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

The analgesic effect produced by electroacupuncture (EA) stimulation in the rat was dose-dependently antagonized by cholecystokinin octapeptide (CCK-8) administered intracerebroventricularly (i.c.v.) or intrathecally (i.th) at a dose range of 0.25-4 ng. This effect had an immediate onset and lasted for at least 4 h. CCK-8 per se, however, did not affect baseline tail flick latency. Rats subjected to prolonged EA stimulation developed EA tolerance as well as cross-tolerance to morphine. These tolerances could be postponed or reversed by i.c.v. or i.th injection of antiserum against CCK-8. While CCK-8 antagonized opioid analgesia, it did not affect analgesia induced by 5-hydroxytryptamine (5-HT) or norepinephrine (NE). Moreover, CCK-8 antiserum did not alter the basic level of nociception, nor did it potentiate EA analgesia in naive rats. It is concluded that prolonged EA stimulation results in a profound release of opioids which may trigger the release of CCK-8 in the central nervous system to counteract the opioid component of EA analgesia. This mechanism may account, at least in part, for the development of EA tolerance.
Pain 1986 Oct
PMID:Cholecystokinin octapeptide (CCK-8): antagonism to electroacupuncture analgesia and a possible role in electroacupuncture tolerance. 349 55

The observation that the narcotic antagonist naloxone could inhibit analgesia produced by electrical stimulation of the brain indicated the involvement of an endogenous chemical in the relief of pain. Multiple endogenous opioid peptides have been identified that have similar pharmacological properties to known narcotic analgesics. The biosynthesis, release, and degradation of opioid peptides have been studied in order to better understand how the manipulation of endogenous opioid systems can be used to produce or augment analgesia. The results of our studies reveal that various conditions and manipulations, such as electrical brain stimulation, acupuncture, stress, and the administration of opioid analgesics, can cause the release of endogenous opioid peptides and possibly endogenous nonpeptide substances. It has also been discovered that nonopioid peptides, such as cholecystokinin, calcitonin, and angiotensin II, can alter the action of opioid analgesics by antagonizing or potentiating their effects. An understanding of the role of endogenous peptides in endogenous opioid mechanisms is necessary for the development of new ways to treat pain and such other disorders as sleep apnea in children (sudden infant death syndrome), head injury, and opioid addiction that involve the activation or alteration of endogenous opioid systems.
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PMID:The role of endogenous peptides in the action of opioid analgesics. 352 91

Plasma cholecystokinin (CCK) responses after ingestion of a test meal in patients with mild chronic pancreatitis having abdominal pain were studied with a radioimmunoassay using the CCK specific antiserum (OAL-656) produced by a novel immunization procedure. Mean concentration of the fasting plasma CCK determined using CCK-8 as a standard was 31.5 +/- 5.8 pg/ml in six patients who had mild impaired exocrine function with pain, and was significantly higher than 10 healthy subjects (9.8 +/- 1.8 pg/ml). In those patients, the ingestion of a liquid test meal led to a peak of 75.1 +/- 25.4 pg/ml at 30 min, and the 120-min integrated CCK response (5427 +/- 1217.3 pg X min/ml) was significantly higher than in healthy subjects (1538 +/- 110.1 pg X min/ml).
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PMID:High plasma cholecystokinin levels in patients with chronic pancreatitis having abdominal pain. 353 53

Pain is a complex phenomenon involving both neurophysiological and psychological components. Pathophysiological mechanisms involve neural pathways, and a variety of pain-producing substances and modulating mechanisms. These include acetylcholine, serotonin, histamine, bradykinin, prostaglandins, substance P, somatostatin, cholecystokinin, vasoactive intestinal polypeptide, noradrenaline and endogenous opioid peptides. In assessing patients with pain, it is essential to evaluate the cause of the pain, its severity, type, location, duration, quality, and response to therapies, among other factors. The measurement of pain is dependent on subjective responses, which are evaluated by methods which have been well developed over the last three decades. Alleviation of pain by non-drug treatments must be considered as well as use of pharmacological treatments. These include psychological support, placebos, relaxation training, biofeedback, hypnosis, heat, cold, physical supports and surgery. Oral drugs are generally preferable to parenteral drugs, as are drugs with few side effects and low addictive liability. Both overtreatment and undertreatment are to be avoided. Patients can be expected to differ in their needs and responses, and economic considerations ought not be ignored. Newer approaches to pain management include self-administration of parenteral drugs, the search for new types of analgesics and appreciation of the relationship between age, sex, race, etc. and the response to analgesics. Tricyclic antidepressants, phenothiazines and the new non-steroidal anti-inflammatory drugs have pointed the way to possible improvements in our ability to tailor specific drugs to the needs of individual patients.
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PMID:The management of pain. 355 78

Prostaglandins have been postulated to be involved in the formation of gallstones and the pain and inflammation of calculous gallbladder disease. This report evaluated prostaglandin E and F levels in patients with acalculous gallbladder disease. Control gallbladders were obtained from patients undergoing cholecystectomy during insertion of hepatic artery catheters for regional, hepatic chemotherapy. Patients without gallstones and with long-standing post-prandial biliary colic with abnormal cholecystokinin administration underwent cholecystectomy for chronic acalculous cholecystitis. A third group of patients underwent cholecystectomy for acute acalculous cholecystitis. Gallbladder mucosa and muscle were separated, and prostaglandin E and F concentrations in mucosal and muscle or mucosa were identified in gallbladders from patients with chronic acalculous cholecystitis compared to gallbladders from patients without biliary tract symptoms. In gallbladders from patients with acute acalculous cholecystitis a seven-fold increase in PGE production by muscle tissue and mucosal cells was found. The more histologically inflamed gallbladders had higher mucosal and muscle prostaglandin E concentrations than were found in less inflamed gallbladders. Prostaglandin F levels were not significantly changed or were decreased, resulting in a significant increase in the ratio of PGE/PGF in acutely diseased gallbladders when compared to normal gallbladders. Prostaglandin E may be a manipulatable intermediary in the sequence of events that results in the development of acute acalculous cholecystitis.
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PMID:The role of prostaglandins E and F in acalculous gallbladder disease. 359 60

Course and prognosis of 125 patients with chronic pancreatitis (CP) were evaluated. Follow-up period ranged from 1-20 years with a median of 6.3 years. The following conclusions were obtained. Recent increase of CP in our clinics was ascribed to alcoholic CP and idiopathic CP in the aged. Of 106 patients with pain, 74 showed improvement or disappearance of pain. Drinking habit and observation period were the main factors determining the rate of pain relief. Serial endoscopic retrograde pancreatography (ERP) showed aggravation in 17/47 patients, cholecystokinin-pancreozymin (CCK-PZ) secretin test in 4/40 patients, and oral glucose tolerance test (OGTT) in 7/25 patients. Exocrine function showed improvement in five patients, whereas endocrine function showed none. Improvement or aggravation of exocrine function was closely related to drinking habit. Main complications included 15 cases of peptic ulcer, 19 of pancreatic pseudocyst, and 15 of bile duct stenosis. Twenty-six patients died, often due to malignant neoplasms and diabetic complications. Those who continued drinking as much showed a lower survival rate than those who discontinued or decreased alcohol intake. The socioeconomic status deteriorated often due to pain or alcoholism. Three patients had to degrade jobs and six fell into inactive social life.
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PMID:Clinical course and prognosis of chronic pancreatitis. 362 35

A deafferentation syndrome can be produced in rats by dorsal root ganglionectomies. This syndrome consists of scratching and/or biting of the anesthetic limb to the point of amputation. This behavior may serve as an experimental model to study certain aspects of chronic dysesthesias and/or pain caused by deafferentation in man. In this study, we made behavioral observations on the deafferentation syndrome and examined the possibility that intraventricular neurotensin and cholecystokinin alter the course of this syndrome. We found that neurotensin accelerated the scratching component without affecting the biting behavior. Cholecystokinin, however, attenuated the release of both components of the syndrome.
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PMID:The deafferentation syndrome in the rat: effects of intraventricular neurotensin and cholecystokinin. 366 78

The cholecystokinin cholescintigraphic findings of fundal adenomyomatosis in a 29-yr-old male with severe post-prandial pain are presented. Planar cholescintigraphy demonstrated a trilobed gallbladder contour. Following the administration of 0.02 micrograms/kg of cholecystokinin at maximal gallbladder filling, fundal dyskinesia was observed. Regional gallbladder ejection fractions were: whole gallbladder, 43%; proximal two-thirds of the gallbladder, 70%; and gallbladder fundus, 32%. First harmonic Fourier phase and amplitude images demonstrated: (a) decreased fundal amplitude values, and (b) a phase shift of the pixels in the gallbladder fundus.
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PMID:Differential gallbladder contractility in fundal adenomyomatosis: demonstration by cholecystokinin cholescintigraphy. 366 68

So-called acalculous gallbladder disease is an ill-defined entity, mainly seen in young women, which could be due to a motility disorder of the biliary tract. Seven young women with relapsing pain in the right upper quadrant of the abdomen or in the epigastrium, with cholesterol crystals in the bile and with normal sonographic and radiologic findings as well as normal gastroscopy, were investigated by hepato-biliary scintigraphy with 99mTc-HIDA. This first group was compared with a second group of 6 young women suffering from irritable colon, and with a third group of 6 asymptomatic control subjects. The half emptying-time of the gallbladder after cholecystokinin injection was 104.36 +/- 43.93 minutes in the first group, 17.92 +/- 23.57 minutes in the second and 20.42 +/- 23.67 minutes in the third group (p less than 0.005). After 6 weeks of ursodeoxycholic acid treatment, regression of pain and a significant reduction in the half emptying-time from 104.36 +/- 43.93 to 74.35 +/- 52.79 minutes (p less than 0.01) was observed in the first group. These results, which need to be confirmed by further studies, show that in acalculous gallbladder disease there is a delay in gallbladder emptying which could explain the formation of cholesterol crystals by bile stasis as described by various authors.
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PMID:[Study of gallbladder emptying using 99m Tc-HIDA in acalculous cholecystopathy]. 367 67

Sixty two patients with a clinical suspicion of biliary dyskinesia were investigated with endoscopic manometry of the sphincter of Oddi before and after intravenous injection of cholecystokinin or ceruletide. In 52 patients injection was followed by decreased pressure in the sphincter of Oddi; 43 of these had normal prestimulatory values (group I), while the values were raised in the other nine patients (group II). A paradoxical response to intravenous injection was observed in 10 women (group III): increased baseline sphincteric pressure occurred in eight and increase in the amplitude of phasic contractions in four patients. The prestimulatory sphincteric pressure was raised in five and normal in the remaining patients. Eight patients were treated with papillotomy (seven) or balloon dilatation of the sphincter (one). They experienced relief of pain during a follow up period of 11-16 months. Intravenous injection of cholecystokinin or ceruletide may disclose a special type of biliary dyskinesia even in patients with normal prestimulatory manometric findings. Hormone injection increases the diagnostic yield of endoscopic manometry in patients suspected of biliary dyskinesia.
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PMID:Paradoxical response of sphincter of Oddi to intravenous injection of cholecystokinin or ceruletide. Manometric findings and results of treatment in biliary dyskinesia. 380 27


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