Gene/Protein Disease Symptom Drug Enzyme Compound
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Query: UMLS:C0344307 (analgesia)
 28,200 document(s) hit in 31,850,051 MEDLINE articles (0.00 seconds)

Tilest 500 contains tiletamine and the water-soluble benzodiazepine zolazepam in the ratio 1:1. The drug was administered intramuscularly in ten dogs at a dosage of 10 mg/kg bwt of tiletamine and 10 mg/kg bwt of zolazepam and tested for its effects on hemodynamics, respiration, and the antagonistic effect of flumazenil. Initial effects occurred quickly, analgesia and muscle relaxation were excellent 10 minutes after administration. There was a highly significant increase in heart rate and a slight decrease in both mean arterial blood pressure and arterial pO2. In a second group of ten dogs the interventricular paraconal branch of the left coronary artery was ligated which induced local myocardial ischemia. Here Tilest 500 showed electrostabilizing and antifibrillatory properties even in the presence of severe arrhythmias. The benzodiazepine compound of this drug combination can be antagonized by flumazenil. To avoid excitatory reactions flumazenil should not be injected earlier than 45 to 60 minutes after administration of Tilest 500.
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PMID:[Anesthesia in dogs with the combination preparation Tilest 500]. 204 1

The potential antinociceptive effects of the selective cholecystokinin-B (CCK-B) antagonist L-365,260 were examined in the squirrel monkey tail withdrawal test. Pain threshold was measured in 6 male monkeys by recording the latency to remove the tail from a warm (55 degrees C) water bath. L-365,260 at doses of 100 ng/kg to 100 micrograms/kg significantly elevated tail withdrawal latencies throughout a 2 h test period. These data provide the first evidence that blockade of CCK-B receptors induces analgesia in primates.
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PMID:Blockade of CCK-B receptors by L-365,260 induces analgesia in the squirrel monkey. 207 89

Two experiments were made showing that opioid involvement coincides with the magnitude of stress-induced analgesia. In Experiment I rats subjected to cold water swims were screened for jump threshold levels on electrified grid and divided into high, medium and low threshold responders' groups. Later on the three groups were given 90 s forepaw footshock. Tail-flick latencies rose highest in the high threshold, and lowest in the low threshold responders. This decrease in nociception was counteracted by naloxone more effectively in high than in medium threshold responders, and not all in low threshold responders. In Experiment II mice selectively bred for high (HA) and low (LA) post-stress analgesia swam at 20 and 2 degrees C. Both stressors were followed by an increase in tail-flick latencies in the order of magnitude HA greater than unselected controls greater than LA line. Naloxone attenuated analgesia after both stressors in the HA line, but was ineffective in LA mice. In unselected controls swimming at 20 degrees C caused naloxone-sensitive, and cold water swims naloxone-resistant analgesia. It is concluded that apart from the kind of stressor, inborn properties of an individual are essential for the development of opioid vs. non-opioid form of post-stress analgesia.
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PMID:Correlation between magnitude and opioid mediation of stress-induced analgesia: individual differences and the effect of selective breeding. 213 37

It is now well established that compounds classified as kappa opioids can, in circumstances where they produce no measurable agonist effects, antagonize the actions of mu opioids. Largely on the basis of studies in vitro, beta-funaltrexamine (beta-FNA) has been classified as a reversible kappa agonist and long acting mu antagonist. The present study investigated the possibility that the mu antagonist profile of this compound could be related to its kappa agonist actions. We used two tests of analgesia (the acetic acid writhing test and the hot-water tail-flick test) and selective kappa agonists and antagonists given at supraspinal and spinal sites in mice. Intrathecal (i.t.) administration of beta-FNA, but not the selective kappa agonist U50,488H, produced long-lasting and dose-related analgesia in the writhing test for periods up to 48 hr after a single dose. In contrast, i.t. beta-FNA had no agonist actions in the tail-flick test. The kappa antagonist, nor-binaltorphimine (nor-BNI) produced no agonist effects in either analgesic test when given i.t. In the writhing test, nor-BNI produced a rightward displacement of the beta-FNA dose-response line regardless of whether beta-FNA was given 10 min or 4 hr before testing, indicating that i.t. beta-FNA was acting as a kappa agonist in this test. As both i.t. morphine and beta-FNA are active in the writhing test, the antagonist actions of i.t. beta-FNA could be evaluated only in the tail-flick test. beta-FNA, but not nor-BNI, blocked the effects of i.t. morphine in the tail-flick test.(ABSTRACT TRUNCATED AT 250 WORDS)
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PMID:Mu antagonist and kappa agonist properties of beta-funaltrexamine (beta-FNA) in vivo: long-lasting spinal analgesia in mice. 215 86

Early in life, Walker Hound pups from several litters, later determined to have peroneal and tibial neuropathy, had been given supplements of either evaporated milk and corn syrup mixed with well water or powdered bitch milk formula mixed with well water. Other pups not given supplements were not affected. Pelvic limb monoparesis, areflexia, analgesia, and muscular atrophy developed by 2 weeks of age. Abnormalities detected by light and electron microscopy included scattered swollen axons containing increased organelles and whorled neurofilaments. The clear association between clinical signs of disease and dietary supplementation of pups among healthy dogs in a kennel, as well as lack of an obvious pattern of inheritance, suggested an environmentally acquired toxin, specifically the well water. Attempts to reproduce neuropathy in a litter of Beagle pups 2 years after initial evaluation of the disease syndrome were unsuccessful. Atomic absorption studies performed on the well water to detect heavy metals did not reveal toxic concentrations. Toxins that may have been responsible for the neuropathy in these pups were not identified.
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PMID:An epizootic of peroneal and tibial neuropathy in Walker Hound pups. 217 Mar 12

The critical care patient population has much to gain from properly administered neural blockade. Effective analgesia alone may make the difference between a patient who is able to compensate for their acute insult and one who cannot. A good example is the patient with multiple fractured ribs, who, after intercostal nerve blocks, no longer requires intubation and mechanical ventilation. The authors believe that effective analgesia is just the beginning of the beneficial effects of neural blockade, because blockade of the afferent limb of sympathetic and sensory nerves may circumvent the neuroendocrine response to acute injury. There is evidence that the stress response is not beneficial in the hospital setting and in fact may be detrimental. Some of the effects include elevated plasma catecholamines, ADH, cortisol, and blood glucose, which contribute to tachycardia, hypertension, increased myocardial work and oxygen consumption, salt and water retention, and a catabolic state with negative nitrogen balance. Whether these changes result in reduced morbidity and mortality has been the subject of several studies, but more studies are needed. It would seem that critically ill patients with little physiologic reserve might be the best population to study because even a small improvement may improve survival. A small beneficial effect in healthy postoperative patients may not be clinically apparent. Most would agree that neural blockade used intraoperatively results in reduced blood loss and a lower incidence of postoperative thromboembolism. The continuation of these techniques into the postoperative period may reduce morbidity and mortality in high-risk patients. A word of caution is in order. The indiscriminate application of the techniques described in this article to critically ill patients would not be in the patients' best interest. Nerve blocks are only safe in the hands of those physicians specifically trained to perform them. In addition, local anesthetics have a low therapeutic ratio, and their administration requires continual observation. The use of epidural or intrathecal opioids alone or in combination with other agents also has potentially serious side effects, and requires continual patient monitoring. The proper performance and maintenance of these techniques requires a large commitment of time, manpower, equipment, and a multidisciplinary approach to include physicians, nursing, and support staff. Nerve blocks and other sophisticated techniques started in the operating room or critical care unit should not necessarily be discontinued when the patient is transferred to a ward bed because the full benefit of this therapy may not have been fully realized.(ABSTRACT TRUNCATED AT 400 WORDS)
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PMID:Nerve blocks in the critical care environment. 218 9

The author points out that when midwives inject sterile water in the lumbar region as a form of analgesia during the first stage of labour, this may prolong delivery. The author has found no documentation to support this method. The labour lasts almost two hours longer in women receiving such injections. There is no adverse effect on Apgar score after one minute. More investigation is necessary in order to examine the effectiveness and/or adverse effects of method.
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PMID:[Intracutaneous injections of sterile water as analgesia during labor]. 221 88

We exposed 24 subjects high in hypnotic susceptibility and 24 subjects low in hypnotic susceptibility to a cold-pressor pain stimulus under either hypnotic or waking conditions, using each of two pain-reduction strategies (analgesia and distraction) separately. Trance depth level was held constant for hypnotized subjects. We used pain-tolerance levels as measures of pain, and we analyzed them by survival analysis. High susceptibles reported significantly lower pain ratings and kept their hands immersed longer in the cold water than low-susceptible subjects. There were no significant differences between hypnotic and waking condition subjects or between the different strategies. We have discussed the results in terms of a relationship in the literature between choice of experimental design (between-subjects or within-subjects) and the effectiveness of a hypnotic induction for suggested pain reduction.
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PMID:Hypnotic susceptibility and experimental pain reduction. 222 Jun 55

The competitive excitatory amino acid antagonist cis-4-phosphonomethyl-2-piperidine-carboxylic acid (CGS 19755) increased the latency for monkeys to remove their tails from warm water (analgesia); larger doses produced ataxia, loss of righting, salivation, and eliminated reactivity to stimulation (anesthesia). CGS 19755 decreased tidal volume and had little effect on frequency of respiration. Although longer lasting, the effects of CGS 19755 were similar to the effects of ketamine, suggesting these effects result from actions at the NMDA receptor complex.
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PMID:Analgesic, anesthetic, and respiratory effects of the competitive N-methyl-D-aspartate (NMDA) antagonist CGS 19755 in rhesus monkeys. 225 91

The effects of the cholecystokinin antagonist devazepide on analgesia and respiratory depression induced by morphine in squirrel monkeys were examined. Pain thresholds were determined using the tail withdrawal procedure, in which monkeys restrained in chairs kept their tails in cool (35 degrees C) water for at least 20 sec, but withdrew them from warm (55 degrees C) water in less than 4 sec. Morphine produced a dose-related increase in tail withdrawal latencies from warm water. Devazepide (injected i.p. or p.o.) had no effect on tail withdrawal latencies when given alone but enhanced the analgesic effects of morphine. The devazepide dose-response curve for morphine enhancement was bell-shaped with doses of 3, 10, 30 and 100 micrograms/kg injected i.p. increasing morphine analgesia whereas higher and lower dose did not. In a separate group of monkeys, morphine produced dose-dependent decreases in respiratory rate and oxygen tension and increases in carbon dioxide tension. In contrast to its effects on morphine analgesia, devazepide had no effect on the various indices of morphine-induced respiratory depression. These data suggest that devazepide may have therapeutic utility as an adjuvant to morphine analgesia allowing lower dose of the opiate to be used to relieve pain and reducing the risk of opiate-induced respiratory depression.
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PMID:The cholecystokinin receptor antagonist devazepide enhances morphine-induced analgesia but not morphine-induced respiratory depression in the squirrel monkey. 226 99


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