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

A general model of the autonomic neuroeffector junction is proposed. In this model, emphasis is placed on the muscle effector bundle with electrotonic coupling between individual cells via gap junctions (or nexuses) and en passage release of transmitter from autonomic nerve varicosities. This release results in transmission to effector cells across junctional clefts ranging from about 20 nm in the vas deferens and iris to as much as 2000 nm in some large arteries. The ultrastructural identification of different autonomic nerve types is described. Current theories on the synthesis, storage, release, and inactivation of transmitter during cholinergic, adrenergic, and purinergic transmission are summarized. Some speculations are made about the possible involvement of purinergic nerves in the innervation of vessels and mast cells in the skin, and whether this involvement results in a functional link between ATP, histamine, bradykinin, and prostaglandin in cutaneous vasodilatation. Another possibility considered as the basis for this reflex is the release of substance P from sensory (pain) nerve collaterals in the skin.
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PMID:Autonomic neuroeffector junctions--reflex vasodilatation of the skin. 1 40

In fourty patients with peripheric atherosclerosis obliterans blood flow was measured by means of venous occlusion plethysmography during an intraarterial and an intravenous infusion of ATP. The intraarterial application showed a significantly higher increase of blood flow than the intravenous in the sick extremities. The "borrowing-lending-phenomenon" happened more seldom than after an intravenous load. This withdrawal of blood occurred most frequently in patients with proximal occlusions, when the infusion reached casually the arteria femoralis profunda only. The "borrowing-lending-phenomenon" can be measured by the poststenotic pressure and by the volume of blood flow in time. Then the patients complain about a begining or an increasing of an ischemic pain at rest.
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PMID:[Investigation by borrowing-lending-phenomenon under conditions of intraarterial induced vasodilatation (author's transl)]. 91 79

Using 31P nuclear magnetic resonance, the following parameters were determined in the resting musculus erector spinae of five patients suffering from chronic low back pain, five patients with fibromyalgia, and five healthy controls: Inorganic phosphate (Pi), phosphocreatine (PCr), ATP gamma, ATP alpha, ATP beta. The intracellular pH was derived from the chemical shift of Pi referenced to the PCr resonance. In addition, the Pi-Index was calculated according to the formula: Pi/(Pi + PCr). We discovered a tendency towards a shift of the Pi resonance in the alcalic direction, which was the larger, the stronger muscle spasm was found on palpation. The pH showed the most reliable relationship to the clinical status of muscle spasm. The surprising finding that there is no acidification within the spasmed muscle indicates that generalized hypoxia does not exist in this tissue. This has already been shown with PO2 measurements. An intracellular acidification is only recorded during maximal isometric contraction. Thus, ischemia cannot be responsible for pain experienced during muscle spasm.
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PMID:[Recording muscle spasm in the musculus erector spinae using in vivo 31P magnetic resonance spectroscopy in patients with chronic lumbalgia and generalized tendomyopathies]. 147 7

Venous stasis is a situation encountered commonly in varicose disorders. The potential implications of this decrease in oxygen levels in terms of the status of the cells of the vein were assessed. When endothelial cells are subjected to hypoxia, there is stimulation of the cells which shows itself as increased synthesis of prostaglandins and of PAF (Platelet Activating Factor). The synthesis of these typical mediators of inflammation results from activation by the calcium of phospholipase A2 which releases the arachidonic acid of phospholipids and this increase in intracellular calcium results itself from a fall in efficacy of calcium pumps due to the fall in ATP caused by hypoxia. Thus the fall in oxygen leads to the production of mediators of inflammation which activate leucocytes and result in local micro-inflammation which can be very rapidly eliminated if the circulation is restored but which can also cause irreversible damage to the vein by changes in venous tissue due to activated leucocytes which release proteases and free radicals after having penetrated the intima of the vein. These processes offer an explanation for the histological changes seen in varicose veins and the onset of localised pain during the development of such disease.
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PMID:[The relation between venous stasis and the occurrence of pain]. 149 30

During the last five years, 672 patients were referred to our esophageal investigation unit; 110 patients (16.3%) of these presented with chest pain of undetermined etiology (CPUE) alone. Since the nature of this pain is intermittent and rarely present during the diagnostic study, acid perfusion and intravenous edrophonium tests were added as provocative tests after baseline esophageal manometry. Following completion of the motility studies, 24-hr pH study was performed to detect gastroesophageal reflux (GER). Twenty-nine patients (26.4%) had positive acid perfusion (APT) test whereas 26 patients (23.6%) had positive edrophonium test (ET). In the group of patients with positive acid perfusion test, 12/29 (41.3%) had GER, 8/29 (27.5%) had both motility disorder and GER, 2/29 (6.8%) had motility disorder, and 7/29 (24.1%) had normal esophageal motility and 24-hr pH studies. In the other group, 13/26 (50%) had motility disorder and 13/26 (50%) had both motility disorder and GER. There were no significant differences between the two tests as far as reproducibility of symptoms was concerned. We conclude that ATP and ET showed the esophageal origin of CPUE in half of our patients and therefore in a substantial percentage of patients the esophageal origin of chest pain will remain very difficult to prove.
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PMID:Acid perfusion and edrophonium provocation tests in patients with chest pain of undetermined etiology. 149 45

Nociceptive dorsal horn neurones, which are involved in the processing of pain-related information, are inhibited by input from vibration-sensitive, large diameter primary sensory fibres (Wall and Cronly-Dillon, 1960; Salter and Henry, 1990a,b). We have reported previously that the inhibition of spinal nociceptive neurones by vibration is mediated by adenosine acting through P1-purinergic receptors (Salter and Henry, 1987). In a number of different types of cell, adenosine is known to activate K+ currents (Gerber et al., 1989; Greene and Haas, 1985; Proctor and Dunwiddie, 1987; Segal, 1982; Trussell and Jackson, 1987) and we have recently found that the adenosine-mediated inhibition of nociceptive neurones by vibration is the result of an inhibitory postsynaptic potential (IPSP), which is, indeed, caused by a K+ conductance (De Koninck and Henry, 1988, 1992). It has been reported that adenosine-activated K+ channels in cardiac muscle cells are the ATP-sensitive K+ channels (Kirsch et al., 1990). Therefore, we questioned whether these channels might mediate the purinergic IPSP we have observed in nociceptive dorsal horn neurones. We report here that glibenclamide, a blocker of ATP-sensitive K+ channels (Ashcroft, 1988; Schmid Antomarchi et al., 1987a,b), blocks the inhibition of nociceptive neurones by vibratory stimulation when this compound is administered locally by iontophoresis or systemically by intravenous injection. In addition, direct intracellular injection of ATP was found to block the IPSP evoked by vibratory stimulation. These data indicate that the purinergic IPSP in nociceptive spinal neurones is mediated via ATP-sensitive K+ channels.(ABSTRACT TRUNCATED AT 250 WORDS)
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PMID:ATP-sensitive K+ channels mediate an IPSP in dorsal horn neurones elicited by sensory stimulation. 163 51

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

A review of metabolic pathways is presented, which are involved in muscular energy production during hypoxia according to recent experimental findings. By means of own exercise examinations the course of reactions providing ATP anaerobically in the muscles of limbs with poor circulation is analysed. Therefore, the arteriovenous differences in the concentrations of lactate, pyruvate, ammonia, hypoxanthine and alanine in the femoral blood of patients with stage II AOD were determined. In addition, the intracellular phosphorus compounds ATP, PCr and Pi as well as the tissue pH were measured noninvasively in the calf muscles using 31P magnetic resonance spectroscopy. The results give evidence for marked activation of the creatine kinase reaction, of glycolysis, of the myokinase reaction and of the purine nucleotide cycle in the ischaemic musculature at loads of short duration, which are in total sufficient to maintain the concentration of ATP even during claudication pain. In spite of salvage pathways like alanine formation, the end products of these "emergency reactions", Pi, H+ and NH4+, accumulate and exert deleterious cytotoxic effects, which are thought to be responsible for rapid muscle fatigue and claudication pain in PAOD.
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PMID:[Regulation of ischemic muscle metabolism in peripheral arterial occlusive disease]. 267 1

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


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