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Biomedical subjects

V Maxwell

Publications and source records attributed to V Maxwell.

34 records · Page 2Linked to original sources
PubMed1984

Similar acid stimulatory potencies of synthetic human big and little gastrins in man.

A newly synthesized human big gastrin (G34) that was prepared according to the revised structure and that contained less than 3% oxidized methionine residues was compared with synthetic human little gastrin (G17) for acid-stimulating activity and clearance in human subjects. Prolonged infusions of each type of gastrin revealed that the time required to approach stable plasma concentrations was much longer for G34 than for G17. The time course of plasma gastrin concentration could be described by one-compartment models with half-lives of 44 min for G34 and 8 min for G17. After rapid intravenous infusion, G34 produced a much larger total acid response than did an equimolar dose of G17, and the responses were directly proportional to the integrated plasma gastrin increments. During the third hour of prolonged intravenous infusions of G34 and G17, the exogenous dosage of G34 required to produce the same blood concentration of gastrin was only one-fourth that of G17. Equivalent blood concentrations of G34 and G17 were associated with similar rates of acid secretion. These results suggest that G34 is more potent than has been thought, that it has an activity similar to that of G17 and that it must not be ignored in estimating total acid-stimulating activity of circulating gastrins. The measurement of total carboxyl-terminal immunoreactive gastrin can produce a good estimate of total acid-stimulating activity.

Adult↗
PubMed1983

Effects of graded amounts of intragastric calcium on acid secretion, gastrin release, and gastric emptying in normal and duodenal ulcer subjects.

We studied effects of graded concentrations of intragastric calcium on acid secretion, residual gastric volume, and serum gastrin and calcium levels. Intragastric titration was performed with solutions of isotonic mannitol or mannitol plus 2.5, 6, 16, 39, and 97 mM CaCl(2) in 10 normal and eight duodenal ulcer subjects. Acid secretion was significantly increased above control values by the two highest CaCl2 concentrations in normal subjects and by the three highest CaCl2 concentrations in ulcer subjects. Highest observed acid output to any concentration of CaCl2 was 55% of peak acid output to pentagastrin in normal subjects and 75% in ulcer subjects. Intragastric calcium also released gastrin; correlation between acid secretion and circulating gastrin was weak (r = 0.43, P less than 0.05). Serum calcium was slightly increased but did not correlate with acid secretion. Residual intragastric volume after both control and CaCl2 solutions was much less in ulcer than in normal subjects; calcium did not alter residual volumes.

Adult↗
PubMed1981

Failure of gastric inhibitory polypeptide to inhibit pentagastrin-stimulated acid secretion in vagotomized human subjects.

Five vagotomized male subjects were given graded doses of pentagastrin without and with a background infusion of 2 microgram/kg/hr of gastric inhibitory polypeptide (GIP). An insulin infusion test (0.1 units/kg/hr) showed that the vagotomies were complete. GIP infusion failed to inhibit pentagastrin-stimulated acid and pepsin secretion even though plasma GIP concentration reached a plateau much higher than that measured after ingestion of a meal. We conclude that GIP does not inhibit pentagastrin-stimulated gastric acid secretion in vagotomized human subjects.

Adult↗
PubMed1981

Bombesin stimulates human gastric function by gastrin-dependent and independent mechanisms.

Studies were performed in six men to determine the relationship between serum gastrin concentration and gastric function during exogenous and endogenous stimulation of gastrin release. When the intragastric pH was maintained at 5.0, there were dose-related increases in gastric acid secretion with increasing serum gastrin concentrations produced either by stepwise increasing doses of intravenous gastrin or bombesin, or by intragastric perfusion with peptone. When intragastric pH was maintained at 2.5, or when intravenous atropine was given hourly, sensitivity to both exogenous and endogenously released gastrin were similarly decreased. Gastric emptying was inhibited in a dose-dependent manner by both bombesin and peptone but not by exogenous gastrin. These results suggest that bombesin and peptone stimulate gastric acid secretion through release of circulating gastrin but inhibit gastric emptying by another mechanism.

Adult↗
PubMed1980

Effect of gastric inhibitory polypeptide on pentagastrin-stimulated acid secretion in man.

Eight male subjects were given pentagastrin by intravenous infusion in doses of 25, 74, 222, 667, and 2000 ng/kg/hr, each dose for 30 min. On another day the same subjects were given the same doses of pentagastrin while gastric inhibitory polypeptide (GIP) was being infused intravenously in a dose of 2 microgram/kg/hr. At the 222 ng/kg/hr dose of pentagastrin, acid output was significantly lower with GIP; at all other doses of pentagastrin, acid output did not differ significantly in tests with and without GIP. Pepsin output in the tests with and without GIP did not differ significantly at any dose of pentagastrin. Plasma concentration of GIP, measured by radioimmunoassay, showed a mean +/- SE plateau level of 7.4 +/- 1.4 ng/ml during GIP infusion and 0.4 +/- 0.1 ng/ml peak level after a standard meal. We conclude that the increase in blood concentration of GIP produced by feeding is probably inadequate to cause significant inhibition of gastric acid or pepsin secretion in man.

Adult↗
PubMed1980

Effect of intravenous lipid on gastric acid secretion stimulated by intravenous amino acids.

Intraduodenal fat is a potent inhibitor of all forms of gastric acid secretion in humans. Studies were performed in random order on 3 separate days in 5 normal subjects to determine if intravenous fat (Intralipid) altered gastric acid secretion stimulated by intravenous amino acids in humans. Mean (+/- SE) gastric acid output during a 4-hr intravenous amino acid infusion (21 g L-amino acids; Freamine II) plus glucose (50 g. to maintain isocaloric and isoosmolar solutions) was 43.2 +/- 3.2 meq/4 hr. Intraduodenal fat fusion (20 g of Intralipid) significantly (P < 0.02) suppressed amino acid-stimulated acid output. Interestingly, intravenous fat (20 g of Intralipid) also significantly (P < 0.02) inhibited acid secretion (14.8 +/- 6.3 meq/4 hr); similar to the effect observed with intraduodenal fat (12.7 +/- 4.9 meq/4 hr). Serum levels of CCK, gastrin, and GIP were measured at 30-min intervals throughout each study. Cholecystokinin and GIP increased significantly from basal during intraduodenal fat infusion. There were no other changes in serum CCK, gastrin, or GIP during any of the other tests. It is concluded that in normal subjects intravenous fat is a potent inhibitor of intraveous amino acid-stimulated gastric acid secretion, similar in effect to intraduodenal fat. The inhibitory effect of intravenous fat on amino acid-stimulated gastric acid secretion is probably not mediated by release of either CCK of GIP. Circulating fat may play a role in the control of some forms of gastric acid secretion.

Adult↗
PubMed1978

The natural antibody response to E. coli includes antibodies of the IgD class.

Antibodies to E. coli of the IgM, IgG and IgA class are readily demonstrable in normal human serum. Using the sensitive red cell-linked antigen-antiglobulin system, it has been demonstrated that antibodies of the IgD class are also part of this normal response. The IgD antibody titre is low and often could only be demonstrated in partially purified IgD preparations. The availability of purified IgD paraproteins and their Fabdelta and Fcdelta fragments, as well as antisera specific for these fragments, allowed the necessary critical specificity controls to be performed.

Antibodies, Bacterial↗
PubMed1976

Clearance and acid-stimulating action of human big and little gastrins in duodenal ulcer subjects.

Acid-stimulating action and clearance of pure natural human big gastriin (HG-34-I) and little gastrin (HG-17-I) were assessed in four male subjects with inactive duodenal ulcer (DU) disease. Disappearance half-times for HG-17-I after intravenous infusion (5.2 min) or rapid intravenous injection (6.4 min) were six to eight times shorter than those for HG-34-I (41.5 and 37.8 min, respectively). Studies of clearance of synthetic human little gastrin (HG-17-I) were performed in three of these same four DU subjects, eight additional male DU subjects, and eleven normal male subjects. The disappearance halftime of synthetic HG-17-I averaged 6.2 min in both the DU subjects and the normal subjects. These data suggest that clearance of exogenous gastrin is not altered in patients with DU. Acid secretion in response to rapid intravenous injection of HG-34-I reached a higher peak and lasted longer than in response to an equimolar dose of HG-17-I; the total response to HG-34-I was about three times that to HG-17-I. During constant intravenous infusion, acid responses to equimolar exogenous doses of the two peptides were similar but the increment in molar concentration of circulating gastrin was six to eight times greater with HG-34-I than with HG-17-I. Chromatography of serum obtained during infusions of HG-34-I revealed no evidence of conversion to HG-17-I, nor was there any increase in circulating G-34 activity during infusions of HG-17-I. The increment in serum gastrin concentration required to produce half-maximal stimulation of gastric acid secretion (D50) was estimated in each subject for each gastrin from curves relating acid secretion to change in serum gastrin concentration produced by infusion of these peptides. After instilling peptone solution into the stomach, acid secretion was measured by intragastric titration, and increases in circulating G-17 and G-34 were determined by chromatography and radioimmunoassay of serum. Increases in circulating G-17 and G-34 in response to the peptone meal, taken together, were equivalent to 1.5 times the D50 determined from infusions of G-34 and G-17. Acid secretion during the same time period averaged 55% of maximal rates. Although G-34 comprised approximately three-fourths of the total molar concentration of circulating gastrin after stimulation, it was estimated to contribute less than half of the acid-stimulating activity.

Dose-Response Relationship, Drug↗
PubMed1976

The effect of various forms of milk on gastric-acid secretion. Studies in patients with duodenal ulcer and normal subjects.

Milk is commonly recommended as therapy for patients with peptic ulcer. The purpose of this study was to examine the effect of various forms of milk and 0.15 M NaCl (control) on gastric-acid secretion in five patients with duodenal ulcer during a period of remission and in five normal subjects. A significant (P less than 0.05) increase in acid secretion in both groups was produced by 240 ml of whole, low-fat, and nonfat milk. The acid secretory responses to milk were equivalent to approximately 20% to 35% of maximal betazole - or pentagastrin-stimulated acid output. Gastric-acid secretion produced a significant (P less than 0.05) increase in acid secretion in the patients with duodenal ulcer but not in the normal subjects. Because milk contains both protein and calcium, and each are stimulants of gastric-acid secretion, there is reason to question its frequent ingestion by patients with peptic ulcer.

Animals↗
PubMed1976

The effect of 16,16-dimethyl prostaglandin E2 on meal-stimulated gastric acid secretion and serum gastrin in duodenal ulcer patients.

The effect of intragastric and intraduodenal 16,16-dimethyl prostaglandin E2 (dm PGE2) on meal-stimulated gastric acid secretion and gastrin release was studied in patients with inactive duodenal ulcer. Compared to placebo, doses of 0.75, 1.00, 1.33, and 1.77 mug per kg of dm PGE2 instilled into the stomach inhibited meal-stimulated gastric acid secretion by 61 to 94% (P less than 0.01). The 1.00, 1.33, and 1.77 mug per kg doses inhibited acid secretion significantly (P less than 0.05) more than an optimal dose of propantheline bromide. Intragastric dm PGE2 (1 mug per kg) was significantly (P less than 0.05) more effective than intraduodenal dm PGE2 (1 mug per kg) in inhibiting both gastric acid secretion and gastrin release. After 1.33 and 1.77 mug per kg, some patients experienced abdominal cramps, or diarrhea, or both, but at doses of 1.00 mug per kg or less no apparent untoward side effects were observed. It is concluded that 16,16-dm PGE2 significantly inhibits meal-stimulated gastric acid secretion and gastrin release, and may be of therapeutic value in patients with peptic ulcer provided it is free of untoward side-effects with chronic administration.

Duodenal Ulcer↗
PubMed1975

Inhibition of gastric acid secretion by cimetidine in patients with duodenal ulcer.

Cimetidine, a non-thiourea-containing H2-receptor antagonist, was studied in seven patients with duodenal ulcer. Oral doses of 100, 200, and 300 mg were tested. Each dose significantly inhibited basal and meal-stimulated secretion. After 300 mg, basal acid secretion was essentially zero for at least five hours. The meal-stimulated three-hour acid output after the 300-mg dose was reduced by 67%. Cimetidine, 300 mg, decreased meal-stimulated acid secretion significantly more than an optimal effective dose of propantheline bromide (P less than 0.05). Inhibition of meal-stimualted gastric acid secretion showed a significant relation to peak blood cimetidine concentration (r is equal to 0.76, P less than 0.01). Cimetidine did not affect meal-stimulated gastrin release. No toxicity was observed after serial doses given during these tests. Cimetidine may be useful in treatment of acid-peptic diseases provided no important toxicity appears on chronic testing.

Administration, Oral↗
PubMed1975

Increased sensitivity to stimulation of acid secretion by pentagastrin in duodenal ulcer.

The effect of graded doses of pentagastrin (2.7-6,000 ng/kg times h) on gastric acid secretion was measured in 20 duodenal ulcer (DU) and 20 non-DU subjects. Confirming many previous studies, the mean observed highest response and the mean calculated maximal response were significantly greater in DU than in non-DU subjects. The mean dose (plus or minus SE) in ng/kg times h for half maximal response, calculated from responses corrected for basal secretion and normalized for maximal secretion, was 92.1 plus or minus 1.7 in DU and 246.8 plus or minus 24.6 in non-DU subjects, a significant difference. By parallel line bioassay non-DU subjects required 2.8 times more pentagastrin (95% confidence limits 2.1-3.7) than DU highest response. Thus, this study shows that, compared with non-DU subjects, DU patients not only secrete more acid in response to stimulation by pentagastrin but also are more sensitive to stimulation by pentagastrin, that is, need smaller doses to achieve the same fraction of maximal response.

Adult↗