Gene/Protein Disease Symptom Drug Enzyme Compound
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Query: UMLS:C0016382 (flushing)
 6,387 document(s) hit in 31,850,051 MEDLINE articles (0.00 seconds)

The effects of naloxone and a met-enkephalin analogue on head pain, vascular responses, and autonomic-associated symptoms were studied in 24 migraine patients, 12 patients suffering from tension-type headache, and 24 normal subjects in whom headache was induced by intravenous injections of increasing doses of histamine (histamine test). A hypersensitivity to histamine was found in migraine patients. Naloxone slightly increased the intensity of pain in migraine and tension-type headache sufferers. The met-enkephalin analogue did not affect the intensity of pain in migraine patients, tension-type headache patients, and normal subjects, but it reduced the intensity and duration of facial flushing (p less than 0.001) and the autonomic symptoms (p less than 0.001) in migraine patients when the pretreatment was not given shortly before histamine. In migraine patients, there seems to be an increased reactivity (receptor supersensitivity?) to the met-enkephalin analogue at the level of systems that inhibit facial vasodilatation and autonomic symptoms.
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PMID:Increased reactivity to a met-enkephalin analogue in the control of autonomic responses in migraine patients. 227 18

The role of opiate receptors in the metabolic response to an intravenous glucose load was determined in eight non-diabetic subjects (four of whom showed a positive chlorpropamide alcohol flush response and four who did not). Subjects were studied in a double blind randomised fashion receiving either a saline control or the specific opiate receptor antagonist, naloxone (0.4 mg/min), as an infusion for 5 minutes before and 20 minutes after an intravenous bolus of glucose (0.5 g/kg body weight). Naloxone decreased the early plasma glucose peak in all subjects by increasing the distribution volume but did not alter the fractional glucose clearance. Insulin and glucagon responses to glucose were not altered by naloxone. Naloxone delayed the normal post-glucose rise in the levels of the gluconeogenic precursors alanine, lactate, pyruvate and glycerol suggesting a delay in the usual inhibition in gluconeogenesis following a glucose load. There was no difference in the metabolic response between those subjects who were liable to chlorpropamide alcohol flushing and those who were not either with or without naloxone. We conclude that opiate receptors may influence distribution volume and gluconeogenesis but do not play a major role in either insulin or glucagon secretion or in glucose disposal following an intravenous glucose load.
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PMID:Opiate receptors and the metabolic response to intravenous glucose. 629 13

Hot flashes have a close temporal relationship with the initiation of LH pulses, suggesting that factors stimulating gonadotropin release are involved in the mechanism of this disturbance. It has been reported that the opiate antagonist naloxone acutely blocked subjective hot flashes, a seemingly paradoxical effect, since the use of this agent in premenopausal women increases the magnitude and frequency of LH pulses. We, therefore, studied the effects of naloxone in 16 postmenopausal women with frequent hot flashes using continuous recordings of finger temperature and skin resistance as objective indices of flushing and perspiration, respectively. After baseline recordings, the subjects were randomized into equal groups, and the recordings were repeated during 8-h infusion of either saline or naloxone (22 micrograms/min). Serum gonadotropin levels were measured at 15-min intervals before and during the last 4 h of the infusion. Naloxone did not change the rate of objectively measured hot flashes, mean serum LH or FSH levels, or the frequencies or amplitudes of gonadotropin pulses. These data suggest that there is a very low input of endogenous opiates on gonadotropin secretion in postmenopausal women and that opioid peptides do not play a role in the initiation of the postmenopausal hot flash.
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PMID:The effects of naloxone on hot flashes and gonadotropin secretion in postmenopausal women. 642 Apr 45

Six postmenopausal women with frequent attacks of flushing were studied by measuring plasma luteinizing hormone (LH), follicle stimulating hormone (FSH), prolactin and noradrenaline concentrations at regular and frequent intervals and at the time of each of 82 flushes. The hormone measurements were made on a control day and on the second day during infusion of either naloxone (22 micrograms/min) or saline. The perception of a flush was associated with a significant increase of plasma LH concentrations. There were no significant changes in plasma FSH, prolactin or noradrenaline concentrations. Naloxone infusion resulted in a highly significant reduction in the frequency of flushes and in the number of LH pulses. We conclude that flushing and its neuro-endocrine correlates are related to activation of opiate receptors. Naloxone may provide the basis for a non-steroidal treatment of climacteric flushing attacks.
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PMID:Climacteric flushing: clinical and endocrine response to infusion of naloxone. 679 84