Search PubMed⌕ Search

Biomedical subjects

A R Cooke

Publications and source records attributed to A R Cooke.

At least 37 records · Page 2Linked to original sources
PubMed1977

Pulmonary alveolar microlithiasis.

A case of pulmonary avleolar microlithiasis is reported. This is of especial interest as it is the first case to be reported from Africa South of the Sahara. The clinical presentation of the patient follows a similar pattern as that of cases already described by other workers. The diagnosis in this case was made in life by a combination of radiological examination and a lung biopsy. The clinical presentat on and aetiology of the condition are briefly discussed.

Calculi↗
PubMed1977

A comparison of intrinsic nerve supplies of two muscular layers of duodenum.

The duodenums of opossums and cats were cut into strips 2 mm wide and 2-2.5 cm long. Strips cut in the direction of the oral-caudal axis were called longitudinal strips, and those cut at 90 degrees to that axis were called circular strips. Each muscle strip was stimulated with trains of electrical rectangular pulses (10 Hz, 50-70 V, 0.5 ms). In the longitudinal strips, electrical field stimulation caused contraction, and this contraction was abolished by atropine, 10(-7) M. In the circular strips, electrical field stimulation caused relaxation. This relaxation was abolished by tetrodotoxin, 10(-7) M, but it was not affected by antagonists to adrenergic and cholinergic transmission, nor by some gastrointestinal hormones. Reserpinization of the opossums or alteration of the frequencies of electrical field stimulation from 0.1-50 Hz did not affect or alter the relaxation of the circular strips or the contraction of the longitudinal strips. These findings suggest that the longitudinal muscle is dominated by an excitatory cholinergic innervation, and the circular muscle is dominated by a nonadrenergic, noncholinergic inhibitory innervation.

Animals↗
PubMed1976

Gastric and duodenal ulcer and their associated diseases.

Assessments of likely associations between ulcer and other diseases are hindered by the frequent lack of controls, by controls which are inadequate, and by inadequate descriptions of techniques used. The inherent biases in some of the techniques have also probably been insufficiently appreciated. Ulcer is common in the community and much of the evidence adduced to suggest ulcer/other-disease associations may well be describing oridinary ulcer frequency which has been underestimated. With such problems in mind, few of the proposed associations bear examination. Ulcer is probably unusually frequent in patients undergoing treatment for chronic renal failure. It is possibly more frequent in association with hyperparathyroidism and in cirrhotics, in cardiovascular disease (except hypertension), and in chronic respiratory disease. Evidence for other associations is not compelling.

Adrenocortical Hyperfunction↗
PubMed1976

Effect of a fixed pyloric opening on gastric emptying in the cat and dog.

The effect of preventing pyloric closure on the rate of gastric emptying without alteration of the gastroduodenal junction was studied in six dogs and four cats with gastric fistulas. Each had a Teflon cannula with an internal diameter of 1.0 or 1.25 cm (dog) and 0.6 cm (cat) sewn into the pyloric channel. At the completion of the initial series of tests, the cannulas were removed and the studies repeated. Test meals were 240 and 480 ml of water, acid (120 mM HC1), and hyperosmotic glucose (555 mM) in the dogs and 50 ml of water, acid (100 mM HC1) and fat (20 mM Na oleate) in the cats. Phenol red was used as a nonabsorbable marker. The residual volumes were collected at 15-40 min in the dogs and 15-20 min in the cats. In both species, the rate of emptying of all the meals was unaffected by the pyloric cannula. In the dog, added secretions were greater with the pyloric cannula in place, suggesting reflux of duodenal contents. This study indicates that while the pylorus is unimportant in the gastric emptying of liquids in the dog and cat, it may have a role in prevention of duodenal reflux.

Alcohols↗
PubMed1976

Osmoltye and tryptophan receptors controlling gastric emptying in the dog.

The effect of three monosaccharides, three disaccharides, two dipeptides, combinations of tryptophan with two hexoses, one hexitol, and two amino acids ongastric emptying was studied in dogs to further define the samll intestinal receptors responsive to osmolytes and tryptophan. On a molar basis the disacchardies and dipeptides were almost twice as potent as their respective constituent monosaccharides or amino acids implying that the osmoreceptor is deep to the brush border disaccharidases and cytosol dipeptidases. Tryptophan probably acts by a mechanism different from the osmoreceptor since slowing of gastric emptying by tryptophan was inhibited by methionine which has no effect on a stimulant of the osmoreceptor mechanism. Lysine unlike methionine does not share the neutral amino acid transport pathway with tryptophan. Lysine did not change the inhibitory effect of tryptophan on gastric emptying. This imples that transport of tryptophan into the intestinal cell is necessary for its slowing effect. Glucose and galactose also inhibited the tryptophan effect whereas a nonabsorbed hexitor, mannitol, was without effect. Interference by the hexoses was also probably by competition with tryptophan for transport into the cell. These studies further indicate that the tryptophan receptor is different from the osmoreceptor.

Alanine↗
PubMed1976

Drugs and gastric damage.

The effects of aspirin, salicylate formulations and substitutes, smoking (nicotine), indomethacin, corticosteroids, phenylbutazone, ethanol, caffeine and reserpine on the gastric mucosa are discussed. The damaging effects of the drugs are considered in terms of the gastric mucosal barrier, gastric erosions, microbleeding and haematemesis and melaena and finally whether they cause peptic ulcer. There is suggestive evidence that unbuffered aspirin is a cause of haematemesis and melaena and of gastric ulcer but the incidence rates for hospital admission are low, being 10 to 15 per 100,000 heavy users per year. Aspirin in solution as acetylsalicylate buffered to maintain a neutral pH protects against gastric damage. Newer aspirin substitutes (mefenamic acid, fenoprofen, naproxen, tolmetin and ibuprofen) appear to cause less faecal blood loss than aspirin but their long-term effects have not been fully evaluated. Smoking is definitely associated with peptic ucler but the mechanism is unknown. Corticosteroids are probably not ulcerogenic despite clinical bias that they are. Indomethacin and phenylbutazone may be ulcerogenic but there is insufficient evidence to make firm judgements. Ethanol, caffeine and reserpine, on available evidence, are probably not ulcerogenic.

Adrenal Cortex Hormones↗
PubMed1976

Effect of tryptophan and its metabolites on gastric emptying of liquid meals in dogs.

The effects of tryptophan and its metabolites were studied to determine whether the known inhibiting effect of tryptophan on emptying was due to local or systemic effects or due to tryptophan metabolites. In five dogs with chronic gastric fistulas, instillation of 300 ml of DL-kynurenine (5mM), 5-hydroxytryptophan (mM), or 5-hydroxytryptamine (20 mM) into the gut did not slow gastric emptying. Furthermore, iv infusion of L-tryptophan (5, 20, 50 mM), DL-kynurenine (2, 5, 10 mM), 5-hydroxytryptamine (2mM, 10 mM), and 3-indolepyruvic acid (2, 5, 10 mM) also did not slow gastric emptying. These studies indicate that tryptophan slows gastric emptying by exciting a receptor in the gut and not by a direct effect on the stomach or brain or via its major metabolites.

Animals↗
PubMed1976

Gastric damage by drugs and the role of the mucosal barrier.

There are six drugs usually implicated in peptic ulceration and these are adrenal corticosteroids, aspirin, phenylbutazone, indomethacin, ethanol and caffeine. The types of data upon which these conclusions rest follows three lines of evidence. First, the production of ulcers in experimental animals; all the drugs mentioned above can produce experimental ulcers. Second, the cause and effect relationship in man, i.e. epidemiological evidence; the epidemiological evidence is very weak except for aspirin. Third, a mechanism suspected of participating in the pathogenesis; the pathogenesis of drug ulceration is not fully understood but aspirin may be the only one with a body of data to support its ulcerogenic effect. The pathogenesis of peptic ulcer is usually considered in terms of the equation, acid-pepsin versus mucosal resistance. Caffeine is a moderately strong stimulus of acid secretion but corticosteroids, phenylbutazone, ethanol and indomethacin are very weak stimulants or have no effect. Aspirin decreases acid secretion...

Animals↗
PubMed1976

Effect of first part of duodenum on gastric emptying in dogs: response to acid, fat, glucose, and neural blockade.

Five dogs were prepared, each with a gastric and duodenal fistula (5 cm distal to the pylorus), to study the inhibitory role of the first 5 cm of the duodenum on gastric emptying. The basic design of the experiments was to instill the test meal (300 ml at 37 degrees C, containing phenol red 40 mg 1(-1)) into the stomach and collect it at 1- or 2-min intervals for 10 or 20 min from the duodenal fistula. As the test meal emptied from the stomach it bathed the first 5 cm of duodenum and thus stimulated the appropriate receptor. A Foley catheter with an inflated balloon prevented passage into the second part of the duodenum. Test meals of hypertonic glucose (15%, 865 milliosmoles kg-1) or 20 and 80 mM of sodium oleate emptied at the same rate as water when allowed to bathe the first 5 cm of duodenum, whereas test meals of 100 mM of HCl were slowed. In further studies using neural blocking agents, the emptying of water meals was slowed with subcutaneous atropine sulfate (0.03 and 0.15 mg kg-1), intravenous hexamethonium chloride (10 mg kg-1), and norepinephrine bitartrate (0.04 mg kg-1). The emptying of 100 to 120 mM HCl meals was slowed by subcutaneous atropine sulfate (0.03 and 0.15 mg kg-1), intravenous norepinephrine bitartrate (0.04 mg kg-1), and the intravenous alpha-receptor blocking agents phenoxybenzamine HCl (2 mg kg-1) and phentolamine (2 mg kg-1), was unaffected by intravenous hexamethonium chloide (10 mg kg-1), and was unchanged (1.0 mg kg-1) or slightly slowed (2.0 mg kg-1) by the beta-receptor blocker propranolol. In contrast, acid test meals were emptied at the same rate as water when treated with intravenous guanethidine monosulfate (2 mg kg-1) or intramuscular reserpine (1 mg kg-1), indicating that the acid inhibition was mediated by an adrenergic mechanism. The emptying of water meals was unchanged by these two drugs. The authors suggest that the first 5 cm of duodenum contain receptors for inhibition of emptying of acid but not for fat or hypertonic glucose. Furthermore, the neural blocking studies indicate that the inhibitory effect of acid in the first part of the duodenum is an adrenergic mechanism which appears to be neither alpha nor beta-receptor-mediated.

Animals↗
PubMed1975

Arthropod-borne viral infections of man in Nigeria, 1964-1970.

During the years 1964 to 1970, 171 arboviruses of 15 different types were isolated from humans in Nigeria. Isolation rates were highest in 1969, and lowest in 1965 and 1967. Monthly arbovirus activity was highest in the rainy season months of June, July and August and lowest in the dry months of January and February. Viruses were isolated from all age groups, with the majority from children one to four years old. The viruses isolated in largest numbers were chikungunya and yellow fever, which caused epidemics in 1969, and dengue types 1 and 2 and Tataguine, which are endemic in Ibadan. Bwamba virus was isolated in 1964 and 1969, and Bunyamwera group viruses were encountered for the first time in 1969. Other viruses recovered less frequently were Zika, Igbo-Ora (an agent related to o'nyong-nyong), two viruses related to the Uganda mosquito virus Ug MP 359, Dugbe, Thogoto, Lebombo and Shuni. Several of these are new agents and have not previously been isolated from man. Clinical details are presented where available.

Adolescent↗
PubMed1975

Effects of essential and nonessential amino acids on gastric emptying in the dog.

Five dogs with gastric fistulas were studied to assess the effect on gastric emptying of two potent cholecystokinin (CCK) releasers (tryptophan and phenylalanine) and six other essential amino acids; the nonessential amino acids alanine, beta-alanine, arginine, asparagine, aspartic acid, citrulline, cysteine, cystine, glutamic acid, glutamine, D-glutamine, histidine, hydroxyproline, ornithine, proline, serine, tyrosine, and D-tryptophan; four peptide and amino acid preparations; and solutions of glucose, glycine, and mannitol. Of the essential amino acids, only tryptophan significantly slowed emptying and it was above 4 mM that there was a difference between control and test meal. The delay in response to tryptophan was dose-related and approached maximum at 40 mM; D-tryptophan had no effect at these concentrations. In concentrations up to 80 mM, none of the nonessential amino acids slowed emptying significantly. The four peptide and amino acid preparations in concentrations ranging from 80 to 700 milliosmoles had dose responses identical to those of D-glucose, glycine, and mannitol at similar osmolalities. It is concluded that L-tryptophan is a uniquely potent delayer of gastric emptying in the dog which is dose-dependent and stereospecific. Phenylalanine, a potent CCK releaser, did not slow emptying, which suggests that CCK release may not be the only mechanism by which tryptophan acts. The peptide and amino acid preparations (casein hydrolysate, Bacto-peptone, Amigen, FreAmine) seem to delay emptying by stimulation of osmoreceptors which is distinct from the mechanism of action of tryptophan.

Amino Acids↗
PubMed1975

Aspirin revisited.

ASA is a safe drug to relieve pain, lessen fever, diminish the inflammatory reaction and treat arthritis. This drug can be given to people in a very safe soluble and buffered form which minimizes its major potential side effect: G.I. bleeding. The G.I. bleeding seen with ASA is due to its local effect on the gastric mucosa. The evidence that exists shows that ASA's effect upon the platelet does not contribute to the gastric bleeding. It is unclear to what extent those diseases mediated by thrombosis can be prevented by ASA and other platelet-suppressive drugs. Thrombosis is not equivalent to hemostasis, but is a distortion of the hemostatic process. Clinical trials are now underway but they will probably be inconclusive. Presently, the literature is contradictory and, therefore, the decision to use ASA as an anti-thrombotic durg remains with the individual physician.

Animals↗