Low back pain. Pain clinics have an important role.
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Humans↗
Biomedical subjects
K Budd
Publications and source records attributed to K Budd.
Chronic pain--challenge and response.
Tramadol is effective in treating both acute and chronic pain, exhibiting a potency equivalent to that of pethidine, and it has an acceptable adverse event profile. Whilst the most common adverse events are nausea, vomiting, drowsiness and dizziness, as would be expected from an opioid, there is a noticeable lack of respiratory depression. This latter property, together with its low potential for the development of tolerance and dependence, make tramadol a most interesting agent for clinical use. The studies reported in this article illustrate the beneficial and adverse effects of tramadol to enable the clinician to judge the value of this agent.
Chronic Disease↗
Recent advances in the treatment of chronic pain.
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Analgesics↗
Drug management of chronic benign pain.
Chronic benign pain usually requires treatment with drugs. Three main classes of drugs are used: opiates, non-steroidal anti-inflammatory drugs, and a miscellaneous group which includes psychoactive drugs and a variety of specific agents for individual conditions. The careful selection and combination of drugs, with adequate and appropriate dosage, will bring pain relief in the majority of patients.
Anti-Inflammatory Agents, Non-Steroidal↗
The use of the opiate antagonist, naloxone, in the treatment of intractable pain.
Thirteen adult patients with established thalamic syndrome, resistant to prior analgesic and other therapy, were treated with intravenous infusions of the opiate antagonist, naloxone. A total of twenty treatments were administered with doses of naloxone varying from 4.0-8.0 mgs. Seven patients exhibited beneficial effects with the duration of the resultant pain relief ranging from four days to two and a half years. In these patients, pain and hyperpathia were completely obtunded in six out of seven and partially in one. Side effects of therapy were minimal and of short duration being mainly confined to the cardiovascular system. During therapy all patients had continuous E.C.G. monitoring. In certain ischaemic conditions of the central nervous system, endogenous opioids possibly reduce cerebral blood flow via. inhibition of the locus coeruleus and subsequent release of noradrenaline: hence naloxone by inhibiting the opioids could increase cerebral perfusion pressure. This study has shown the benefit of treating patients with cerebral ischaemic lesions with an opioid antagonist. The rapidity of onset of pain relief in these patients would appear to indicate a mode of action by increasing cerebral perfusion.
Aged↗
The treatment of chronic pain by the use of meptazinol administered into the epidural space.
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Adult↗
High dose buprenorphine for postoperative analgesia.
Buprenorphine was given intravenously to produce analgesia in the immediate postoperative period, the dose being titrated against the response of each patient in order to obtain complete freedom from pain. In 50 patients following lower segment Caesarean section under general anaesthesia, buprenorphine in the dose range 0.4-7.0 mg was found to be a potent, long lasting and safe analgesic. Serial blood gas estimations performed on ten of the patients confirmed the clinically observed lack of respiratory depression.
Adult↗
Inducible plasmid-determined resistance to arsenate, arsenite, and antimony (III) in escherichia coli and Staphylococcus aureus.
Plasmids in both Escherichia coli and Staphylococcus aureus contain an "operon" that confers resistance to arsenate, arsenite, and antimony(III) salts. The systems were always inducible. All three salts, arsenate, arsenite, and antimony(III), were inducers. Mutants and a cloned deoxyribonucleic acid fragment from plasmid pI258 in S. aureus have lost arsenate resistance but retained resistances to arsenite and antimony, demonstrating that separate genes are involved. Arsenate-resistant arsenite-sensitive S. aureus plasmid mutants were also isolated. In E. coli, plasmid-determined arsenate resistance and reduced uptake were additive to that found with chromosomal arsenate resistance mutants. Arsenate resistance was due to reduced uptake of arsenate by the induced plasmid-containing cells. Under conditions of high arsenate, when some uptake could be demonstrated with the induced resistant cells, the arsenate was rapidly lost by the cells in the absence of extracellular phosphate. Sensitive cells retained arsenate under these conditions. When phosphate was added, phosphate-arsenate exchange occurred. High phosphate in the growth medium protected cells from arsenate, but not from arsenite or antimony(III) toxicity. We do not know the mechanisms of arsenite or antimony resistance. However, arsenite was not oxidized to less toxic arsenate. Since cell-free medium "conditioned" by prior growth to induced resistant cells with toxic levels of arsenite or antimony(III) retained the ability to inhibit the growth of sensitive cells, the mechanism of arsenite and antimony resistance does not involve conversion of AsO2- or SbO+ to less toxic forms or binding by soluble thiols excreted by resistant cells.
Antimony↗
Psychotropic drugs in the treatment of chronic pain.
The psychotropic drugs in the treatment of chronic pain have value in several areas. They not only influence the mood of the patient but also provide hypnosis, augment the activity of the analgesics and exhibit analgesic potency in their own right. They may be used alone, or in combination with analgesic agents or with each other. The three most valuable groups are the antidepressants, tranquillizers and anticonvulsants, all of which exert their effect by influencing the intracerebral levels of various neurotransmitter amines.
Anticonvulsants↗
Psychologic and social implications of scientific care for pregnant diabetic women.
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Diabetes Mellitus↗
Influence of exogenous sugars and polyols on C1-influx and efflux by the ascomycete Neocosmospora vasinfecta.
Glucose and other transportable sugars and polyols inhibited Cl- influx very soon after addition to mycelium in the process of Cl- accumulation. Under the usual experimental conditions (0.1 mM KCl, glucose greater than or equal to 2 mM) the mean percentage of inhibition of Cl- influx by glucose was 54.1 +/- 8.0 (+/- standard error; N = 26). Transport of the exogenous carbohydrate was necessary for inhibition of Cl- influx. Thus, the estimated Ki for glucose inhibition of Cl- influx (28 muM) was close to the Km for glucose transport; glycerol did not inhibit Cl- influx unless it was itself transported, and the degree of inhibition exerted by various carbohydrates correlated with their uptake rates. Inhibition was not caused by the accumulated sugar itself, as high levels (ca. 60 mM) of intramycelial 3-O-methylglucose gave rise to a stimulation of Cl- influx when the exogenous sugar was removed. It is suggested that interaction of Cl- and carbohydrate transport arises from competition for a common energy-coupling mechanism in the cell membrane. Both glucose and 3-O-methylglucose elicited Cl- efflux, but the maximal Cl- efflux rates were observed only after 40 min of incubation and only in the presence of the readily metabolizable glucose. Removal of the exogenous glucose, even after maximal Cl- efflux had been established, resulted in the rapid cessation of efflux. Studies under anaerobic conditions gave further evidence that glucose uptake was necessary and that efflux was not due to temporary depletion of energy reserves. It is proposed that glucose-induced leakage of Cl- is due to reversal of the Cl- uptake system, even though the Km for efflux is much greater than that for influx.
Alcohols↗
Evidence for a negative membrane potential and for movement of C1- against its electrochemical gradient in the ascomycete Neocosmospora vasinfecta.
The iodides of three lipid-soluble cations (dibenzyldimethylammonium; tribenzylmethylammonium, TBMA+; ethyldimethylbenzylammonium) were synthesized by the reaction of 14C-labeled methyl or 14C-labeled ethyl iodide with the appropriate secondary of tertiary amine and used in an attempt to measure the transmembrane electrical potential difference in Neocosmospora. Only mycelium containing high levels of Na+ accumulated measureable amounts of these cations and only above pH 6. Uptake was reduced in the presence of exogenous K+, Na+, Mg2+, or tris(hydroxymethyl)aminomethane. The velocity of TBMA+ uptake was proportional to its concentration between 46 and 427 muM. Neither the rate nor the extent of TBMB+ uptake was greatly affected by the presence of a fivefold excess of either dibenzyldimethylammonium or ethyldimethylbenzylammonium, even though these cations were themselves accumulated. The uncoupler m-chlorophenylhydrazone induced loss of previously accumulated TBMA+ from the mycelium. Anaerobiosis and cold (5 degrees C) temperature both inhibited TBMA+ uptake but did not induce the loss of previously accumulated TBMA+. The uptake of lipophilic cations by Na+-rich mycelium indicated a minimum transmembrane electrical potential of -60 to -70 mV (inside negative). Net uptake of these cations appeared to be strongly influenced by the availability of endogenous exchangeable cations and by the presence of other exogenous cations, as well as by the membrane potential. Despite these limitations, transport of C1- by Na+-rich mycelium appeared to take place against the electrochemical gradient for C1-.
Anaerobiosis↗
Meptazinol--a new analgesic effects on hemodynamic stability.
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Analgesics↗
Potassium fluxes in Neocosmospora vasinfecta.
The unidirectional K+ fluxes across the mycelial surface of Neocosmospora vasinfecta were determined using 42K. Influx was mediated by at least two kinetically distinct systems, one having an apparent Km of 6-5 mu-equiv. K+/l and the other of about 1-0 m-equiv. K+/l. The VMAX for both systems was in the range 18 to 22 mu-equiv. K+/100 mg mycelial dry matter/h (1-0 to 1-2 m-equiv. K+/l cell-water/min). Influx was strongly inhibited by 2,4-dinitrophenol, sodium azide, sodium arsenate and anaerobiosis. K+ efflux was dependent on the external K+ concentration and ranged from 3 to 10% of mycelial K+/h. The maximum efflux rate was always considerably less than the initial influx rate for the K+ concentrations examined. During incubation in dilute KCl solutions, K+ influx decreased to a value approaching the K+ efflux rate. It is considered that equilibrium with external K+ is attained primarily by the regulation of K+ influx, and that this may be the principal mechanism controlling cytoplasmic K+ levels. Adsorption of K+ was also observed throughout the K+ concentration range examined and can be attributed to two distinct K+-binding entities at the mycelial surface, half-saturating at approximately O-I mM-and 4-4 mM-KCl respectively.
Adsorption↗
Halide uptake by the filamentous ascomycete Neocosmospora vasinfecta.
The uptake of Cl minus by the ascomycetes Neocosmospora vasinfecta was investigated. Intramycelial concentrations of more than 55 mM (890-fold the external concentration) were reached. Accumulation was as inorganic Cl minus and nystatin induced total loss of mycelial Cl minus without extensive protein loss, implying that Cl minus retention was not due to binding to macromolecules. Cl minus transport was largely unidirectional with efflux being low under all conditions. Uptake was temperature dependent (maximal Arrhenius activation energy of 18.0 kcal/mol) and was severely reduced by KCN, dicyclohexylcarbodiimide, and anaerobiosis. A comparison with the inhibition of oxygen uptake under the same conditions implied that Cl minus transport was not directly coupled to aerobic electron transport. Cl minus uptake was a saturatable function of the external Cl minus concentration, and apparent Km values of 6.4 times 10-6 M and 10-4 M were calculated. Of the anions tested, only Br minus effectively inhibited Cl minus uptake and I minus, NO3 minus, SO4 minus 2, HCO3 minus, and H2PO4 minus were without effect. Cl minus uptake did not require concomitant cation uptake.
Anaerobiosis↗