Search PubMed⌕ Search

Biomedical subjects

M I Grossman

Publications and source records attributed to M I Grossman.

At least 37 records · Page 2Linked to original sources
PubMed1981

Gastric acid and gastrin response to decaffeinated coffee and a peptone meal.

We compared five graded doses of decaffeinated coffee and a widely used protein test meal (Bacto-peptone) as stimulants of acid secretion (intragastric titration) and gastrin release (radioimmunoassay) in eight healthy men. In each subject, for both acid and gastrin, the sums of the responses to all five doses were greater to decaffeinated coffee than to peptone. The mean +/- SE peak acid output in millimoles per hour was 18.5 +/- 2.9 to decaffeinated coffee and 14.7 +/- 2.7 to peptone, representing 70% and 55%, respectively, of the peak acid output to pentagastrin. The mean +/- SEM peak increment over basal rate in serum gastrin in picograms per milliliter was 84.8 +/- 4.4 to decaffeinated coffee and 44.8 +/- 2.1 to peptone. At equal concentrations, decaffeinated coffee was a more potent stimulant of acid secretion and of gastrin release than peptone. The ingredient(s) of decaffeinated coffee that accounts for its high potency in stimulating acid secretion and gastrin release has not been identified.

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

A therapeutic trial of 15 (R)-15-methyl prostaglandin E2 in rheumatoid arthritis patients with gastroduodenal lesions.

Thirteen patients who had rheumatoid arthritis and gastroduodenal lesion (erosions, ulcers) received 200 micrograms/d of 15(R)-15-methyl prostaglandin E2 (MPGE2) for one month in a controlled, randomized, double-blind crossover study. The patients continued their usual arthritis medications. Serial assessments were made with endoscopy and multiple antral biopsies. Seven patients improved on MPGE2 and 3 improved on placebo. Two patients worsened on MPGE2 compared with 3 on placebo. No dramatic benefit was observed after one month of therapy with MPGE2, although a moderate benefit could have been missed in a small study of this type. Our experience with this study suggests that future studies in rheumatoid arthritis should first establish the natural history of lesions in a given group of patients, that a cross-over design may actually hamper interpretation and that therapy should be more prolonged.

Adult↗
PubMed1981

Effect of atropine on pancreatic response to HCl and secretin.

In dogs with gastric and pancreatic fistulas, we studied the effect of atropine on the pancreatic secretory response to secretin and intestinal HCl. Atropine sulfate (20 micrograms.kg-1.h-1 iv) significantly depressed basal bicarbonate and protein output. Atropine depressed bicarbonate responses to low doses (62.5, 125, 250, and 500 ng.kg-1.h-1) of secretin but had no significant effect on responses to high doses (1,000 and 2,000 ng.kg-1.h-1). Secretin, with or without atropine, did not stimulate pancreatic protein output above basal. Atropine depressed bicarbonate responses to low loads (3, 6, and 12 mmol.h-1) of HCl but had no significant effect on responses to high loads (12, 24, and 48 mmol.h-1). Intraduodenal HCl produced a dose-dependent increase in protein output. Atropine abolished protein responses to low loads (3 and 6 mmol.h-1) but did not affect responses to high loads (24 and 48 mmol.h-1) of HCl. These findings are compatible with the hypotheses that a) endogenous cholinergic activity augments the pancreatic bicarbonate response to secretin, and b) the pancreatic protein response to intraduodenal HCl is, at least in part, mediated cholinergically.

Animals↗
PubMed1981

Effect of adding albumin to solutions of secretin on pancreatic volume and bicarbonate response.

In six conscious dogs with gastric and pancreatic Thomas fistulas, we studied the pancreatic bicarbonate response to intravenous bolus injections of synthetic secretin dissolved either in 5 ml of 0.15 M NaCl alone or in the same amount of NaCl to which dog albumin had been added, to give a 0.1% solution. The pancreatic bicarbonate (micromol . 10 min-1) response to the four lowest doses of secretin (12.5, 25, 50, 100 ng . kg-1) used was significantly (p less than 0.05) higher when secretin was dissolved in NaCl plus albumin than in NaCl alone. The pancreatic response to higher doses of secretin (200, 400, 800, 1600 ng . kg-1) was not significantly altered by the addition of albumin. The D50 of secretin was about 2.6 times greater in the absence than in the presence of albumin. This study suggests that albumin should be added to dilute solutions of secretin to preserve biological activity.

Albumins↗
PubMed1981

Peptic ulcer: new therapies, new diseases.

Although hospitalizations and deaths attributable to peptic ulcer have decreased notably during the past decade, it is not certain whether this decrease is because of reduced incidence of new cases or changes in other factors, such as the severity of the disease. Several genetic traits associated with peptic ulcer have been recognized. Hyperpepsinogenemia I is the most prevalent. Peptic ulcer is a heterogeneous group of disorders with multiple genetic and environmental causes. One manifestation of the diversity of ulcer disease is the variety of physiologic abnormalities seen in patients. The use of endoscopy has enabled more reliable evaluation of new treatments. Histamine H2-receptor antagonists are the dominant mode of treatment, but increasing attention is being given to agents that enhance the resistance of the mucosa to injury, such as prostaglandins. Because of the lower frequency of side effects, proximal gastric vagotomy is gradually replacing truncal vagotomy with drainage. The possibility that endoscopic treatments, such as laser coagulation, may reduce mortality from bleeding ulcers is being investigated.

Duodenal Ulcer↗
PubMed1980

Comparison of human urine gastric inhibitor (HUGI) and bacterial endotoxin as inhibitors of acid secretion.

In conscious cats with gastric fistulas, 10 micrograms . kg-1 of human urinary gastric inhibitor (HUGI) given as an intravenous bolus injection increased mean rectal temperature 1.4 degree C and inhibited mean gastrin-stimulated acid secretion by 64%. The sample of HUGI contained an amount of beta-hydroxymyristic acid corresponding to a 5% contamination of the HUGI with bacterial endotoxin. Injection of bacterial endotoxin in an amount corresponding to the beta-hydroxymyritic acid content of HUGI mimicked, both in magnitude and time course, the increase in body temperature and the inhibition of acid secretion produced by HUGI. We conclude that inhibition of acid secretion by HUGI may be due to the presence of an endotoxin-like contaminant.

Animals↗
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

Physiological abnormalities in duodenal ulcer: a brief review.

Patients with duodenal ulcer may have one or more of the following abnormalities: (1) larger than normal volume of gastric mucosa containing correspondingly more acid and pepsin secreting cells which is reflected in (2) increased mean concentration of pepsinogen-I in plasma, and (3) increased maximal rates of secretion of acid and pepsin in response to stimuli such as histamine, gastrin, insulin, or food; (4) increased sensitivy to stimulation by gastrin as reflected by decreased dose of gastrin needed to evoke half maximal response; (5) increased gastrin response to meals; (6) decreased inhibition of gastrin release and of acid secretion in response to acidification of the gastric contents; and (7) increased rapidity of gastric emptying. Items 2, 5, and 7 are heritable autosomal dominant traits in at least some patients. Although mean values of each of these 7 items are significantly different from normal, the range is wide and most individual duodenal ulcer patients fall within the normal range. The diversity of physiological abnormalities found in patients with duodenal ulcer shows that it is a heterogeneous disease with many different factors operating in its pathogenesis.

Duodenal Ulcer↗
PubMed1980

Effect of atropine on secretion from intact and transplanted pancreas in dog.

In dogs with a fistula of the intact pancreas and a transplanted portion of pancreas, we studied the effect of atropine on the pancreatic secretory response to intravenous caerulein and to intestinal perfusion with tryptophan, both given with a secretin background. Atropine (50 micrograms . kg-1 given as an intravenous bolus injection followed by 20 micrograms . kg-1 . h-1 iv infusion) depressed bicarbonate and protein secretion from intact pancreas during stimulation by secretin alone (250 ng . kg-1 . h-1) but did not suppress the increment in bicarbonate secretion in response to caerulein or tryptophan given against the secretin background. In intact pancreas, atropine suppressed protein secretion in response to tryptophan but not in response to caerulein. Atropine had no significant effect on the secretion of bicarbonate and protein from transplanted pancreas in response to secretin, caerulein, or tryptophan. Thus, the only significant effect of atropine on bicarbonate and protein secretion from intact and transplanted pancreas in response to intravenous caerulein or intraduodenal tryptophan, both given against a background of secretin, was inhibition of the protein response to tryptophan in the intact pancreas. These findings are compatible with the hypothesis that pancreatic protein secretion in response to intraduodenal tryptophan is mediated in part by a cholinergic enteropancreatic reflex.

Animals↗
PubMed1980

Latency of pancreatic enzyme response to intraduodenal stimulants.

In six dogs with pancreatic fistulas, secretin (500 ng . kg-1 . h-1) was given to provide a flow of pancreatic juice of about 1 drop/s. Amylase concentration was measured in each drop before and after rapid intraduodenal injection of L-tryptophan, sodium oleate, and NaCl or after rapid intraportal injection of cholecystokinin (CCK). Latency of response (time between injection and a sustained increase in amylase output greater than the mean + 3 SD of prestimulation output) was 0.30 min to tryptophan and 0.33 min to oleate. These were significantly (P less than 0.01) less than the latency to intraportal CCK (0.53 min). Atropine and truncal vagotomy increased the latency to tryptophan and oleate 10-fold but had no effect on the latency to intraportal CCK. We conclude that, since the latency of amylase response to intraduodenal stimulants was shorter than to intraportal CCK, the initial response is probably not due to release of hormones. The finding that atropine and vagotomy increased latency of response to intraduodenal stimulants indicates that a vagovagal cholinergic reflex mediates the early pancreatic enzyme response to intestinal stimulants.

Amylases↗
PubMed1980

Intravenous indomethacin and aspirin reduce basal gastric mucosal blood flow in dogs.

The effect of two known inhibitors of prostaglandin synthesis, indomethacin and aspirin, on blood flow was studied in six Heidenhain pouch and three antral pouch dogs. The unstimulated gastric mucosa was bathed with 0.15 M HCl and clearance of [14C]-aminopyrine was used as an index of changes in mucosal blood flow. [14C]aminopyrine clearance was measured during three 15-min predrug periods and five 15 min-postdrug periods. Either indomethacin (10 mg . kg-1), aspirin (100 mg . kg-1), or 0.15 M NaCl were given intravenously as a bolus. Indomethacin reduced mucosal blood flow in the Heidenhain pouch 52% (P less than 0.05) and in the antral pouch 52% (P less than 0.05). Aspirin reduced Heidenhain pouch mucosal blood flow 31% (P less than 0.05). Indomethacin caused no significant change in electrical potential difference or in net flux of H+ or Na+ in Heidenhain pouches. Indomethacin (10 mg . kg-1 iv) produced no change in mean arterial pressure. We conclude that indomethacin and aspirin reduce unstimulated gastric mucosal blood flow, suggesting that endogenous prostaglandin may contribute to its maintenance.

Animals↗
PubMed1980

Effects of gastrointestinal polypeptides on hormone content of endocrine pancreas in the rat.

Although trophic actions of gastrointestinal peptides on exocrine pancreas have been shown, little is known regarding their effects in endocrine pancreas. Therefore, we measured the contents of somatostatin-like immunoreactivity (SLI), insulin and glucagon, in pancreatic extracts from rats that had been treated three times a day for 10 days with saline; 1 microgram/kg caerulein; 5, 25, and 100 microgram/kg secretin; 1 microgram/kg caerulein plus 5, 25, and 100 microgram/kg secretin; 25 microgram/kg pancreatic polypeptide; 15 microgram/kg glicentin; or 15 microgram/kg gastric-inhibitory polypeptide. Pancreatic SLI content was significantly increased in rats treated with glicentin and caerulein plus secretin at the two higher doses. No difference was noted between the control and the caerulein plus 100 microgram/kg secretin groups in delta-cell number per islet when examined by the immunoperoxidase technique. These data suggest that because of their effect on SLI content gastrointestinal polypeptides may modulate pancreatic endocrine function.

Animals↗