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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

A useful method is described in this paper for studying the mediators released from tooth pulp of the dog during the electrical stimulation of dentine. This method is based upon the perfusion of the pulp and superfusing the return continuously over the isolated, in cascade, cat jejunum and rat stomach fundus strip. The presented evidences in this study indicate the possibility of the release of bradykinin and prostaglandin - like materials from the tooth pulp during the electrical stimulation of dentine. Possible relationship of these mediators and tooth pain due to the electrical stimulation of dentine is discussed.
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PMID:A method for studying the peripheral mediators of the dental pain induced by electrical stimulation. 5 34

1. Injections of algesic chemicals were made into the arterial circulation of the triceps surae muscles in anaesthetized monkeys. 2. The responses of a sample of primary muscle afferents suggest that what is known about the activation of muscle afferents in the cat by algesic agents applies also to the monkey. One exception to this is the activation of many group I afferents by KCl in the monkey, but not in the cat. 3. Many spinothalamic tract cells were powerfully excited by the intra-arterial injection of algesic chemicals (bradykinin, 5-hydroxytryptamine (5-HT), KCl) in preparations in which the hind limb was denervated except for the nerves to the triceps surae muscles. The excitatory action of bradykinin had a slower time course than did that of 5-HT or KCl. 4. A number of the spinothalamic tract cells which failed to respond to chemical activation of muscle afferents were located in lamina I of the spinal cord. 5. Repeated injections of bradykinin produced similar responses, whereas the effects of 5-HT injections showed marked tachyphylaxis. 6. No evidence was obtained that activation of muscle spindle afferents by succinylcholine injections resulted in the excitation of spinothalamic tract neurones in the population sampled. 7. Injections of hypertonic NaCl into muscle or tendon produced a prolonged excitation of many spinothalamic tract cells. 8. It is concluded that a substantial proportion of primate spinothalamic tract cells receive a convergent input from cutaneous and muscle receptors. The muscle receptors involved appear to include primary afferents of group III and IV calibre. The possibility is suggested that such cells could play a role in the production of poorly localized pain.
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PMID:Effects of mechanical and chemical stimulation of fine muscle afferents upon primate spinothalamic tract cells. 10 91

In chemical terms the mediators of inflammation can be divided in amines (histamine, serotonine), peptides (ECF-A, bradykinin), proteins (lysosomal enzymes), and lipids. They mainly act at three levels: 1.) They induce vascular reactions and are responsible for the classical symptoms of inflammation, 2.) they define and modulate the cellular response towards the inflammatory stimulus such as the morphology of the tissue infiltrate, 3.) they act on haemostasis by interaction with platelets. While in the past investigations on classical mediators have dominated research, recently the biological role of lipid mediators has been appreciated. They can be detected only in minute quantities; they often have a short half-life and are not preformed within the cells. The most common precursor of the lipid mediators is arachidonic acid. This unsaturated fatty acid is generated from phospholipids after phospholipase activation of cells and is transformed by the enzyme cycloxygenase to a series of compounds such as the prostaglandins. They induce the classical signs of inflammation such asvescular dilatation, increase in permeability, pain, hyperalgesia etc. By the same process, the thromboxanes and prostacycline are generated which mainly act on the coagulation system. Various products are obtained from arachidonic acid via lipoxygenase activation. To these belong a factor chemically not completely defined with classical SRS-A activity; there is strong evidence that PAF and ECF are formed on the same line. Experiments in recent years have supported the idea that neutrophils and mononuclear cells are by far the main producers of lipid mediators, thus indicating the cellular interdependence during the inflammatory process.
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PMID:[Origin and biological role of lipid mediators during inflammation (author's transl)]. 12 Mar 7

1. In order to determine the nervous outflow from skeletal muscle during chemically induced muscle pain, the impulse activity of various types of muscle afferents in response to close intra-arterial injections of pain-producing substances (bradykinin, 5-hydroxytryptamine, histamine and potassium) was studied in anaesthetized cats using a single fibre recording technique.2. By administration of algesic agents in doses which produce pain in man and pain reactions in animals, about half of the group IV and two thirds of the group III muscle afferents could be activated. In contrast, group II and group I afferent units were usually not excited by chemical noxious stimulation. If effects at all occurred in the thick myelinated afferents, they consisted of a depression of the fibre activity rather than of an activation.3. The qualitative features of the discharges of group III muscle afferents induced by chemical stimulation resembled those of the group IV units very closely. The group III units differed from the group IV afferents in that their responses to a given dose of bradykinin were of greater magnitude.4. It is concluded that the chemically induced muscle pain is probably mediated by certain portions of the group IV and group III afferents, whereas the reactions of group II and group I units to algesic agents are such that a contribution to muscular chemo-nociception seems improbable.
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PMID:Nervous outflow from skeletal muscle following chemical noxious stimulation. 14 96

An anti-inflammatory factor (AIF) was highly purified from normal bovine serum. The purified AIF was a polysaccharide which was formed from a low molecular substance Pro-AIF by macromolecularization. AIF showed potent inhibitory activities against carrageenin induced edema in rats and PMN-leucocyte chemotaxis. It showed no inhibition in cutaneous reaction with serotonin, bradykinin or a mediator releaser compound 48/80. No inhibition was also observed in thermally induced pain, reversed passive Arthus reaction and adjuvant polyarthritis in rats. With these results, the role of AIF in inflammation was discussed.
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PMID:Purification and characterization of an anti-inflammatory factor (AIF) from bovine serum. 15 Jul 78

The purpose of this study was to define, in hyperventilated and unanesthetized cats, the role of the posterior thalamic nuclei in pain mechanisms. Unit activities of these structures were compared to those of the ventro-posterior nucleus during non-noxious (touch, brushing) and noxious stimulations (pinches and intra-arterial injections of bradykinin into the limbs). 135 cells with somatic inputs and clear peripheral excitatory receptive field were studied. The cells driven by noxious stimulations were located in the posterior group nuclei as anatomically defined by Rinvik. These units, preferentially excited from contralateral receptive fields, were localized in POm, POl, suprageniculate nuclei, the magnocellular division of the medial geniculate body (Mgmc) and the ventral part of the lateral posterior nucleus. At this level two groups of units were found: those driven only by noxious stimulations and those driven by both noxious and non-noxious stimulations. On contrast, cells recorded at the levels of the VPm and VPl were not activated by noxious stimuli. These results emphasize the role of the posterior thalamic nuclei in pain processing.
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PMID:Single units activities in ventral posterior and posterior group thalamic nuclei during nociceptive and non nociceptive stimulations in the cat. 19 52

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

1. Bradykinin (0.02-5 microgram) applied to the epicardium of the left ventricle in the open-chest, anaesthetized dog, elicits dose-related reflex pressor effects and acceleration of the heart rate. 2. Bradykinin-induced reflex tachycardia was suppressed after the blockade of beta-adrenoceptors with propranolol, whereas reflex pressor responses were prevented by blocking the alpha-adrenoceptor sites with phenoxybenzamine. 3. Vagotomy and atropine treatment did not affect reflex hypertension and tachycardia to epicardial bradykinin. 4. After spinal section at C1, the pressor responses to epicardial bradykinin were significantly reduced, but still present in all but one experiment. A small acceleration of the heart occurred in two out of five spinal dogs with intact vagi and was absent in three vagotomized spinal dogs. 5. The results indicate the reflex activation of the sympathetic outflow to the heart and blood vessels, mediated mainly at a supraspinal level as a predominant mechanism for the cardiovascular response initiated by bradykinin-induced stimulation of cardiac pain receptors.
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PMID:Sympathetic cardiovascular reflex initiated by bradykinin-induced stimulation of cardiac pain receptors in the dog. 26 62

A rat uterine smooth muscle contracting substance was released into the superfusate of the dog's exposed canine pulp after noxious stimulation of the pulp by pricking, heat and electrical stimulation. This active substance was acid- and heat-resistant and was decomposed by carboxypeptidase B and alpha-chymotrypsin, but not by carboxypeptidase A and trypsin. This substance was also tested on several types of smooth muscle. Electrical activity of nerve cells in the reticular formation, which were sensitive to stimulation of the instep of the foot by pinching, was activated by the intrafemoral administration of the active substance. The algesic activity of this substance was examined in cantharidin blister base in man. This study conclusively demonstrated that the active substance of the pulp released by noxious stimulation produced pain and it was identified as bradykinin.
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PMID:Bradykinin as an algesic (pain producing) substance in the pulp. 42 98


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