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

Geriatric patients are preferentially involved in ischemic bowel disease. The sudden occlusion of the large mesenteric arteries (a. mesenterica superior (more frequently) and inferior) is followed by intestinal gangrene and peritonitis with a poor prognosis and a high letality (greater than 90%). In chronic intestinal ischemia the leading clinical symptom is postprandial pain ('claudicatio intestinalis'). In some cases of acute mesenteric artery occlusion no embolus or thrombus will be found. In these cases the circulation in the arteriosclerotic vessels falls below a critical value due to cardiac insufficiency, shock, digitalis overdose and others. In less severe ischemia the mucosa is involved being most sensitive to O2 deprivation. It usually regenerates within a few days. This form is found more frequently in the colon than in other parts of the gut (about 40%): ischemic colitis. The therapy - if possible in acute, fulminant ischemia or if necessary in chronic intestinal ischemia - is surgical consisting in reconstructive procedures of the mesenteric circulation.
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PMID:[Ischemic bowel disease (author's transl)]. 1 31

It is suggested that the early-morning growth-hormone release associated with slow-wave sleep is due to inhibition of somatostatin secretion from the hypothalamus. It is also associated with inhibition of gastrointestinal somatostatin, causing a release of gastrin and insulin. Because the levels of glucocorticoid hormones are concurrently low, the insulin effect is unopposed and increases gut motility through augmented vagal tone. This results in an increased delivery of acid to the duodenum. In duodenal-ulcer patients, whose duodenal buffering capacity is reduced because of a relative deficiency of secretin response, this leads to pain.
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PMID:Nocturnal ulcer pain associated with slow-wave sleep. 7 1

Sites in the gut that are related to pain are reviewed with respect to the special psychophysiological factors that operate locally. Topics considered are the irritable bowel, appendicitis and appendicectomy, duodenal ulceration and biliary disorders. Psychological states that promote the complaint or experience of abdominal pain are discussed. Possible psychological mechanisms are considered for abdominal pain with the reservation that we still do not know even the main physical mechanisms of pain related to gut disturbance.
Pain 1978 Aug
PMID:Abdominal pain and the emotions. 69 72

The horse with an abdominal crisis caused by acute gastro-intestinal tract obstruction develops hypovolaemia, haemoconcentration, electrolyte depletion, metabolic acidosis and shock. During preparation for operation, treatment with fluids, antibiotics and bicarbonate will impede metabolic imbalance. Stomach decompression may slow the passage of sodium, water and potassium to the gut lumen, reduce pain and minimize the risk of stomach rupture. Selected laboratory determinations and the monitoring of arterial and venous pressures will provide a measure of security, and serve as a guide to replacement therapy. In the post-surgical period, vigilance must be directed towards potassium and bicarbonate imbalance and adequate hydration.
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PMID:Metabolic management of the horse with an acute abdominal crisis. 110 Aug 23

A washout technic with intestinal infusion of an inert gas mixture was used to study the relation of gas to functional abdominal symptoms. The volume of gas in the intestinal tract (176 plus or minus 28 ml S.E.M.) of 12 fasting patients with chronic complaints of excess gas did not differ significantly (P greater than 0.10) from that of 10 controls (199 plus or minus 31 ml). Similarly, there was no difference in the composition or accumulation rate of intestinal gas. However, more gas tended to reflux back into the stomach in patients who complained of abdominal pain during infusion of volumes of gas well tolerated by controls. Six patients with severe pain during the study had intestinal transit times of gas (40 plus or minus 6 minutes S.E.M.) that were significantly (P less than 0.05) longer than those of the control group (22 plus or minus 3 minutes). Thus, complaints of bloating, pain and gas may result from disordered intestinal motility in combination with an abnormal pain response to gut distention rather than from increased volumes of gas.
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PMID:The role of intestinal gas in functional abdominal pain. 115 77

Loose ligation of the sciatic nerve with 4-0 chromic gut sutures in rats produces behavioral evidence of neuropathic pain. In the present experiments we examined the involvement of capsaicin-sensitive afferents in mediating the thermal hyperalgesia produced by this model. Male Sprague-Dawley rats, treated as neonates (within 48 h of birth) with capsaicin (50 mg/kg, s.c.) or vehicle, were used at 16-18 weeks of age. Chromic gut sutures (4-0) were tied around the left sciatic nerve and withdrawal latencies of both hind paws to radiant heat were determined on postoperative days 3, 5, 10 and 20. Whereas there was a pronounced thermal hyperalgesia which lasted for up to 20 days in vehicle-treated rats, there was no evidence of thermal hyperalgesia in capsaicin-treated rats. There was no difference in baseline (pre-surgery) withdrawal latencies between the two groups. Radioimmunoassay revealed that there was a significant depletion of substance P (43.8%) and calcitonin-gene-related peptide (72.6%) in the lumbar spinal cord of neonatal capsaicin-treated rats compared to vehicle-treated rats. These results demonstrate that the chromic gut-induced thermal hyperalgesia is mediated by capsaicin-sensitive afferents and suggest that central mechanisms which process and control the reflex response to heat are different than mechanisms involved in thermal hyperalgesia.
Pain 1992 Dec
PMID:Neonatal capsaicin treatment prevents the development of the thermal hyperalgesia produced in a model of neuropathic pain in the rat. 128 62

The irritable bowel syndrome (IBS) is a very common condition in gastroenterology clinics, but yet it is one of the pooly understood. A international working team in Rome, 1988, proposed that IBS is a functional intestinal disorder with chronic or recurrent gastrointestinal symptoms without structural or biochemical abnormalities. IBS was sub-classified into 3 groups; abdominal pain as the prominent feature with diarrhea, with constipation, with both while painless diarrhea and simple constipation without pain were excluded from IBS. There is a lot of data suggesting that IBS has a gut dysmotility, which is influenced by many stimuli (food, hormone, drug, menses, mechanical dilatation), including psychological stress. Moreover, currently available evidences implicate that IBS is a more generalized disorder of smooth muscle function not only in the intestine but also outside of the intestine.
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PMID:[Irritable bowel syndrome--criteria, sub-classification, etiology]. 128 43

Recent advances in the investigation of brain-gut interaction in irritable bowel syndrome (IBS) were reviewed. Brain is suggested to play an important role in the pathophysiology of IBS on the basis of the following evidence. (1) Stress often induces major symptoms of IBS patients (Drossman et al., 1982), simultaneously with colonic hypermotility (Fukudo et al., 1987) or dysmotility of the small intestine (Kumar et al., 1985). (2) IBS patients rarely express symptoms or small intestinal dysmotility during sleep (Kellow et al., 1990). (3) IBS patients complain of more pain with balloon distension of the colon or rectum than normal controls; visceral perception is enhanced in IBS (Whitehead et al., 1990). (4) IBS patients often show psychoneurotic symptoms and extra-colonic somatic symptoms (Young et al., 1976). (5) There are some animal (Williams et al, 1987) or human (Dinan et al, 1990) experiments which indicate the possible involvement of brain peptide or brain monoamine in IBS. (6) Dysrhythmia or increased beta power in electroencephalogram is observed more often in IBS patients than in the normal controls (Fukudo et al, 1991) in addition to abnormal REM sleep in IBS patients (Kumar et al., 1992). These observations support our hypothesis that not only the gut but also the brain show dysfunction and exaggerated responsivity to the stimuli in IBS. Further research on brain-gut interaction in IBS is warranted.
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PMID:[Brain-gut interactions in irritable bowel syndrome: physiological and psychological aspect]. 133 64

Recent evidence has shown that activation of the N-methyl-D-aspartate receptor mediates the thermal hyperalgesia produced in a model of neuropathic pain. As the acute nociceptive effects of N-methyl-D-aspartate have been reported to be mediated through production of nitric oxide and activation of soluble guanylate cyclase, these experiments were designed to determine whether the thermal hyperalgesia produced in a rat model of neuropathic pain is also mediated through the production of nitric oxide and activation of soluble guanylate cyclase. Loose ligation of the sciatic nerve with chromic gut sutures, but not bilateral sham rats, demonstrated evidence of a marked thermal hyperalgesia on day 3 post-surgery. In bilateral sham rats, intrathecal administration of either an alternate substrate for nitric oxide synthase, NW-nitro-L-arginine methyl ester, or the soluble guanylate cyclase inhibitor, Methylene Blue, did not produce any change in thermal nociceptive withdrawal latencies. These same treatments blocked the thermal hyperalgesia in rats with chromic gut ligatures for a period of 2 and 4 h, respectively. These results suggest that a sustained production of nitric oxide and subsequent activation of soluble guanylate cyclase in the lumbar spinal cord mediate the thermal hyperalgesia produced in a model of neuropathic pain in the rat.
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PMID:Nitric oxide mediates the thermal hyperalgesia produced in a model of neuropathic pain in the rat. 140 61

Twenty consecutive patients with recurrent Tolosa-Hunt syndrome were studied. One had a parent who suffered from recurrent Tolosa-Hunt syndrome. Thirty-three percent of the patients had also recurrent periods of weeks to months of unilateral periorbital pain without ophthalmoplegia. One patient had cluster headache before the Tolosa-Hunt syndrome started. Some patients had involvement of cranial nerves outside the cavernous sinus region during Tolosa-Hunt syndrome and also between episodes. The same systemic symptoms, i.e. back pain, cold feet, arthralgia, gut problems, varices, vertigo, chronic fatigue, thrombophlebitis, memory deficiency and signs of inflammation in serum, occurred in Tolosa-Hunt syndrome as earlier found in patients with orbital venous vasculitis. Seventy-three percent of the patients had pathologic orbital phlebograms. All patients treated with steroids reacted promptly; four who developed chronic pain syndromes were treated satisfactorily with azathioprine.
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PMID:Recurrent Tolosa-Hunt syndrome. 155 57


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