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)

We carried out a review of 358 patients undergoing cholecystectomy during a seven-year period. Twenty-one patients were found to have classic biliary colic with a normal oral cholecystogram. All patients were female and had symptoms for three to 120 months (mean, 24 months). Cholecystosonography, upper gastrointestinal (GI) tract x-ray series, and infusion tomography of the gallbladder, when performed, were normal. Twelve patients underwent cholecystokinin (CCK) cholecystography. Failure of normal contraction of the gallbladder was noted in all 12. All 21 underwent cholecystectomy; three months postoperatively, all patients were relieved of their pain, and 15 of the 16 available for long-term follow-up (averaging 22 months) were completely cured of their symptoms. We conclude that the young woman with typical biliary colic and a normal oral cholecystogram, gallbladder ultrasound study, and upper GI tract x-ray series should undergo CCK cholecystography. If the results are positive, these patients can be reliably cured by cholecystectomy.
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PMID:Biliary colic and functional gallbladder disease. 710 15

Combined biliary drainage-cholecystokinin cholecystography (BD-CC) was evaluated in 81 patients with pain indistinguishable from biliary colic, but normal conventional diagnostic tests. The test was performed using a new technique of intubation and aspiration, with a steerable catheter and sump duodenal tube. Both positive and negative groups were followed. One third of patients had positive tests, and almost all had pathologic gallbladders, and a symptomatic outcome equal to that obtained by cholecystectomy for cholelithiasis diagnosed by conventional means. Some patients with severe pain had cholecystectomy despite a negative report. Pathologic findings were significantly fewer, and symptomatic outcome less satisfactory but sufficiently good to suggest that painful functional gallbladder abnormalities, not amenable to diagnosis by BD-CC exist. Hypercontraction was found to be a reliable index of gallbladder pathology. A false bilirubin precipitate was identified in some patients; this precipitate may be recognized by microscopy and pH testing. This finding should reduce false-positives in BD-CC.
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PMID:Results of combined biliary drainage and cholecystokinin cholecystography in 81 patients with normal oral cholecystograms. 714 12

The spinal cord dorsal horn contains neural mechanisms which can greatly facilitate pain. We have recently shown that 'illness'-inducing agents, such as intraperitoneally administered lipopolysaccharide (LPS; bacterial endotoxin), can produce prolonged hyperalgesia. This hyperalgesic state is mediated at the level of the spinal cord via activation of the NMDA-nitric oxide cascade. However, prolonged neuronal depolarization is required before such a cascade can occur. The present series of experiments were aimed at identifying spinal neurotransmitters which might be responsible for creating such a depolarized state. These studies show that LPS hyperalgesia is mediated at the level of the spinal cord by substance P, cholecystokinin and excitatory amino acids acting at non-NMDA sites. No apparent role for serotonin or kappa opiate receptors was found.
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PMID:Illness-induced hyperalgesia is mediated by spinal neuropeptides and excitatory amino acids. 753

Until recently, basic science studies, both behavioural and electrophysiological, have concentrated on the antinociceptive actions of opioids primarily gauged against acute nociceptive responses. However, of more relevance to clinical situations are the actions of opioids in more persistent/prolonged pain states. This review sets out to examine the central actions of opioids against nociception of inflammatory origins. The first section deals with the response of the endogenous opioid system to the development of an inflammatory state and the second examines the ability of exogenous opioids to modulate inflammatory nociception. There are complex changes in the roles of endogenous opioids, in particular dynorphin, at the spinal level after inflammation although the physiological consequences remain unclear. With regard to exogenous opioids, the effectiveness of spinal morphine is rapidly enhanced after inflammation, likely to be due to changes in the interaction between the peptide cholecystokinin and the mu opioid receptor. The ability of inflammatory processes to alter both endogenous opioids and morphine analgesia at the spinal level illustrates the considerable degree of plasticity observed in opioid function.
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PMID:Spinal opioid systems in inflammation. 758 17

Given an indication for surgery in patients with chronic pancreatitis, such as distal common bile duct obstruction, duodenal stenosis, or dilated pancreatic duct with stones and congestion, the surgeon must decide the type of operation to perform. A duodenopancreatectomy, the Whipple procedure, is widely considered to be the gold standard. It is highly effective in relieving pain and eliminating the structural abnormalities noted above. Duodenum-preserving resection of the head of the pancreas (DPRHP) seems to be an attractive alternative to pancreaticoduodenectomy (PD) in the treatment of chronic pancreatitis. In a clinical prospective randomized trial the efficiency of both operative methods was investigated. Between 7/1987 and 12/1993 43 patients were randomly assigned to undergo either a Whipple procedure (n = 21) or DPRHP (n = 22). Data on postoperative course, mortality, and postoperative morbidity were compiled. As concerns long-term results, postoperative hormonal status (insulin, neurotensin, cholecystokinin, gastrin) was checked, basal and stimulated with a standardized meal, using standard hormonal assay kits. All patients with PD survived, whereas one with DPRHP died from peritonitis. Patients with DPRHP had a significant more rapid convalescence (16.5 vs. 21.7 days). The range for postoperative follow-up is from 36 months to 5.5 years. In the DPRHP group 18 patients are in good condition. Two had diabetes and one developed carcinoma. In the PD group one died from hepatic coma, 14 are in good condition and 6 developed diabetes. All gained body weight with an average of 6.4 vs. 4.9 kg, DPRHP vs. PD. A difference between DPRHP and PD was obvious for the postoperative hormonal status. Results are satisfactory in both groups. For patients with DPRHP however, we see a quicker convalescence and a significant benefit as concerns postoperative hormonal status.
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PMID:[Pancreatic function and quality of life after resection of the head of the pancreas in chronic pancreatitis. A prospective, randomized comparative study after duodenum preserving resection of the head of the pancreas versus Whipple's operation]. 763 46

Carrageenan-induced inflammation of the rat hindpaw has been used as a model for persistent pain of inflammatory origin. The induction of inflammation resulting from carrageenan injection in the rat hindpaw has been shown to elicit an increase in the antinociceptive potency of morphine, an effect postulated to be related to reduced levels of spinal cholecystokinin (CCK). Recent findings have related the anti-opioid effect of CCK to a decrease in activation of delta-opioid receptors. For this reason, we have examined the effects of the delta-opioid antagonist naltrindole (NTI) on the modulation of morphine antinociceptive potency resulting from carrageenan-induced inflammation. Rats with carrageenan-induced hindpaw inflammation received several doses of morphine in the absence or presence of NTI and were tested in the hot plate (HP) and tail flick (TF) tests. These results were compared to those of non-carrageenan injected rats. Morphine was significantly more potent in inflamed, than in control, rats in both tests. While NTI did not affect morphine antinociceptive potency in control rats in either test, this opioid delta antagonist blocked the increase in morphine potency resulting from carrageenan inflammation in nearly every case. The blockade of the enhancement of morphine potency was such that the effect of a given dose of morphine was similar in control rats and carrageenan-injected rats with NTI. We suggest that carrageenan-induced inflammation may alter endogenous enkephalin levels, perhaps by a decrease in CCK availability. The enhancement of morphine antinociceptive potency may result from the well-established synergism seen following the activation of opioid delta receptors by enkephalins.
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PMID:The increase in morphine antinociceptive potency produced by carrageenan-induced hindpaw inflammation is blocked by naltrindole, a selective delta-opioid antagonist. 771 40

The endogenous peptides enkephalins and cholecystokinin appear to play an opposite role in the control of pain. In this work, the effect of the selective CCKB receptor antagonist PD-134,308 on antinociceptive effects induced by morphine or by a complete inhibitor of enkephalin-metabolizing enzymes, RB 101, was studied using the formalin test. In mice, s.c. injection of formalin into the dorsal surface of the hindpaw had a biphasic effect: an early nociceptive response followed by a late response. Morphine (2 mg/kg i.p.) caused naloxone (0.5 mg/kg s.c.) but not naltrindole (0.5 mg/kg s.c.) reversible antinociceptive responses in the early and late phases of the assay, suggesting a preferential involvement of mu-opioid receptors in these responses. In contrast, RB 101 (50 mg/kg i.p.) produced antinociceptive effects in the early and late phases which were both antagonized by the delta-selective opioid receptor antagonist naltrindole (0.5 mg/kg s.c.). The antinociceptive response elicited by morphine on the late but not the early phase of the formalin test was potentiated by the CCKB antagonist PD-134,308 (1 mg/kg i.p.). This compound was unable to facilitate the analgesic effects produced by RB 101 on both phases, in contrast to what was observed in the hot plate test with mice and the tail flick test with rats. Therefore, in the formalin test with mice, the facilitating effects of opiate-induced analgesia by CCKB receptor antagonists seem to be restricted to mu-opioid receptor-mediated responses.
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PMID:A selective CCKB receptor antagonist potentiates, mu-, but not delta-opioid receptor-mediated antinociception in the formalin test. 773 8

Recent studies have suggested that cholecystokinin may have a role in modulating the effects of the endogenous opioid system in physiological functions such as thermoregulation and pain control. However, the possible interaction of cholecystokinin and morphine in epileptogenesis is unknown. We studied the effect of subcutaneous morphine and intracerebroventricularly administered cholecystokinin octapeptide sulphate ester and receptor antagonists CCK-A (MK 329) and CCK-B (L 365,260) on seizures provoked by maximal electroshock in male Sprague-Dawley rats. Seizures were induced through electrode-gel-coated ear clip electrodes by a high voltage, high internal resistance constant current generator, 30 minutes after morphine administration and 10 minutes after cholecystokinin-8-SE, CCK-A and CCK-B infusion. Morphine decreased the length of the tonic component of the seizure and cholecystokinin potentiated this decrease. Cholecystokinin antagonists blocked the effects of both cholecystokinin and morphine. The results suggest that cholecystokinin acts as an endogenous agonist with opioids in the regulation of seizure susceptibility through both CCK-A and B receptors and may be responsible for part of the anticonvulsant action of morphine.
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PMID:Cholecystokinin potentiates morphine anticonvulsant action through both CCK-A and CCK-B receptors. 774 54

We have recently developed a rat model of chronic pain states after spinal cord injury. Thus, after severe, but incomplete, ischemic spinal cord injury, some rats chronically exhibited responses indicative of pain to innocuous mechanical stimuli (allodynia) in the rostral dermatomes involving the injured spinal segments. These responses have some characteristics in common with chronic central pain in patients with spinal cord injury. We now report that systemic CI988, a specific antagonist of the cholecystokinin (CCK) type B receptor, effectively relieved the allodynia-like symptom, an effect that was reversed by the opioid receptor antagonist naloxone. Furthermore, in rats which did not develop the allodynia-like symptom after spinal cord lesion, systemic naloxone induced typical allodynia. In contrast, naloxone failed to produce allodynia in normal animals. It is thus suggested that the abnormal sensory processing initiated by spinal cord ischemic lesion is under tonic opioidergic control and dysfunction of this control by the upregulated endogenous CCK system is responsible for the development of painful sensations in these rats.
Pain 1994 Mar
PMID:Chronic pain-related behaviors in spinally injured rats: evidence for functional alterations of the endogenous cholecystokinin and opioid systems. 791 21

The periaqueductal gray (PAG) is an important integration site for pain, autonomic functions, vocalization, fear and anxiety. Cholecystokinin (CCK) is a major neurotransmitter in the PAG and CCK receptors are heterogeneously distributed within the PAG. Since CCK antagonists are anxiolytic and potentiate morphine analgesia, it is possible that these effects of CCK are mediated through alteration of neuronal activities in the PAG. The goals of this study were to examine the anatomical and physiological properties of the PAG CCK containing systems. The distribution of CCK-containing axons and boutons in PAG was examined using immunohistochemical procedures. These studies show that CCK-like immunoreactive (CCK-LIR) fibers and terminals are present throughout PAG, but are particularly heavily concentrated in a focal column that runs longitudinally throughout the rostrocaudal axis of dorsolateral PAG and in nucleus cuneiformis which represents a caudolateral extension of PAG. The physiological effects of CCK on PAG neurons were examined in both in vivo and in vitro preparations. In the in vivo experiments multibarreled electrodes were used to record from PAG neurons and to apply CCK and the CCK antagonists, CR1409 and proglumide. Of 37 neurons recorded in vivo, CCK caused excitation in 25 cells, inhibited 7 cells and had no effect on 5 cells. The excitatory effect was blocked by CR1409 in 11/11 cells tested. Proglumide blocked the excitatory response of CCK in 12/14 cells. Proglumide blocked the inhibitory effect in 2 of 7 cells, but CR1409 had no effect on CCK-evoked inhibition in 7 cells tested. Extracellular, conventional intracellular and whole cell patch clamping procedures were used to study CCK actions in the in vitro slice preparation. In the extracellular recording experiments, responses of PAG cells to CCK were measured in slices that were maintained at 22 degrees C (room temperature) and at 32 degrees C. CCK excited 40/56, inhibited 7/56 and had no effect on 9/56 cells; excitatory responses were blocked by CR1409 in 32/36 cells and by proglumide in 25/27 cells tested. Inhibitory responses to CCK were unaffected by CR1409, but were blocked in 3/7 cells by proglumide. Conventional intracellular recordings were made from 13 cells.(ABSTRACT TRUNCATED AT 400 WORDS)
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PMID:Characterization of the effect of cholecystokinin (CCK) on neurons in the periaqueductal gray of the rat: immunocytochemical and in vivo and in vitro electrophysiological studies. 803 4


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