Changes in rat bladder function following exposure to pain and water stimuli. 755 95

1. K channels are a diverse and ubiquitous class of proteins that regulate a number of biological functions. 2. Ligands for the study of a variety of K channels are available. These include "openers" and antagonists for the ATP sensitive K channel and peptide toxins such as apamin and charybdotoxin that block other subtypes. 3. Antagonists of the ATP sensitive K channel are useful in the treatment of type II diabetes while "openers" of this channel are being tested in asthma and cardiovascular disease. 4. Intracerebroventricular administration of K channel "openers" block experimentally induced seizures in rodents through a hyperpolarization of neurons. K channel openers may also be useful in the treatment of neurodegenerative diseases, pain and cerebral ischemia. 5. A key to the development of psychopharmacological agents to modify brain K channel function is CNS selectivity. The promise of the ATP sensitive K channel openers suggests a bright future for this mechanism.
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PMID:ATP sensitive potassium channels: potential drug targets in neuropsychopharmacology. 784 82

Masseter muscle metabolism is poorly understood. 31P Magnetic Resonance Spectroscopy (MRS) provides an opportunity for non-invasive study of muscle metabolism during rest, exercise, and recovery. The aim of this study was to investigate the changes in high-energy phosphates and pH in human masseter muscle associated with exertional pain. Phosphates and pH were measured with 31P Magnetic Resonance at 2.0 Tesla. The bite force was simultaneously measured with a force transducer. Continuous biting at maximum voluntary bite force (MVBF) and two intermittent biting exercises with different duty cycles were performed to pain intolerance. The light intermittent exercise did not produce pain. Brief MVBF requested at the beginning, during, and end of each exercise showed no decay. Qualitatively, changes in phosphates were similar to those reported from comparable limb muscle exercises: increased inorganic phosphate (Pi), decreased phosphocreatine (PCr), and no changes in ATP level. Quantitatively, however, the Pi/PCr ratio did not reach the levels reported in limb muscles during similar exercises. Also, the pH changed very little. Thus, the lack of fatigue was no surprise, since the level of changes in Pi/PCr and pH, reported to be associated with fatigue in limb muscles, was far less in the masseter. Pain development toward the end of the heavy exercises prevented further depletion of metabolites. Thus, the lack of fatigue generally postulated for the masseter muscle may not be due to resistance to fatigue of these fibers, but rather to the presence of pain preventing the fatigue. However, no specific metabolic changes associated with exertional pain were found.
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PMID:Phosphorus magnetic resonance spectroscopy of human masseter muscle. 787 27


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