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)

2-Deoxy-D-glucose (2DG) analgesia, mediated in part by endogenous opiate and hypothalamo-hypophysial systems is presumably activated by its stress-related properties. Recently 2DG hyperphagia, but not 2DG hyperglycemia was reduced by central pretreatment with the pancreatic beta-cell toxin, alloxan; this deficit was eliminated by co-administration of 3M D-glucose. The present experiment examined whether intracerebroventricular pretreatment with alloxan (40 or 200 micrograms) altered 2DG analgesia (400 or 700 mg/kg, IP) on the tail-flick and jump tests, and whether 3M D-glucose co-administration ameliorated any deficits. Both alloxan doses significantly reduced 2DG analgesia (400 mg/kg) on both tests. 2DG analgesia (700 mg/kg) was significantly reduced by both alloxan doses on the jump test, but only by the higher alloxan pretreatment on the tail-flick test. 3M D-glucose co-administration ameliorated alloxan-induced analgesic deficits more effectively at the lower 2DG dose. Neither alloxan nor alloxan/3M D-glucose treatments altered basal thresholds. These data pertain both to alloxan's effects upon coding of 2DG effects as stressful, and to the role of diabetes and/or central glucoreceptors in analgesic processes.
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PMID:Intracerebroventricular alloxan reduces 2-deoxy-D-glucose analgesia. 339 8

The increase of plasma catecholamines that occurs during surgery can be reduced by administration of morphine. To test the hypothesis that morphine specifically blocks nociceptive stimulation during surgery, we compared the effects of morphine administration on the plasma catecholamine response to a laparotomy in pentobarbital-anesthetized dogs with the effect of morphine on the plasma catecholamine response to the neuroglucopenic agent, 2-deoxy-D-glucose (2DG, 300 mg/kg iv). In control dogs, plasma epinephrine (Epi) and plasma norepinephrine (NE) both increased progressively with time following a midline laparotomy (delta Epi by 50 min, +133 +/- 42 pg/ml, P less than 0.01 and delta NE by 50 min, +108 +/- 38 pg/ml, P less than 0.01, mean +/- SE, n = 12). 2-Deoxy-D-glucose produced a similar increase of both plasma NE and Epi. In dogs that received the anesthesia alone, plasma catecholamines did not increase from base line during the experiment. The analgesic morphine (15 mg iv), given 15 min after the completion of laparotomy, not only prevented the progressive rise of plasma catecholamines after laparotomy, but also caused a small but significant decline (P less than 0.05). Naloxone (0.4 mg iv) totally reversed the suppressive effects of morphine, restoring both catecholamines to the levels of their time-related control. In marked contrast, neither morphine nor naloxone affected the plasma NE and Epi increases following the administration of 2DG. These data suggest that morphine suppression of plasma catecholamines during surgery is not due to a generalized attenuation of sympathetic outflow, but rather to a specific interaction with an opiate receptor that either mediates analgesia or lies within the neural pathway stimulated by laparotomy but not by 2DG.
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PMID:Morphine suppresses plasma catecholamine responses to laparotomy but not to 2-deoxyglucose. 708 32