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Biomedical subjects

G L Kauffman

Publications and source records attributed to G L Kauffman.

81 records · Page 5Linked to original sources
PubMed1979

Effects of prostacyclin and a stable analogue, 6-beta-PGI1, on gastric acid secretion, mucosal blood flow, and blood pressure in conscious dogs.

We studied the effect of prostacyclin, PGI2, its chemical decomposition product, 6-oxo-PGF1 alpha, and a stable 5-6-dihydro analogue, 6-beta-PGI1, on gastric acid secretion, mucosal blood flow (14C-aminopyrine clearance), and mean arterial pressure in unanesthetized dogs. During submaximal acid secretion from a gastric fistula induced by intravenous histamine dihydrochloride (20 microgram kg-1 h-1), prostacyclin and its stable analogue, 6-beta-PGI1, reduced acid output with ID50s (dose causing 50% inhibition) of about 0.2 and 3.0 microgram kg-1 min-1 i.v., respectively, whereas 6-oxo-PGF1 alpha was inactive at 100 times the effective dose of prostacyclin. The ratio of mucosal blood flow to acid output remained unchanged during prostacyclin administration and was significantly elevated during 6-beta-PGI1 infusion, suggesting that with both compounds the changes in mucosal blood flow were not the cause of the antisecretory action. For doses causing equivalent antisecretory action, 6-beta-PGI1 lowered systemic arterial blood pressure much less than prostacyclin, indicating selectivity of action. Prostacyclin is unlikely to be a circulating antisecretory agent, but may play a role as a local humoral modulator of secretion and blood flow in the gastric mucosa.

Aminopyrine↗
PubMed1979

Serum gastrin during intestinal phase of acid secretion in dogs.

These studies were designed to determine whether the intestinal phase of gastric acid secretion is accompanied by an increase in serum gastrin concentration. Seven dogs with a gastric fistula and a duodenal fistula prepared so as to allow perfusion into the duodenum without reflux into the stomach were used. Gastric secretion and blood samples for serum gastrin determination were collected during intestinal perfusion with either 0.15 M NaCl or 5% liver extract at 200 ml hr(-1) for 2 hr. The mean +/- SE gastric acid secretory response during the second hour of perfusion with 0.15 M NaCl was 3.1 +/- 1.0% of the maximal acid output (MAO) to histamine, significantly (P less than 0.05) greater than the control value with no intestinal perfusion (0.18 +/- 0.07%). The mean +/- SE response during the second hour of perfusion with 5% liver extract was 7.4 +/- 2.2% of MAO, significantly (P less than 0.05) greater than both control and NaCl perfusion values. There was no significant change in peripheral serum gastrin concentration during the response to perfusion with either NaCl or liver extract. We conclude that, under the conditions of the present study, the intestinal phase of gastric acid secretion was not accompanied by an increase in serum gastrin concentration.

Animals↗
PubMed1978

Prostaglandin and cimetidine inhibit the formation of ulcers produced by parenteral salicylates.

Antral ulcers were produced in unanesthetized rats in 3 hr by simultaneous intravenous administration of acetylsalicylic acid (ASA) and gastric perfusion with 0.15 M HCl. Intravenous infusion of ASA alone or gastric perfusion with HCl alone produced no antral ulcers. Plasma salicylate levels ranged from 250 to 350 microgram ml-1. 16-16 Dimethyl prostaglandin E2 (DMPGE2) (0.04, 0.40, 4.0 microgram kg-1 hr-1) and cimetidine (10, 50 mg kg-1 hr-1) significantly decreased the severity of antral ulcers in a dose-dependent fashion. In a separate group of unanesthetized rats prepared with gastric fistula and pylorus ligation, pepsin output during administration of parenteral ASA and gastric perfusion of HCl was reduced by the highest doses of 16-16 DMPGE2 and cimetidine. However, addition of exogenous pepsin to the HCl perfusate had no effect on the inhibition of ulceration afforded by 16-16 DMPGE2 and cimetidine. We conclude that both 16-16 DMPGE2 and cimetidine protect antral mucosa against injury by parenteral ASA plus topical HCl by some means other than their effect on acid and pepsin output.

Animals↗
PubMed1978

Pacreaticoduodenectomy.

Pancreaticoduodenectomy, the Whipple operation, is a reasonable operation for carcinoma if used in the absence of distant metastases or regional spread to vital structures. It can be performed with an acceptable in-hospital mortality. It is primarily a palliative surgical procedure. Occasionally, a patient will survive more than five years. At times, the operation is fully justified or cannot be avoided for nonmalignant conditions.

Adult↗
PubMed1975

Titration of sodium channels in canine gastric mucosa.

Net Na+ flux from mucosa to lumen, potential difference, and volume and plasma protein outputs were measured in vagally denervated, separated pouches of the dog's oxyntic or pyloric glandular mucosa when the pouches were irrigated with Na+-free solutions whose pH ranged from 1.5 to 12.2. The apparent permeability to Na+(P'Na) was calculated. P'Na is lowest when the mucosa is bathed with acid and increases 2- to 3-fold when the pH is raised to 10. In the range of pH 10.0--11.2 P'Na is greater by an order of magnitude, but volume output is small, and no plasma proteins are shed. When the pH is above 11.2 there is an abrupt increase in P'Na, and the mucosa sheds a large volume of fluid containing plasma proteins. The change effected by raising the pH to the range of 10.0--11.2 occurs within 10 sec, and it is reversible. The change effected by raising the pH above 11.2 also occurs within 10 sec, and it is partly reversible.

Animals↗
PubMed1975

Plasma shedding by the canine oxyntic and pyloric glandular mucosa induced by topical action of acetylcholine. Effect of atropine and physostigmine.

Irrigation of the canine oxyntic or pyloric glandular mucosa in vagally denervated pouches with a solution of acetylcholine causes the mucosa to shed plasma proteins and the potential difference across the mucosa to fall. The response is dose-related with the threshold concentration of acetylcholine bromide ranging from 0.1 to 1 g per 100 ml. Topical application or intravenous injection of atropine prevents both plasma shedding and decline in potential difference. The minimal effective intravenous dose of atropine sulfate is about 0.007 mg per kg. The effect of irrigation with low concentrations of acetylcholine is enchanced by concurrent irrigation with physotigmine. The action of topical acetylcholine is not affected by concurrent irrigation with hexamethonium chloride (0.5 g per 100 ml) or by intravenous injection (5 mg per kg). Topical application of gallamine triethiodide (0.5 g per 100 ml) or d-tubocurarine (0.15 g per 100 ml) does not prevent the effects of acetylcholine in causing plasma shedding. Topical application of succinylcholine chloride (1 g per 100 ml) does not cause plasma shedding or a fall in potential difference.

Acetylcholine↗