Search PubMed⌕ Search

Biomedical subjects

M A Chapman

Publications and source records attributed to M A Chapman.

At least 37 records · Page 2Linked to original sources
PubMed1995

Complications of the ileal pouch: is the pouchogram a useful predictor?

A series of ileal pouchograms from 25 consecutive patients has been analysed retrospectively. Ileal pouchography may demonstrate abnormalities which delay closure of the covering ileostomy. The aim was to determine whether disruption of the ileoanal anastomosis and/or leak at pouchography correlated with pelvic sepsis after ileostomy closure. Disruption of the stapled ileoanal anastomosis is a sensitive (88%) but not specific predictor (57%) for subsequent pelvic sepsis. The predictive value of a negative test is high (89%). Leak of contrast from the anastomosis is specific (81%) but not sensitive (56%) for pelvic sepsis. No significant relationship was demonstrated between width of the presacral space and the presence of pelvic sepsis. No significant relationship was demonstrated between diameter of the ileoanal anastomosis and symptoms of stricture. The presence of anastomotic disruption or leak at pouchography prior to ileostomy closure are useful predictors of potential pelvic sepsis.

Adolescent↗
PubMed1994

Chronic haloperidol, but not clozapine, produces altered oral movements and increased extracellular glutamate in rats.

Rats administered chronic haloperidol or clozapine in their drinking water for 6 months were monitored for changes in oral movements using a computerized video analysis system. Haloperidol-treated animals exhibited late onset increases in small amplitude oral movements and an increase in the percentage of oral movements in the 1-2 Hz range, accompanied by a decrease in oral movements in the higher frequency range (> 6 Hz) as determined by fast fourier analysis. In contrast, clozapine-treated rats showed a decrease in medium-sized amplitude oral movements, but did not demonstrate significant changes in the distribution of oral movements across frequencies. Extracellular concentrations of gamma-aminobutyric acid (GABA) and glutamate in the ventrolateral striatum were then assessed by intracranial microdialysis during oral drug administration and 3 days after drug withdrawal. Extracellular GABA and glutamate levels were not significantly different between groups during drug administration. However, 3 days after drug withdrawal, there was a significant increase in glutamate in the haloperidol-treated rats. No changes were noted for glutamate levels in clozapine-treated rats or for GABA levels in either group following withdrawal. These results confirm the atypical profile of clozapine in an animal model of tardive dyskinesia and suggest that alterations in striatal glutamatergic function follow typical, but not atypical, antipsychotic drug administration.

Administration, Oral↗
PubMed1994

Butyrate oxidation is impaired in the colonic mucosa of sufferers of quiescent ulcerative colitis.

The short chain fatty acids, acetate, propionate, and butyrate are produced by colonic bacterial fermentation of non-starch polysaccharides. Butyrate is the major fuel source for the colonic epithelium and there is evidence to suggest that its oxidation is impaired in ulcerative colitis. Triplicate biopsy specimens were taken at colonoscopy from five regions of the large bowel in 15 sufferers of ulcerative colitis. These patients all had mild or quiescent colitis as assessed by clinical condition, mucosal endoscopic and histological appearance. The rate of oxidation of glucose, glutamine, and butyrate through to carbon dioxide was compared with that in biopsy specimens from 28 patients who had no mucosal abnormality. Butyrate (272 (199-368)) was the preferred fuel source for the colitic mucosa followed by glutamine (33 (24-62)) then glucose (7.2 (5.3-15)) pmol/micrograms/hour; medians and 95% confidence intervals, p < 0.01. There was no regional difference in the rate of utilisation of these metabolites. In the group with colitis the rate of butyrate oxidation to carbon dioxide was significantly impaired compared with that in normal mucosa decreasing from 472 (351-637) pmol/micrograms/hour to 272 (199-368) pmol/micrograms/hour; median and 95% confidence intervals, p = 0.016. The rate of glucose and glutamine utilisation were not significantly different between normal and colitic mucosa. These data confirm that in quiescent ulcerative colitis there is an impairment of butyrate oxidation.

Adult↗
PubMed1994

The consequences of long-term antipsychotic drug administration on basal ganglia neuronal function in laboratory animals.

Antipsychotic drugs (APDs) have been widely utilized in the treatment of a variety of psychiatric disorders, most prevalently for schizophrenia. In addition to their desired therapeutic effects, repeated administration of APDs often produces various motor side effects. Experimental evidence has implicated alterations in the nuclei of the basal ganglia as the basis for the motor dysfunctions that may arise during APD treatment. Because APDs are invariably administered for extended periods of time, a great deal of research has focused on the effects of prolonged drug exposure. Animal models have been a particularly valuable tool for studying APD effects on basal ganglia function following several weeks (subchronic) to months or years (chronic) of administration. The present paper reviews the scope of studies that have assessed various aspects of basal ganglia function in laboratory animals treated with APDs for prolonged period of time. Possible mechanisms of action are reviewed regarding subchronic and chronic APD effects on basal ganglia function as well as directions for future research.

Animals↗
PubMed1993

New technique to measure mucosal metabolism and its use to map substrate utilization in the healthy human large bowel.

A new method of assessing substrate utilization in gastrointestinal mucosal specimens is described. Small human endoscopic biopsy specimens with wet weights ranging between 1.4 and 12.2 mg were used to quantify the oxidation of three metabolic substrates, glucose, glutamine and butyrate, through to carbon dioxide over a 2-h period. The technique proved to be reproducible and capable of distinguishing variations in mucosal metabolism between individuals (P < 0.0001 for each substrate). Results were similar to those obtained previously using human and rat colonocytes. To characterize the metabolism of the healthy large bowel, specimens were obtained from five regions in 15 patients who had a normal colonoscopic examination. The results show that butyrate is the preferred fuel source of large bowel mucosa, followed by glutamine, then glucose (P < 0.01). There was no significant regional variation in utilization of the three substrates between the five regions; with respect to glutamine, this is contrary to previous findings.

Adult↗
PubMed1992

Chronic neuroleptic administration decreases extracellular GABA in the nucleus accumbens but not in the caudate-putamen of rats.

The extracellular levels of gamma-aminobutyric acid (GABA) in the caudate-putamen and the nucleus accumbens of rats following administration of haloperidol decanoate, fluphenazine decanoate, or vehicle for 8 months were assessed using intracranial microdialysis. Basal levels of extracellular GABA were significantly decreased in the nucleus accumbens of both neuroleptic-treated groups while levels of GABA in the caudate-putamen were not significantly different between groups. These results provide evidence for selective chronic neuroleptic-induced effects on in vivo GABA function in different terminal regions containing dopamine receptors.

Animals↗
PubMed1992

Comparison of chronic intermittent haloperidol and raclopride effects on striatal dopamine release and synaptic ultrastructure in rats.

The effects of chronic intermittent administration (7 months) of two neuroleptics, haloperidol (HAL) and raclopride (RAC), were compared using several different measures. Both drugs were administered weekly by subcutaneous injection at 7.0 mg/kg. Both neuroleptics consistently produced catalepsy throughout the treatment period, although HAL was generally more cataleptogenic than RAC. Assessment of dopamine (DA) release in the caudate putamen (CPu), through the use of in vivo microdialysis, showed that chronic HAL or RAC administration caused a prolonged decrease of DA release in response to a low dose of the DA D2 agonist quinpirole (0.03 mg/kg, sc). Injection of the muscarinic agonist pilocarpine (1.0 mg/kg, IP) did not have any significant within-group effects, although both neuroleptic treatment groups showed decreased DA release when compared to controls. Ultrastructural analysis of the dorsolateral CPu showed that both HAL and RAC treatment resulted in a significant increase in the number of perforated synapses, which contain a discontinuous density along the postsynaptic membrane. These results demonstrate that two different DA D2 receptor antagonists produce a similar effect on DA function and ultrastructural changes within the CPu following chronic, intermittent treatment.

Animals↗
PubMed1992

Neurotensin increases extracellular striatal dopamine levels in vivo.

This study employed intracranial microdialysis to assess the effects of neurotensin (NT) infusion on extracellular dopamine (DA) and DA metabolite concentrations in the rat striatum and nucleus accumbens, and the effects of NT on alterations in extracellular DA levels induced by cocaine and the DA D-2 receptor agonist, quinpirole. Direct NT infusion (.10, 1.0, 10.0 microM) did not significantly affect extracellular DA in the nucleus accumbens, but did produce a significant increase in the DA metabolite homovanillic acid (HVA). In contrast, direct NT infusion produced an increase in striatal DA levels, without altering DA metabolites. Neurotensin infusion (.10 microM) into the striatum significantly attenuated the peak DA increase induced by an intraperitoneal (IP) injection of a low dose (10.0 mg/kg) but not a high dose (30.0 mg/kg) of cocaine. Neurotensin infusion (.10 microM) did not affect the decrease in DA and its metabolites induced by an IP injection of a low dose of quinpirole (.03 mg/kg), but did alter the decrease in HVA induced by a high dose of quinpirole (.10 mg/kg). These results suggest that NT differentially affects in vivo DA release in the striatum and nucleus accumbens, and further strengthens the assertion that NT is an important modulator of dopaminergic function.

3,4-Dihydroxyphenylacetic Acid↗
PubMed1991

In vivo assessment of release and metabolism of dopamine in the ventrolateral striatum of awake rats following administration of dopamine D1 and D2 receptor agonists and antagonists.

The ability of specific dopamine (DA) receptor agonists and antagonists to modify the release and metabolism of DA in the ventrolateral striatum of awake rats was assessed using in vivo microdialysis. The specific DA D2 receptor antagonist, raclopride (0.1, 0.5 and 2.0 mg/kg, i.p.), dose-dependently increased release of DA and levels of the metabolites DOPAC and HVA, while the D2 receptor agonist, quinpirole (0.03, 0.1 and 0.3 mg/kg), decreased levels of DA, DOPAC and HVA. The DA D1 receptor antagonist, SCH23390 [(R + (+)-8-chloro-2,3,4,5-tetrahydro-3-methyl-5-phenyl- 1H-3-benzazepin-7-ol) (0.01, 0.05 and 0.25 mg/kg), produced an increase in DA, DOPAC and HVA but of a lesser magnitude than raclopride. The D1 agonist SKF38393 (1-phenyl-2,3,4,5-tetrahydro-(1H)-3-benzazepine-7,8-diol) (1.0, 3.0 and 10.0 mg/kg) failed to affect the release of metabolism of DA at any dose. These results support previous findings that activation of D2 receptors has greater control over in vivo DA function, than drugs specifically affecting D1 receptors.

2,3,4,5-Tetrahydro-7,8-dihydroxy-1-phenyl-1H-3-ben↗
PubMed1991

Cholinergic modulation of oral activity in drug-naive and chronic haloperidol-treated rats.

The cholinergic agonists pilocarpine, physostigmine, oxotremorine, and arecoline were administered IP at various doses to rats. Oral activity was assessed in these animals with a computerized video analysis system that determined the number and form of jaw openings and closings (computer scored movelets "CSMs"). The different cholinergic drugs produced distinctive changes in the number of CSMs at various amplitudes and in the frequency distribution of CSMs as determined by fast fourier analysis. Rats treated for 28 weeks with haloperidol showed a previously described, late onset oral dyskinesia characterized by increases in small amplitude CSMs, decreases in CSM slope, increased energy at the 1-3 Hz range and decreased energy at the 5-7 Hz range. Administration of pilocarpine (1.0 mg/kg) reversed all of these effects, while the anticholinergic drug, scopolamine (0.05 mg/kg), had no effect. These results indicate that different cholinomimetics can uniquely alter oral activity in rats and that symptoms of late onset, neuroleptic-induced oral dyskinesia are modified by a cholinergic agonist.

Animals↗
PubMed1991

Motor racing accidents at Brands Hatch, 1988/9.

Little is known about the incidence of injury to race track motor-cyclists and car drivers. In a 1-year study at Brands Hatch, 70 of 33,184 competitors required hospital treatment. We found this injury rate to be higher than on the public highway. However, the anatomical distribution of injury caused by motor-bike accidents is similar to that found on the public highway. Motor-cyclists are more likely than car drivers to sustain limb trauma requiring outpatient treatment only. The number of participants requiring admission to hospital is broadly similar for car and bike races, being less than 0.1%.

Accidents↗