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Query: UMLS:C0030193 (pain)
 261,466 document(s) hit in 31,850,051 MEDLINE articles (0.00 seconds)

Cholecystokinin cholecystography represents a study designed to identify patients with acalculous extrahepatic biliary tract disorders. In this study, a positive cholecystokinin cholecystogram (CCK-GB) was defined as both reproduction of the patient's biliary tract-type pain plus one or more of various roentgen abnormalities. Using these criteria, 20 patients had a positive CCK-GB. After failure of medical management, 19 of these patients came to surgery. Seventeen of 18 available for follow-up were cured of their biliary tract pain by surgery. Follow-up of this group of patients has ranged from one month to 60 months. In view of our findings plus those in other reported series, we conclude that CCK-GB provides a reliable study for the diagnosis of acalculous extrahepatic biliary tract disorders.
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PMID:Cholecystokinin cholecystography in the diagnosis of acalculous extrahepatic biliary tract disorders. 74 10

The effect of oxytocin (OT) and cholecystokinin octapeptide (CCK-8) on EA analgesia was studied in rats. The increase of 20.8-39.8% and 9.0-45.0% in pain threshold was observed respectively when ICV of CCK-8 or naloxone was combined with EA, these increases were lower than that in saline-EA group significantly, while the simultaneous ICV of OT and CCK-8 or OT and naloxone in combination with EA produced the increase of 76.2-116.6% and 41.8-104.5% in pain threshold separately. These results showed that only a small part in the role of OT enhancing EA analgesia was blocked by CCK-8 and naloxone. The data suggest that the role of OT in EA was not entirely dependent upon the endogenous opiate peptides.
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PMID:[Effect of oxytocin and cholecystokinin octapeptide (CCK-8) on electroacupuncture (EA) analgesia]. 128 28

Clues to the pathogenesis of functional pain syndromes may be derived from the study of stimuli that precipitate or aggravate symptoms. In this study, cholecystokinin octapeptide (CCK-8, 0.06 microgram/kg) and placebo were given by intravenous infusion (5 min) in random order to control subjects and four groups of patients with unexplained abdominal pain. Induction of pain and nausea were assessed by linear analogue scales while sympathoadrenomedullary responses were assessed by serial changes in plasma concentrations of noradrenaline, adrenaline and dopamine. Scores for pain and nausea were low after infusion of placebo. After infusion of CCK-8, pain scores were significantly higher in patients with spontaneous pain than in control subjects, but significant increases in nausea were restricted to patients with irritable bowel syndrome and a subgroup of patients with pain after cholecystectomy. Although some groups showed increases in plasma concentrations of catecholamines after the infusion of CCK-8, the size of these increases was neither consistent among patients within each group nor predictive of scores of pain and nausea in individual subjects. Pain during the infusion of CCK-8 was a feature common to patients with diverse functional pain syndromes, and did not appear to be attributable to activation of the sympathetic nervous system.
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PMID:Responses to cholecystokinin octapeptide in patients with functional abdominal pain syndromes. 161 Oct 17

The peripheral territories of sheep trigeminal neurons which send their central process to the brainstem through the oculomotor nerve were investigated by the use of fluorescent tracers in double-labeling experiments. For this purpose Diamidino yellow (DY) injection into the oculomotor nerve was combined with Fast blue (FB) injection either into the extraocular muscles (EOMs), or the cornea, or the superior eyelid. Double-labeled DY + FB cells were found in the ophthalmic region of the trigeminal ganglion in addition to single-labeled DY or FB cells. The DY and DY + FB-labeled trigeminal cells were analysed immunocytochemically for their content of substance P (SP)-, calcitonin gene-related peptide (CGRP)-, and cholecystokinin-8 (CCK-8)-like. All single-labeled DY cells showed SP-, CGRP- or CCK-8-like immunoreactivity. Double-labeled DY + FB neurons innervating the EOMs were immunoreactive for each of the three peptides, whereas double-labeled neurons supplying the cornea were only CGRP-like positive. The findings suggest that, in the sheep, trigeminal neurons which send their process centrally through the oculomotor nerve supply the EOMs, the cornea, and the superior eyelid and contain neuropeptides which are usually associated with pain sensation.
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PMID:Peripheral territory and neuropeptides of the trigeminal ganglion neurons centrally projecting through the oculomotor nerve demonstrated by fluorescent retrograde double-labeling combined with immunocytochemistry. 171 31

The contractility of human gallbladders without calculi of 10 patients with typical biliary pain was investigated in vivo (n = 7; pharmacosonography) and in vitro (n = 10; isometric registration). In 6 out of 7 cases, investigated in vivo as well as in vitro, the contractility was identical--therefore the smooth-muscle-preparation in the organ-bath could be an interesting model for studies with CCK-antagonists. 3 of the in-vitro-preparations showed hypomotility consecutive to acetylcholine- and CCK-stimulation. Histologically, the destruction of the normal gallbladder wall structure by scars, chronic inflammation and the evidence of so-called Rokitansky-Aschoff-sinuses could be proved. The importance of these findings probably causal to the process of cholelithogenesis is discussed.
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PMID:[Comparative studies of in-vivo and in-vitro contraction behavior of gallbladders with impaired function]. 192 46

Pancreatic secretion is involved in circadian regulation of the whole organism. This observation was obtained in animals and humans with pancreatic fistulas. We report on three patients in whom the pancreas was removed totally or subtotally because of chronic pancreatitis with severe pain. A segment of the removed gland was transplanted into the thigh in order to preserve endocrine function. The pancreatic duct was drained by a polyethylene tube until pancreatic duct occlusion. Postoperatively juice volume increased within 3 days and remained constant afterwards with 300 ml in 24 hours. Secretin, cholecystokinin and food intake are able to stimulate the transplanted segment in a typical manner. The secretion showed circadian changes. In all patients the pancreatic juice content of protein, amylase, trypsinogen, calcium, and zink decreased till 11 p.m. After 11 p.m. the content of all substances increased and reached maximal values at 6 a.m. Flow rates and therefore output per minute decreased greatly till 6 a.m. The large juice volume of 300 ml in 24 hours is perhaps the consequence of a break down of the feedback mechanism between intraduodenal trypsin activity and CCK-release. The changes during the night may be of pathogenetic relevance. In the early morning pancreatic juice is highly concentrated and the flow rate is very low. High protein concentrations, high calcium concentrations, and reduced flow rates may lead to protein and calcium carbonate precipitates. This mechanism is under discussion in the pathogenesis of chronic pancreatitis.
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PMID:[Exocrine function of a heterotopically transplanted pancreas segment in humans]. 195 40

Specific abnormalities of colonic and small bowel motility are identifiable and associated with symptoms in IBS. Characteristic abnormalities in colonic motility include a prolonged increase in 3-cycles/min colonic motor activity after a meal, an exaggerated increase in 3-cycles/min motor activity in response to stressors and CCK, and increased visceral sensitivity and motor activity in response to balloon distention. Symptoms in patients with IBS correlate in some cases with the abnormal gastrocolonic response and with pain induced by distention at various sites in the colon. Small bowel motility abnormalities identified reproducibly in IBS include an increase in daytime jejunal DCCs, an increase in daytime ileal PPCs, and more frequent cycling of daytime MMCs (in diarrhea-predominant IBS only). DCCs and PPCs are strongly associated with symptoms in IBS, and PPCs associated with altered ileocecal transit may be an important mechanism of symptoms in some patients with IBS. Esophageal and gastroduodenal motility abnormalities are inconsistently identified in IBS, and most symptoms in IBS appear to be secondary to small bowel or colonic dysfunction. Because of the paroxysmal nature of these motor abnormalities in IBS, prolonged motility recordings are required to better understand the pathophysiology of this syndrome. Patients with IBS may have altered visceral sensation and changes in afferent reflex mechanisms that modulate GI motility. These patients do not have a generalized increase in pain perception, but may have a distinct sensitivity to visceral afferent stimulation in both gastrointestinal and other viscera. Whether the altered "setpoint" to visceral afferent stimulation in IBS is intrinsic to the smooth muscle of viscera or secondary to CNS and ANS modulation is not known. Many of the symptoms and abnormalities of small bowel and colonic motility in IBS probably result from these changes in afferent sensation and reflex mechanisms. These findings support the concept that IBS is an abnormality of intestinal motility in conjunction with a "sensitive" gut.
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PMID:Motility disorders in the irritable bowel syndrome. 206 53

This chapter focuses on studies dealing with the feedback mechanism of pancreatic exocrine secretion in animal and man. Clear evidence is presented that this feedback mechanism is working in the rat and the pig and that this feedback is mediated in the rat by the gastrointestinal hormones pancreozymin (enzyme secretion) and secretin (volume and bicarbonate secretion). Two novel peptides have been described--the 'CCK-releasing peptide' originating from the small intestinal mucosa, and the 'monitor peptide' cosecreted together with the enzymes in the pancreatic juice--to account for the stimulation of pancreatic enzyme secretion by the release of CCK. A similar feedback regulation of pancreatic secretion is working in man. It remains as yet controversial whether the feedback in humans is regulated via hormonal or neural pathways. It is also a matter of debate whether this feedback regulation of pancreatic enzyme secretion could be utilized for therapeutic aims in the treatment of pain in patients with chronic pancreatitis.
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PMID:Feedback regulation of pancreatic exocrine secretion in animal and man. 212 96

The effects of sulfated cholecystokinin octapeptide (CCK-8s) and CCK-8s antagonist, proglumide, given intrathecally (i.t.) on inhibition of the tail-flick and hot-plate paw-licking responses induced by beta-endorphin and morphine given intracerebroventricularly (i.c.v.) were studied in male ICR mice. Both CCK-8s (up to 0.5 ng) and proglumide (up to 10 micrograms) injected alone did not affect significantly the control latencies of the tail-flick and paw-licking responses. I.t. injection of CCK-8s as doses from 0.125 to 0.5 ng dose dependently attenuated inhibition of the tail-flick response induced by i.c.v. administered beta-endorphin. The antagonistic effect of CCK-8s on beta-endorphin-induced inhibition was blocked by the co-i.t. injection of proglumide (0.1-1 micrograms) in a dose-dependent manner. High doses (2.5-10 micrograms) of proglumide given i.t. dose dependently enhanced inhibition of the tail-flick response induced by i.c.v. administered beta-endorphin. However, i.t. injection of CCK-8s and proglumide did not affect inhibition of the paw-licking response induced by i.c.v. administered beta-endorphin. The inhibitions of the tail-flick and paw-licking responses induced by i.c.v. administered morphine were not affected by i.t. injection of CCK-8s or proglumide. Our results suggest that CCK-8s in the spinal cord may play an important modulatory role in attenuating the descending pain inhibition induced by i.c.v. administered beta-endorphin but not morphine.
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PMID:Differential effects of sulfated cholecystokinin octapeptide and proglumide injected intrathecally on antinociception induced by beta-endorphin and morphine administered intracerebroventricularly in mice. 214 90

It has been reported that proglumide and L-364,718 potentiate opioid-induced antinociception. However, their mode of action in pain modulation is still not understood. To evaluate a possible interaction with opioid receptors, we determined the affinities of the CCK antagonists proglumide, lorglumide, benzotript and L-364,718 on mu, delta and kappa binding sites, using guinea pig brain crude synaptosome preparations. These affinities were compared to that of the central CCK binding site, using rat brain slide-mounted sections. At 100 microM, proglumide competed for 13% and 17% of mu and kappa binding sites, but did not interact with delta and CCK sites. At this concentration, lorglumide reduced mu, delta, kappa and CCK specific binding by 44%, 69%, 35% and 88%, whereas benzotript diminished it by 16%, 13%, 38% and 48%, respectively. L-364,718 did not interact with opioid receptors (assay limit of solubility, 10 microM) but had a high affinity for CCK binding sites (IC50, 126nM). The lack of selectivity of proglumide, lorglumide and benzotript for CCK receptors suggests that their reported ability to potentiate morphine analgesia may be related to an interaction with opioid receptors.
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PMID:Cholecystokinin antagonists proglumide, lorglumide and benzotript, but not L-364,718, interact with brain opioid binding sites. 217 22


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