Gene/Protein Disease Symptom Drug Enzyme Compound
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Query: UMLS:C0030193 (pain)
 261,466 document(s) hit in 31,850,051 MEDLINE articles (0.00 seconds)

Improved knowledge about biochemical mechanisms underlying pain suppression by CNS electric stimulation is one condition for the further advancement of this form of treatment. In 6 patients treated with PVG stimulation and in 14 with spinal cord stimulation the concentration of substance P-like immunoreactivity in lumbar CSF increased significantly following stimulation. However, these changes may be unspecific and not directly related to the suppression of pain. Measurements of somatostatin, cholecystokinin, vasoactive intestinal polypeptide, neurotensin and monoamine metabolites in CSF showed no changes related to stimulation and the ensuing pain relief. Possible reasons for these negative findings are discussed.
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PMID:Possible neurohumoral mechanisms in CNS stimulation for pain suppression. 242 25

Trigeminal sensory innervation of cerebral vessels and the surrounding dura is responsible for most intracranial head pain. Small-diameter fibers containing substance P (Sub P) have been observed in the periadventitia around feline cerebral blood vessels, and it has been suggested that these fibers are the trigeminal substrate for vascular pain associated with cluster and migraine headaches. Calcitonin gene related peptide (CGRP) coexists with Sub P in some of these fibers and with some Sub P containing neurons in the trigeminal ganglion. In addition, a population of trigeminal neurons containing CGRP but not Sub P has been observed. We now report that the population of trigeminal ganglion cells projecting to the cerebral vasculature is enriched in CGRP-containing neurons, and especially in the population of neurons containing CGRP and not Sub P. Using retrograde tracing of fluorescent tracers combined with immunocytochemistry after explant culture, we found approximately 32% of trigeminal ganglion cells projecting to the cerebral vasculature contained CGRP. Approximately 18 and 17% of these cells contained Sub P and cholecystokinin (CCK), respectively. The 32% of ganglion cells projecting to the cerebral vasculature that contain CGRP stands in contrast to the 12% CGRP positive seen in the population of ganglion cells projecting out to another target (the forehead), and the 21 and 23% CGRP positive observed in the mandibular branch and entire ganglion, respectively. Sub P and CCK are not enriched in the trigeminal innervation of the vasculature compared with their presence in cells throughout the ganglia.(ABSTRACT TRUNCATED AT 250 WORDS)
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PMID:Enrichment of a vasoactive neuropeptide (calcitonin gene related peptide) in the trigeminal sensory projection to the intracranial arteries. 247 Aug 72

The appearance of biliary pain after cholecystectomy in patients with normal ultrasonic and cholangiographic studies has been attributed to functional alterations of the Sphincter of Oddi. We performed dynamic cholescyntigraphic studies of the biliary tract in 32 cholecystectomized patients, at least six months after the operation: 27 were asymptomatic (control group) and 5 had clinical and laboratory findings suggesting temporary functional obstruction of the Sphincter of Oddi. In this group we demonstrated an emptying delay of the biliary tract that was modified by the IV infusion of Cholecystokinin Octapeptide. Biliary Cholescintigraphy appears as a good screening method to evaluate functional alterations of the Sphincter of Oddi.
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PMID:[Biliary scintigraphy in patients with functional disorders of Oddi's sphincter]. 251 63

The potential clinical utility of drug interactions between morphine and the cholecystokinin antagonist proglumide was examined in 80 postoperative patients suffering from moderate to severe pain. Four groups of ASA I-III patients (mean age 51 years, mean weight 72 kg) recovering from major abdominal or gynecological surgery (mean duration of surgery 141 minutes) performed under balanced anesthesia (midazolam, droperidol, fentanyl, N2O, enflurane) were randomly assigned to self-administer morphine-proglumide mixtures on the first postoperative day (ODAC; morphine demand dose 3 mg; infusion rate 0.36 mg/hr; lockout time 2 minutes; hourly maximum dose 15 mg/hr; proglumide doses per demand 0, 50 micrograms, 100 micrograms, or 50 mg). Morphine consumption, actual as well as retrospective pain scores (0-5) and side effects were evaluated. Mean duration of patient-controlled analgesia (PCA) in the subgroups was 17-19 hours, during which time 24.6 +/- 9.5 to 28.0 +/- 3.4 micrograms morphine.kg-1.hr-1 was given. There were no statistically significant differences between the groups either for drug consumption, pain scores, or side effects. It is therefore concluded that proglumide does not potentiate morphine analgesia in a clinical (postoperative) setting.
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PMID:Failure of proglumide, a cholecystokinin antagonist, to potentiate clinical morphine analgesia. A randomized double-blind postoperative study using patient-controlled analgesia (PCA). 264 68

Proglumide, an antagonist of cholecystokinin, has been shown to potentiate morphine analgesia in animal and human experimental pain models. This study was undertaken to determine whether proglumide enhances morphine analgesia for patients experiencing postoperative pain. At onset of pain after the removal of impacted third molars, patients (n = 60) received intravenously either 4 mg morphine, 8 mg morphine, or 4 mg morphine plus proglumide (0.05, 0.5, or 5 mg). The administration of 8 mg morphine significantly reduced pain, in comparison with baseline and 4 mg morphine, for the first 30 minutes. The addition of 0.05 mg proglumide resulted in a significant increase in the magnitude and duration of the analgesic activity of 4 mg morphine; 0.5 and 5.0 mg proglumide did not produce this effect. No difference was seen in respiratory rate or in the frequency of side effects among the various forms of treatment. These data indicate that a low dose of proglumide potentiates both the magnitude and the duration of morphine analgesia in a clinical model of acute pain, without any detectable increase in side effects.
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PMID:Proglumide potentiates morphine analgesia for acute postsurgical pain. 265 36

This paper compares two methods of evaluating gall-bladder function after stimulation with cholecystokinin (CCK); One, the echographic method, permits the gall-bladder contraction study by determining variations in face area of the organ. The other, the scintigraphic method (HIDA-CCK test), studies of the gall-bladder emptying registering the decreases of activity by external counts. Out of 20 studies performed: 8 cases presented a contractile response and normal emptying; 7 had an abnormality late initial response (Ti) and contraction and emptying (defined by T1/2) slower than normal. In the 5 patients the gall-bladder traced with HIDA did not respond to CCK. Within this group, one patient had an incomplete painful contraction, evaluation by echography. The onset of pain or sub-costal discomfort was a variable finding within the different study groups. The linear coefficient correlation for the normal group and for the patients with late response was 0.8255 (x = 2.216 gamma-4.59). Based on these data and taking into account cheaper cost, patient comfort, and greater availability of equipment, the echographic method for studying gall-bladder contraction after administration of CCK, can be used instead of the HIDA-CCK procedure.
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PMID:[A comparative study of gallbladder function using echography and HIDA-CCK]. 269 31

The effects of cholecystokinin octapeptide sulphated (CCK) and the potent CCK antagonist MK-329 (L-364, 718) on analgesia induced by morphine in the paw pressure test in the rat were examined. Both CCK (4-16 micrograms/kg) and MK-329 (0.1-8.0 mg/kg) had no significant effect on thresholds for pain when given alone, whereas morphine (2-16 mg/kg) induced dose-dependent analgesia. Cholecystokinin (4-16 micrograms/kg) abolished the analgesia induced by 8 mg/kg morphine. In contrast, doses of 1 and 2 mg/kg MK-329 enhanced the analgesia induced by 8 and 4 mg/kg morphine, respectively. The present data are consistent with previous reports that CCK blocks, and CCK antagonists enhance, opiate-induced analgesia in response to thermal pain stimuli. In addition, the results show that CCK/opiate interactions extend to mechanical pain stimuli. Recent ligand binding studies have shown that CCK receptors in the spinal cord of the rat (where CCK/opiate interactions are thought to occur) are predominantly of the CCK-B subtype. The drug MK-329 has a relatively weak (micromolar) affinity for CCK-B receptors and a high affinity (nanomolar) for CCK-A receptors. As relatively large doses (1-2 mg/kg) of MK-329 are required to enhance opiate-induced analgesia in the paw pressure test and tail flick test in rats it appears that CCK/opiate interactions in this species involve CCK-B receptors.
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PMID:Morphine-induced analgesia in the rat paw pressure test is blocked by CCK and enhanced by the CCK antagonist MK-329. 272 51

Cholecystokinin (CCK) mRNA was detected by in situ hybridization at high magnification in some rat brain regions where CCK octapeptide (CCK-8) is thought to produce its pharmacological effects. The labeling of the dentate gyrus and the sparse but intensively stained cells found in the CA1 layer, stratum radiatum and hilus could correspond to interneurons involved in hippocampal neural activity, in agreement with excitatory responses induced by local injection of CCK-8. The intense labeling of the Edinger-Westphal nucleus and more generally the presence of CCK mRNA in the periaqueductal gray and thalamus ventrobasal nuclei could account for the various effects of CCK in pain transmission.
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PMID:Distribution of CCK mRNA in particular regions (hippocampus, periaqueductal grey and thalamus) of the rat by in situ hybridization. 281 34

The peripheral control of appetite is effected by two digestive hormones produced by the stomach and intestine. Bombesin, induced by gastric distension, might act as a messenger informing the nervous centres that the subject is satiated. The pharmacological satiating effect of cholecystokinin, probably mediated by the afferent fibres of the vagus nerve, is well established, but its physiological effect has not yet been demonstrated. Centrally, appetite is controlled by neurotransmitters, satiating and orexigenic properties being shared between monoamines, benzodiazepine-receptors and GABA-receptors. Among digestive hormones present in the central nervous system, the most satiating in pharmacological doses seem to be cholecystokinin and calcitonin, but their physiological role remains obscure. Insulin might be the signal informing the hypothalamus on body fat mass. Endorphins exert an orexigenic effect, reversed by naloxone, which is particularly marked in case of stress, in obese subjects and in the presence of highly palatable food. The control of appetite therefore is complex. It cannot be separated from other functions, such as pain and pleasure, which are regulated by intracerebral peptides.
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PMID:[Mechanisms of the control of appetite]. 286 55

The recent discovery that cholecystokinin (CCK) is present in the nervous system has prompted studies that have nearly proven its neurotransmitter status. Pain modulation appears to be a major effect of CCK and proglumide, its antagonist. CCK's inhibitory effect and proglumide's potentiating effect on opiate analgesia may have clinical application; proglumide's inhibitory effect on opiate tolerance may help in management of chronic pain. More research is required before the CCK/opiate interaction can be exploited on a large scale to relieve pain.
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PMID:Cholecystokinin and pain: a review. 287 41


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