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Biomedical subjects

E L Blair

Publications and source records attributed to E L Blair.

At least 19 recordsLinked to original sources
PubMed1980

A systems model for burn care.

The problem of projecting the number of tertiary service beds needed by a population is materially different for rare events than for medical events of more common occurrence. Demand for inpatient burn treatment services has been carefully measured in 57 countries in New York State. A survey provided data describing the rate of ocurrence, severity, and average length of stay for 5,791 hospitalized burn patients. Existing planning formulae which were designed for events of common occurrence were found to project conditions of overflow and underutilization incompletely when applied to regional burn units. Objective planning models designed specifically for intensive burn care were therefore developed. These models show that there is no number of intensive care burn beds which will provide both reasonably high occupancy and reasonable assurance of meeting the normally erratic demand of a small system. Conditions of overload and underutilization are inevitable and therefore planning efforts should be directed at minimizing these impacts. If all of the regional burn treatment facilities are regarded as components of a well-integrated statewide system, a much more effective efficient and economic service will result.

Burns↗
PubMed1980

Gastric acid and pepsin-stimulating activity of non-sulphated fragments of gastrin in the cat.

The gastric acid and pepsin-stimulating activities of several C terminal fragments of non-sulphated human gastrin were investigated in the conscious cat prepared with cannulated gastric fistulae with a reproducible, continuous infusion method to construct dose-response curves. The gastric acid-stimulating activities were quantified by reference to the ED50 and were compared with the activity of synthetic non-sulphated human gastrin 17 (SHG17NS) and cat gastrin 17 (SCG17NS). SHG17NS had an ED50 of 0.329 nmol kg-1 h-1. SHG16NS, SHG15NS and SHG13NS all showed similar activities to SHG17NS. SCG17NS tested at low doses had similar activity to SHG17NS. SHG10NS, G5 and G4 and peptavlon showed progressively lower acid-stimulating activities: 26, 12, 9 and 9%, respectively, compared with SHG17NS. The gastric acid-stimulating activities of all the peptides were paralleled by similar pepsin-stimulating activities. The ratios of pepsin secretion:acid secretion were similar for all the peptides (1--2 microgram pepsin/microEq H+). The results are discussed in relation to the biological activity of the circulating gastrin components in the cat compared with other species and it is argued that component IV (corresponding to gastrin tetradecapeptide or minigastrin) is a major, physiologically active, circulating form of the hormone in the cat.

Animals↗
PubMed1979

The effect of stimulation by meat on gastrins in pyloric antral mucosa of anaesthetized cats.

Chloralose anaesthetized cats were prepared with fundic and antral pouches. After stimulation with meat extract suspension in the antral pouches, the antral mucosae were collected, homogenized and subjected to subcellular fractionation to produce whole homogenates, debris, mitochondrial, granule and microsomal fractions and the cell supernatant. Total gastrin concentration and the quantities of gastrin components were measured in these cell fractions and compared with values obtained from a group of control animals which were not stimulated. Stimulation significantly increased the concentration of total gastrin in whole homogenates and in the cell supernatant. In whole homogenates the concentrations of gastrin components I, II, III and void volume gastrin all increased significantly after stimulation. In granules the concentration of Component III significantly increased. In microsomes the concentration of Componenet IV increased significantly. In cell supernatant the total amounts of Components III and IV increased significantly. It is concluded there was synthesis of gastrin under the experimental conditions used. The concentrations of those gastrin components which are larger than the predominant storage form (Component III) are increased and these larger components may be biosynthetic precursors. The significant increase in Component IV concentration in the cell supernatant and microsomes may suggest that Component IV is formed at least in part by antral tissue as well as by the known conversion process which occurs in cat blood.

Animals↗
PubMed1978

The effect of anaesthesia on pentagastrin stimulated gastric acid secretion in the cat.

1. The effect of Saffan (alphaxalone and alphadolone acetate) and Nembutal (pentobarbitone) anaesthesia on gastric acid secretion stimulated by I.V. bolus injections of pentagastrin was investigated in the gastric fistula cat. The effect of Saffan anaesthesia was also tested on I.V. near-maximal and sub-maximal infusions of pentagastrin. 2. Neither anaesthetic reduced the acid secreted in response to bolus injections of pentagastrin. Increased acid secretion with the anaesthetic was noted at some doses of pentagastrin in both intact and vagotomized animals. 3. Saffan anaesthesia had no effect on near-maximal gastric acid secretion stimulated by pentagastrin 8 microgram kg-1 hr-1 but increased the response to pentagastrin 1 microgram kg-1 hr-1. 4. It is suggested that the differences in the acid secretory responses of the anaesthetized acutely prepared animal compared with the conscious animal are a consequence of the surgical procedures rather than the state of consciousness.

Alfaxalone Alfadolone Mixture↗
PubMed1977

Comparison of vagal and meat stimulation on gastric acid secretion and serum gastrin.

The gastric acid secreted per unit of serum gastrin concentration or per unit of gastrin delivered to the gastric mucosa was significantly greater during electrical vagal stimulation than during stimulation by meat extract in the pyloric antrum. There was no significant difference in the concentrations of big, big gastrin or Components I and II in gastric venous serum during the two forms of stimulation. There were significantly greater concentrations of Components II and IV in gastric venous serum during meat extract stimulation than during vagal stimulation. The gastrin in gastric venous serum when meat extract was in the pyloric antrum was comprised of Component IV in addition to Component III whereas gastrin in extracts of cat antral mucosa was predominantly Component III. Gastric acid secretion in response to vagal stimulation was greater than can be accounted for by the action of gastrin alone and cannot be explained by differences in the known gastrin variants in the circulation during the two forms of stimulation.

Animals↗
PubMed1977

The effects of somatostatin and metiamide on tachyphylaxis of pentagastrin stimulated gastric acid and pepsin secretion in the conscious cat.

1. Pentagastrin stimulated gastric acid and pepsin secretions show parallel rates of tachyphylaxis in the conscious cat. The responses to histamine show only slight tachyphylaxis. 2. Somatostatin 10 microng.kg(-1).hr(-1) inhibits pentagastrin but not histamine stimulated acid secretion and inhibits pentagastrin stimulated pepsin secretion. 3. The inhibition of pentagastrin stimulated acid and pepsin secretion by Somatostatin delays the tachyphylaxis of these responses, but the rates of tachyphylaxis when they do subsequently occur are identical. 4. Metiamide 10 mg-kg(-1)-hr(-1) equally inhibits histamine and pentagastrin stimulated acid secretion but does not inhibit pentagastrin stimulated pepsin secretion. 5. Inhibiton of acid secretion during metiamide infusion neither prevents nor delays acid nor pepsin tachyphylaxis. 6. It is suggested that tachyphylaxis of acid and pepsin secretion is a gastrin receptor phenomenon and that Somatostatin occupies or modifies the behaviour of these receptors, preventing tachyphylaxis. Metiamide, however, exerts its action only on the histmine H2-receptor and not the gastrin receptor mechanism, and this apparently does not prevent or delay acid tachyphylaxis.

Animals↗
PubMed1977

Comparison of the effect of somatostatin on gastrointestinal function in the conscious and anaesthetized cat and on the isolated cat pancreas.

1. Somatostatin, 10 microgram kg-1 hr-1, inhibited gastric acid and pepsin secretion stimulated by pentagastrin, 8 microgram kg-1 hr-1, in conscious and anaesthetized cats with chronically implanted gastric fistulae. In the acutely surgically prepared anaesthetized cat, Somatostatin inhibited pepsin secretion but produced little inhibition of gastric acid secretion or mucosal blood flow. 2. Secretin stimulated pancreatic juice volume was not significantly reduced in acutely prepared anaesthetized cats, but there was a limited reduction of cholecystokinin-pancreozymin stimulated pancreatic amylase secretion and gall bladder contraction. 3. Somatostatin had neither stimulatory nor inhibitory effects on electrolyte and amylase secretion in the isolated saline-perfused cat pancreas. 4. The results suggest that some of the effects of Somatostatin may depend on the interaction on the target cell of other factors, nervous or humoral which may vary in different experimental preparations.

Amylases↗
PubMed1977

A possible origin of circulating gastrin component IV in cats.

1. Blood circulating in the cat is known to contain relatively large concentrations of gastrin components corresponding to Rehfeld's Components III and IV, whereas human blood has mostly Components II and III. 2. Synthetic cat gastrin 17NS was continuously injected into chloralose anaesthetized cats and at 1, 10 and 40 min after the start of injection there were significantly greater concentrations of immunoreactive gastrin Component IV than Component III in arterial blood (P less than 0.025 in each case). These concentrations were also greater than the total arterial gastrin concentration in the basal state. 3. Cat blood with EDTA incubated at 37 degrees C with synthetic cat and natural porcine gastrins 17NS produced Component IV. Hunan blood with EDTA incubated in a similar way with natural and synthetic human gastrins 17NS did not produce any detectable Component IV. Cat blood incubated with natural porcine and synthetic cat gastrin 17NS at 0 degrees C did not produce any Component IV. 4. We conclude that there may be an enzyme or enzymes in cat blood which cause the conversion of gastrin 17NS to Component IV.

Animals↗
PubMed1976

The effect of metramide on the prolonged serum gastrin response to feeding observed in patients with duodenal ulcer.

The response of serum gastrin to a meal has been studied in 11 normal subjects and 16 patients with duodenal ulceration. The mean serum gastrin concentration rises after a meal to similar peak values in both normal subjects and duodenal ulcer patients, and fall to basal values with 3 hours in normal subjects. In duodenal ulcer patients the peak concentration is sustained throughout the 3 hour test period, and this response is not affected by the administration of Metiamide. It is concluded that the control of gastrin release is defective in duodenal ulceration, and this may be due to a failure of the antral pH feedback mechanism. Gastrin may be a primary pathogenetic factor in duodenal ulceration.

Adult↗
PubMed1975

Metiamide in the Zollinger-Ellison syndrome.

The histamine H2-receptor antagonist metiamide is an inhibitor of endogenous and stimulated gastric-acid secretion. It appears to have therapeutic possibilities in duodenal-ulcer disease. Three patients exhibiting the Zollinger-Ellison syndrome have been treated with this drug for six months or more. Rapid symptomatic improvement occurred in each case, followed by ulcer healing. There were also reductions in gastric secretion and consistent changes in the fasting serum-gastrin concentration. On patient relapsed temporarily during therapy. There have been no side effects. It is concluded that, in the short term, metiamide is of benefit in the Zollinger-Ellison syndrome.

Adult↗
PubMed1975

The mechanism whereby growth hormone-release inhibiting hormone (somatostatin) inhibits food stimulated gastric acid secretion in the cat.

Growth hormone-release inhibiting hormone (somatostatin) inhibits the gastric acid response to food in concious cats. We have confirmed that this tetradecapeptide blocks the food stimulated gastrin release. However, the inhibition of gastrin release is delayed relative to that of acid secretion, &howing that the inhibition of food stimulated acid secretion is by primary effect on the acid secretory mechanism. No evidence was found of potentiation of either the gastric acid output or serum concentration of gastric in response to food.

Animals↗