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)

The hot plate method was used to assess tolerance in rats following daily injections of morphine. Following analgesia assessment, or a time equated rest period, rats were injected with either saline or a pituitary peptide. Arginine vasopressin, but not ACTH 4-10, prolonged the retention of morphine tolerance when assessed five weeks after the last injection. Neither the rate nor the degree of tolerance development were influenced by either peptide. These hormones had no effect on retention of tolerance development were influenced by either peptide. These hormones had no effect on retention of tolerance in rats not assessed for analgesia during the period of tolerance development. The effects of pituitary peptides on morphine tolerance are analogous to the effects they have on learning and memory processes, suggesting that similar adaptational processes are occurring in both phenomena.
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PMID:Arginine vasopressin enhances retention of morphine tolerance. 631 68

15 patients (12 women and 3 men) undergoing cholecystectomy were randomized into two groups. 8 patients were operated on under continuous thoracic epidural anaesthesia in combination with light general anaesthesia. Postoperatively they were kept painfree by continuous infusion of an 0.125% solution of bupivacaine via epidural catheter at a rate of 0.25-0.3 ml/kg X h over a period of four days. The 7 patients in the control group were operated on under neuroleptanalgesia. Piritramide was given for postoperative analgesia. All patients received 40 ml/kg X day of electrolyte solution during the period of investigation. Blood was collected at 8 am, 12 am, 4 pm, 8 pm, and 12 pm on the day of operation and on the third postoperative day, at 8 am on the first and second postoperative day, and at 8 am, 12 am, and 4 pm on the fourth postoperative day. Plasma glucose, ACTH, cortisol, T4, T3, and reverse T3 were measured. During the operation and for 12 h thereafter a mild hyperglycaemia was observed in the neuroleptanalgesia group but not in the epidural group. The differences were significant. A rise in ACTH was seen in both groups during and shortly after operation. The increase in cortisol concentration following this ACTH release was significant only in the neuroleptanalgesia, but not in the epidural group. From the first to the fourth postoperative day ACTH levels were low and cortisol concentrations within the normal range. On the third day it appeared that a diurnal variation in cortisol levels was again present. Cortisol suppression following the administration of 2 mg dexamethasone on the fourth postoperative day was detectable in both groups. Of the thyroid hormones, T4 remained unchanged and at a normal level during the investigation. T3 decreased and reverse T3 increased significantly, the maximum rise being observed on the second day. There were no differences between the groups. These changes are defined as low T3 syndrome, following caloric deprivation, injury, and stress. The metabolic and hormonal alterations caused by cholecystectomy are marked only during operation and shortly thereafter and only in this period are they influenced by epidural analgesia. From the first postoperative day onwards they are almost negligible so that a mitigation by using continuous epidural analgesia is not to be expected.
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PMID:[Blood glucose, ACTH, cortisol, T4, T3 and rT3 after cholecystectomy. Comparative studies of continuous peridural anesthesia and neuroleptanalgesia]. 632 95

Analgesia induced in rats by cold-water swim stress and measured by the tail-flick and hot-plate methods was significantly antagonized after IP pretreatment for 3 days with 8 mg/kg dexamethasone. The analgesia developed by the cold-water swim stressor was also attenuated by 1 mg/kg naloxone. These results suggest that the corticosteroids may have a role in modulating stress-induced analgesia and that the adrenal-pituitary axis modulates the endogenous opiate system. These conclusions are based on recent reports that indicate the release of the opiate-like peptide beta-endorphin and adrenocorticotropin (ACTH) from the pituitary are increased by acute stress and inhibited by administration of the synthetic glucocorticoid dexamethasone.
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PMID:Dexamethasone and stress-induced analgesia. 640 29

The nucleus reticularis gigantocellularis (NRGC), including the nucleus reticularis paragigantocellularis (NRPG), of male Sprague Dawley rats was destructed bilaterally by DC 0.5 mA for 40 sec (D-rats). Morphine analgesia estimated by the tail pinch method in 4 and 10 days morphine treated sham operated rats (S-rats), of which the test doses were 40 and 80 mg/kg, respectively, was equal to or smaller than the analgesia by 5 mg/kg in non-treated S-rats. Morphine analgesia at 5 mg/kg in non-treated D-rats was weaker than that in S-rats. Morphine analgesia in 4 and 10 days morphine treated D-rats, of which the test doses were 40 and 80 mg/kg, respectively, was stronger than the analgesia by 5 mg/kg but weaker than that by 20 mg/kg in non-treated D-rats. These results indicate development of morphine tolerance in S- and D-rats. Reverse of diurnal variation in body weight and disappearance of diurnal variation in body temperature and in plasma corticosterone concentration (Pcs) were observed similarly in S- and D-rats during morphine treatment. Body weight loss, increase in Pcs and plasma ACTH concentration, and increase in adrenal weight were elicited by morphine withdrawal in both morphine treated S- and D-rats. These signs during morphine treatment and after morphine abstinence indicate the development of morphine dependence in D-rats. These results suggest that the NRGC participates in development of morphine analgesia, but does not participate in development of morphine tolerance and dependence.
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PMID:[Morphine tolerance and dependence liability in NRGC-destructed rats]. 654 Feb 24

125 rats which were divided into five groups were deprived of food or given orally D- (a potent inhibitor for L-asparaginase) and/or L-aspartic acids (Asp) for one week. The body weights before and at the end of the experiment were determined as well as post mortem the weights of brain, liver and kidneys, their protein contents, and the liver triglyceride and glycogen contents. D- and D+L-Asp caused significant decreases in the weights of body and liver, and in daily fluid intake; in addition liver and kidney protein, and liver triglyceride and glycogen contents were found to be lower than control. On the other hand, the food-deprived group which was subjected to more or less the same body weight loss due to food deprivation showed only a decrease in the liver triglyceride content. Since D-amino acids cause naloxone reversible analgesia which is, thus, considered as an involvement of endorphinergic system and of vasopressin, the effects of D-Asp were attributed to the changes in the availability of opioids and vasopressin, which simultaneously have an effect on each other as well as an effect of the release of ACTH. L-Asp appeared to antagonize the effects of D-Asp. Because L-Asp antagonizes the acute and chronic effects of morphine, including that on L-asparaginase activity, the hypothesis is proposed that the antagonizing effects of L-Asp observed may be caused at the level of L-asparaginase activity.
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PMID:The effects of D- and/or L-aspartic acids on the total weight of body, the weights of certain organs, and their protein, triglyceride and glycogen content. 688 74

We have seen that exposure of an organism to any of a wide range of stressful situations can induce alterations in sensitivity to pain that outlast the exposure. Not all stressors induce analgesia; among those that do not are some that produce maximal elevations in plasma beta-endorphin, ACTH, and adrenal corticosteroids. Some examples of SIA are sensitive to opiate receptor blockade by naloxone, but others are not. Hypophysectomy produces a similarly uneven profile of effects across different stressors. This diversity has often been interpreted as evidence for the existence of an array of pain inhibitory systems, with differing physiological properties and activated by different stressors. However, it might also suggest that stressors can prompt a variety of behavioral changes, many of which can be interpreted as analgesia if a pain reflex test is employed as the dependent measure.
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PMID:The role of endorphins in stress-induced analgesia. 696 59

In a completely crossed, double blind designed study, six rats received intraventricular injections of 0.1, 1.0 and 10 micrograms of alpha-MSH and a placebo. The rats were tested for response to painful thermal stimuli with the tail-flick test. All of the doses of alpha-MSH produced hyperalgesia during the first 20 min of testing. Only the 1.0 microgram dose of alpha-MSH produced hyperalgesia throughout the 80 min course of the experiment. This study, coupled with previous reports that MSH/ACTH fragments may attenuate morphine-induced analgesia, suggest that MSH can have opposite actions from those of the endorphins. It is possible that alpha-MSH and related peptides may be endogenous anti-opiates.
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PMID:Intraventricular administration of MSH induces hyperalgesia in rats. 729 Oct 44

Early evidence has indicated the presence and involvement of specific neural systems which can inhibit the responses to painful stimuli. More recently, further advances suggest that the opiate system may interact with other systems to modulate the analgesia produced by the opiates or various stressors. Since corticosteroids were found to be elevated under the conditions of different stress-induced analgesia (SIA), there may be interactions between the pain-inhibiting systems and the corticosteroids. Recently it was reported that acute stress or long-term adrenalectomy can result in release of beta-endorphin (beta E) and ACTH from the pituitary gland, which can be blocked by dexamethasone. In our early studies we have shown partial antagonism of the SIA by dexamethasone and complete antagonism after naloxone. In this report it was found that chronic treatment of the rats with 0.02% metyrapone in drinking water for 8 weeks resulted in minor hyperalgesia. The chronic pretreatment with metyrapone resulted in a significant potentiation of the analgesia induced via the cold swim stress model, which was reversed by 1 mg/kg (IP) naloxone. Also, hyperalgesia was noted 18 days after the bilateral adrenalectomy of the rats as measured in our laboratory by the hot plate method and as reported by Heybach and Vernikos-Danellis in 1978. These results suggest that the corticosteroid modulation (pituitary-adrenal axis) may have a role in regulating the SIA, and this may implicate the interactions of the corticosteroids with pain-inhibiting systems.
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PMID:Corticosteroid modulation and stress-induced analgesia in rats. 730 Oct 53

The abdominal constriction test was used to explore the effects of cold stress (4 degrees C) of varying duration on the antinociceptive effects of morphine in mice. It was found that after 15 min exposure to cold significant endogenous analgesia was observed, together with a significant potentiation of the antinociceptive effects of morphine. However, after more prolonged exposure to 4 degrees C, the endogenous analgesia was no longer seen and, in addition, the antinociceptive effects of morphine diminished progressively, and after 2 h or longer exposure it was significantly less than control values. It was sown that, in the absence of cold stress, pretreatment with corticosterone, dexamethasone or ACTH reduced the potency of morphine in a manner similar to that seen after 4 h cold stress. It was also shown that the potency of morphine in adrenalectomized mice was not affected by 3 h cold stress. It is concluded that adrenal corticoids, released in response to the stressor effect of exposure to cold, are responsible for the antagonism of the antinociceptive action of morphine seen in mice after extended exposure to cold. It is suggested that the initial potentiation of the antinociceptive potency of morphine is due to the release of endogenous opioids. With more prolonged stress, the stores of these substances may become progressively depleted, possibly as a result of raised corticosteroid levels, so that the component of analgesia contributed by them is steadily reduced and ultimately abolished.
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PMID:The possibility that a component of morphine-induced analgesia is contributed indirectly via the release of endogenous opioids. 742 38

Using the behavioral pharmacological approach, we have studied the influence of ACTH on the analgesia mediated by three types of opioid receptors (mu, delta, kappa). The mechanisms by which ACTH antagonizes opioid analgesia were explored at receptor level and post-receptor second messenger level. The expression of Fos protein induced by ACTH was also observed in rat brain. The main results show that ACTH selectively antagonizes spinal opioid analgesia mediated by mu and delta, but not kappa receptors. The proposed mechanisms of the anti-opioid effect of ACTH are that ACTH can modulate opioid-induced decrease of intracellular cAMP content and the suppression of calcium influx. ACTH has been shown to induce Fos protein expression in selected brain areas including the nuclei involved in pain modulation. These brain areas may serve as sites of action for ACTH to exert its anti-opioid effect.
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PMID:[Adrenocorticotropic hormone (ACTH): antagonistic effect on opioid analgesia in central nervous system of the rat and its possible mechanisms of action]. 765 13


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