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Query: UMLS:C0344307 (analgesia)
28,200 document(s) hit in 31,850,051 MEDLINE articles (0.00 seconds)

Sprague-Dawley rats were allowed ad lib access to a 20% sucrose solution in addition to their normal diet to investigate the relationship between the prolonged consumption of a high carbohydrate diet and opioid function as evidenced by opioid dependence and withdrawal. Morphine dependence, assayed by tailflick, was induced, followed by naloxone-precipitated withdrawal, gauged by weight loss. Sucrose-fed animals developed lowered pain thresholds prior to dependence induction relative to those of control animals, but failed to exhibit any differences from controls in the development of dependence. Weight loss during withdrawal was increased by the discontinuation of sustained sucrose-feeding. In addition, the induction of dependence first decreased, then increased the animals' preference for sucrose. It is concluded that changes in opioid function caused by sustained sucrose-feeding are insufficient to affect the development of tolerance to morphine analgesia, but do aggravate the symptoms of precipitated withdrawal when access to sucrose is denied prior to the injection of naloxone.
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PMID:Discontinuation of sustained sucrose-feeding aggravates morphine withdrawal. 235 87

The difficulties of interpretation of blood sugar level changes during the postoperative period in the anaesthetic management of insulinoma are discussed. Several specific means reduced the errors in the assessment of the hyperglycemic rebound which occurred after the removal of the tumour. They consisted of continuous sugar infusion accorded to measured glucose levels, in order to maintain a constant blood sugar value between 50 and 70 mg X 100 ml-1 before removal of the insulinoma. Furthermore, analgesia was provided by high doses fentanyl. Sugar containing solutes were avoided during the procedure. Glucose levels rose slowly after tumour removal and reached 170 mg X 100 ml-1 at 120 min. This rebound was known to be of no help in ascertaining complete resection. Simultaneous determinations of blood glucose and insulin were obtained. The value of portal blood insulin was found to be normal (12.3 mU X l-1) 30 min after insulinoma removal. Turner's index calculated every 30 min decreased simultaneously (143) and reached a normal value at 120 min (39). These results, obtained during the surgical procedure all the more easily because of rapid laboratory procedures, could be better arguments in determining whether tumour removal has been complete.
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PMID:[Anesthesia for surgery of insulinoma]. 303 Jan 63

1. There is evidence that sweet-tasting substances such as sucrose and saccharin can interact with endogenous opioid systems. Further evidence showed that feeding mice different concentrations of sucrose and saccharin alter the latency in the tail-flick test. 2. In the current study, the effects of a 12-day regimen of different sweetening agents [sucrose (32%), saccharin (0.08%) and aspartame (0.16%)] on morphine-induced analgesia with the formalin test were investigated. 3. Male albino mice (20-27 g) were used for the experiments. Animals were given 12 days to adapt to dietary conditions. Animals were first given saline or morphine subcutaneously (1.5, 3.0, 6.0, or 9.0 mg/kg) 30 min before the observation period. The recording of the early phase started immediately and lasted for 10 min. The recording of the late response started 20 min after formalin injection and lasted for 10 min. Statistical analysis was performed by using analysis of variance followed by Newman-Keuls test, and P < or = 0.05 was considered significant. 4. Sucrose and aspartame increased morphine analgesia in the early phase, but saccharin had no effect on the early phase. On the other hand, saccharin and sucrose decreased the effect of morphine in the late phase, but aspartame increased the effect of morphine-induced analgesia. 5. In conclusion, the present data provide further evidence for an important role for dietary variables in determining the effects of exogenous opioids on pain sensitivity.
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PMID:Effects of sweetening agents on morphine-induced analgesia in mice by formalin test. 935 6

An initial analgesia followed by hyperalgesia to phasic noxious stimuli occurs after ingestion of sucrose ad libitum. However, the mechanism underlying hyperalgesia is not known. The present study was designed to explore the role of VMH in the mediation of the hyperalgesic effect of sucrose ingestion. Adult male albino rats received sucrose solution (20% p.o.) in addition to laboratory food pellets and tap water ad libitum. Their behavioural responses to various phasic and tonic noxious stimuli were recorded after 6, 12 and 48 h during pre and post-sucrose fed states in both the control and VMH lesion groups of rats. Sucrose feeding to control rats significantly reduced the tail flick latency (TFL) and threshold of vocalization during stimulus (SV) and after discharge (VA) indicating hyperalgesia, while the threshold of tail flick remained unaffected. The average pain rating during the formalin test (tonic pain) decreased significantly indicating analgesia. VMH lesion decreased the latency (mean +/- SD) for tail flick (11.26 +/- 4.65 from 15.61 +/- 5.12 s), threshold (median) for tail flick (0.04 from 0.08 mA), vocalization during stimulus (0.05 from 0.1 mA) and vocalization after discharge (0.15 from 0.2 mA), while the tonic pain rating increased, thereby suggesting a hyperalgesic state. However, sucrose feeding to lesioned rats neither potentiated nor attenuated their hyperalgesia. The results suggest that sucrose feeding for 6-48 h ad libitum produces hyperalgesia to phasic noxious and analgesia to tonic noxious stimuli, while VMH lesion produces hyperalgesia to both phasic and tonic noxious stimuli. Secondly, sucrose ingestion by VMH lesion rats does not affect their responses to pain, suggesting the possible role of VMH in the mediation of sucrose-fed nociceptive responses.
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PMID:Effect of VMH lesion on sucrose-Fed nociceptive responses. 1108 37

Treatment of pain in newborns is associated with problematic drug side effects. Previous studies demonstrate that an intraoral infusion of sucrose and other sweet components of mother's milk are effective in alleviating pain in infant rats and humans. These findings are of considerable significance, as sweet tastants are used in pain and stress management in a number of clinical procedures performed in human infants. The ability of sweet stimuli to induce analgesia is absent in adult rats, suggesting that this is a developmentally transient phenomenon. However, the age range over which intraoral sucrose is capable of producing analgesia is not known. We investigated the effects of intraoral sucrose (7.5%) on nocifensive withdrawal responses to thermal and mechanical stimuli in naive and inflamed rats at postnatal days (P) P0-21. In some rats, Complete Freund's adjuvant (CFA) was injected in a fore- or hindpaw to produce inflammation. In non-inflamed animals, for noxious thermal stimuli, sucrose-induced analgesia emerged at P3, peaked at P7-10, then progressively declined and was absent at P17. For mechanical forepaw stimuli, sucrose-induced analgesia emerged, and was maximal at approximately P10, then declined and was absent at P17. By contrast, maximal sucrose-induced analgesia for mechanical hindpaw stimuli was delayed (P13) compared to that for the forepaw, although it was also absent at P17. In inflamed animals, sucrose reduced hyperesthesia and hyperalgesia assessed with mechanical stimuli. Sucrose-induced analgesia in inflamed animals was initially present at P3 for the forepaw and P13 for the hindpaw, and was absent by P17 for both limbs. Intraoral sucrose produced significantly greater effects on responses in fore- and hindpaws in inflamed rats than in naive rats indicating that it reduces hyperalgesia and allodynia beyond its effects on responses in naive animals. These findings support the hypothesis that sucrose has a selective influence on analgesic mechanisms and that an enhanced sucrose effect takes place in hyperalgesic, inflamed animals as compared to naive animals. Taken together, these results indicate that intraoral sucrose alleviates transient pain in response to thermal and mechanical stimuli, and also effectively reduces inflammatory hyperalgesia and allodynia. Sucrose-induced analgesia is age-dependent and limited to the pre-weaning period in rats. The age-dependency of sucrose-induced analgesia and its differential maturation for the fore- and hindpaw may be due to developmental changes in endogenous analgesic mechanisms and developmental modulation of the interaction between gustatory and pain modulatory pathways.
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PMID:Age-dependency of analgesia elicited by intraoral sucrose in acute and persistent pain models. 1203 83

Previous studies demonstrated that nursing or intraoral infusion of certain components of mother's milk (e.g. sugars and fats) produces calming and opiate receptor-dependent analgesia in newborn rats and humans. However, the neural circuitry underlying such analgesia is unknown. The aim of the present study was to specify the central pathways by which taste stimuli engage neural antinociceptive mechanisms. For this purpose, midcollicular transactions were used to investigate the role of the forebrain in analgesia elicited by intraoral infusion of 0.2 M sucrose in neonatal rats. Sucrose-induced analgesia persisted, and was enhanced, following midcollicular transection, indicating that it did not require neural circuits confined to the forebrain. Fos immunohistochemistry was used to identify brainstem neurons activated by a brief (90 s) intraoral infusion of a small volume (90 microl, 0.2M) of sucrose or a salt solution (0.1 M ammonium chloride) in 10-day-old rat pups. Compared with control groups (intact, cannula, distilled water), both sucrose and ammonium chloride induced Fos expression in the rostral nucleus tractus solitarius, the first relay in the ascending gustatory pathway. Sucrose also elicited Fos expression in several brainstem areas associated with centrally mediated analgesia, including the periaqueductal gray and the nucleus raphe magnus. Taken together, these findings demonstrate that analgesia elicited by intraoral sucrose does not require involvement of the forebrain. Intraoral sucrose activates neurons in the periaqueductal gray and nucleus raphe magnus, two key brainstem sites critically involved in descending pain modulation.
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PMID:A brainstem substrate for analgesia elicited by intraoral sucrose. 1589 46

Sucrose ingestion has been shown to alleviate pain and distress in rats, human infants as well as adults. Sucrose induced analgesia is related to the reward value associated with its sweet taste. The sweet taste of sucrose is a stimulus for the activation of endogenous opioid pool. The opioids in turn modulate pain perception. It has been demonstrated in a number of animal and human studies that sucrose ingestion increases the hypothalamic/CSF opioid levels. This gains support from the results obtained from naloxone challenge test, a neuro-endocrine method for assessment of endogenous opioid tone. Moreover, the analgesic effects of sucrose can be reversed by administration of opioid antagonists such as naloxone. On the other hand, long-term sucrose ingestion leads to hyperalgesia in rats and it has been hypothesized to result from a complex interaction of sucrose with the endogenous opioid system leading to a deficiency of opioids. In the present article mechanisms underlying sucrose induced analgesia including the interaction of the palatability and reward value of food with the neural substrates and its neuro-chemical basis have been reviewed in the light of both animal and human studies. In addition, clinical application of the knowledge about sucrose and its modulatory effect on the endogenous opioid system has been suggested.
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PMID:Antinociceptive effect of sucrose ingestion in the human. 1657 91

Both magnetic field (MF) exposure and sucrose ingestion produce opioid mediated analgesia, independently. This article addresses the query whether or not sucrose ingestion potentiates the analgesia of MF exposure. The pain threshold, as reflected by withdrawal of tail (thresholds of tail flick, TF), vocalization during stimulus (VD), and vocalization after stimulus (VA) were determined in 7 sessions at 0, 5, 10, 15, 30, 45, and 60 min, respectively (control rats). After an interval of 24 h the rats were provided with sucrose solution and were allowed to ingest it for 10 min. The pain thresholds were determined (Control sucrose-fed rats). The rats then received exposure to magnetic field (50 Hz, 17.9 microT) for 7 d (8 h/d) (MF-exposed rats) and the effect of sucrose ingestion was repeated (MF-Sucrose-fed rats). The basal threshold of pain did not vary in between the control and MF-exposed rats. Pain threshold during sessions II-VII did not vary in control rats but it increased in MF rats. Moreover, the pain thresholds were elevated in MF rats as compared to control rats. Sucrose-ingestion elevated the threshold of TF in controls but not in MF-exposed rats; while the thresholds of VA and VD were elevated more in control than MF rats. The results suggest that the MF exposure (50 Hz, 17.9 microT, 8 h/d) for 7 d did not affect the basal thresholds of pain, increased stress induced analgesia, and attenuated the sucrose ingestion-induced analgesia.
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PMID:Threshold of pain in chronic magnetic field- (50 Hz, 17.9 microT) exposed rats: effect of sucrose ingestion. 1882 Dec 1

This study determined the effects of cumulative exposure to painful needle procedures and sucrose analgesia on the development of remote hyperalgesia in newborn infants, defined as an increase in response to a normally painful stimulus at a site distal from the site of injury. One-hundred and twenty healthy newborns and 120 healthy newborn infants of diabetic mothers equally randomized to sucrose analgesia or placebo prior to all needle procedures in the first two days after birth were divided into two exposure groups according to number of needle procedures they had undergone [high (> or =5) or low (< or =4)] using the median cut-off technique. Compared to the low exposure group, infants in the high exposure group had a higher pain response during a subsequent venipuncture distal to the site of previous injury, assessed by the Premature Infant Pain Profile (PIPP) [7.1 vs. 8.4; p=0.012] and Visual Analog Scale (VAS) [2.5 cm vs. 3.2 cm; p=0.047], and a trend for longer cry duration [25.7 s vs. 33.8 s; p=0.171]. PIPP scores did not differ during a routine diaper change, suggesting a nociceptive specific mechanism for the remote hyperalgesia to venipuncture. Sucrose reduced PIPP, VAS, and cry duration scores during venipuncture, but did not prevent hyperalgesia (p>0.05). There was a preponderance of infants of diabetic mothers in the high exposure group; however, the analysis did not demonstrate this to be a confounding factor. In conclusion, sucrose analgesia for repeated painful procedures in the first day of life does not prevent development of remote hyperalgesia in newborns.
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PMID:Influence of repeated painful procedures and sucrose analgesia on the development of hyperalgesia in newborn infants. 1937 23

Sucrose ingestion is reported to produce an initial (20-30min) analgesia and late (<5h) hyperalgesia. However, the influence of the characteristics of noxious stimuli and sweet substances on the pattern of transition from analgesia to hyperalgesia is not known. Therefore, we investigated the effect of sucrose (20%, sucrose fed group), saccharin (0.1%, saccharin fed group) and water ingestion (control group) on pain responses to various noxious stimuli for 5h. Latency of motor response of tail (TFL), paws to noxious thermal stimuli, threshold for elicitation of motor responses to electrical stimulation of tail nociceptive afferents in 5 sessions (0, 0.25, 1, 3 and 5h) and pain-related behavior to tonic noxious stimulus in 3 sessions at 1, 3 and 5h were recorded. In sucrose fed rats as compared to controls, the TFL sequentially increased (9.29+/-0.47s from 8.41+/-0.25; p<0.01), recovered to base-line and decreased (6.61+/-0.61sec; p<0.0001) in sessions II, III and V indicating analgesia, eualgesia and hyperalgesia, respectively. In saccharin fed rats the initial analgesia extended until session III followed by eualgesia and hyperalgesia in sessions IV and V. Pain related behaviour to tonic noxious stimulus also indicated an initial analgesia (0-5min), intermediate eualgesia and late hyperalgesia (3-5h) in sucrose fed rats, whereas only analgesia in saccharin fed rats. The results of our study suggest that sucrose ingestion for 5h leads to a bi-phasic response to both phasic and tonic noxious stimuli, albeit there are variations in their durations. Therefore, the temporal relationship of the nociceptive responses to palatable food is a function of the stimulus quality of both.
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PMID:Pattern of biphasic response to various noxious stimuli in rats ingesting sucrose ad libitum. 2058 Jun 42


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