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Biomedical subjects

J Hotz

Publications and source records attributed to J Hotz.

At least 73 records · Page 4Linked to original sources
PubMed1986

Gastroparesis after radiation. Successful treatment with carbachol.

Following abdominal radiation, a 16-year-old male developed persistent vomiting, metabolic alkalosis, and cachexia secondary to gastric stasis, atony, and dilatation in the absence of mechanical obstruction. Fluoroscopically and manometrically, antral motility was found to be severely impaired. Antral motor activity was not influenced by metoclopramide, but stimulated by carbachol. During oral maintenance carbachol therapy, gastric emptying of food was restored and sufficient oral nutrition could be resumed. The improvement persisted even after termination of therapy four months later. Systematic investigations on the effects of abdominal radiation on gastrointestinal motility appear to be necessary.

Adolescent↗
PubMed1986

Bile secretion in acute and chronic hypercalcemia in the cat.

The reported coincidence of primary hyperparathyroidism and cholelithiasis led us to investigate the effects of acute and chronic hypercalcemia on bile secretion in cats. Acute hypercalcemia (6-7 mmol/liter) was induced by an intravenous calcium infusion. Chronic hypercalcemia (3-4 mmol/liter) was induced and maintained for 8-10 weeks by treatment with subcutaneous vitamin D3, oral dihydrotachysterol, and feeding a calcium-rich diet. Bile secretion was then studied in acute experiments. We found that calcium concentrations in serum and hepatic bile were similar during all experimental normo- or hypercalcemic conditions (y = 1.12x - 0.85; r = 0.76). Biliary volume outputs were significantly decreased during both acute (P less than 0.002) and chronic (P less than 0.05) hypercalcemia compared with normocalcemic controls. Acute hypercalcemia also decreased total bile acid outputs (P less than 0.05), but had no effect on biliary bile acid concentrations. The inhibitory effect of acute hypercalcemia on biliary fluid and bile acid secretion was dose dependent and not antagonized by atropine. These findings suggest that calcium is secreted in hepatic bile at similar concentrations as present in the serum and that elevations of serum calcium concentration inhibit biliary volume and bile acid secretion in cats. Similar effects of hypercalcemia on bile composition in humans might promote calcium salt precipitation in bile.

Acute Disease↗
PubMed1986

Stimulatory effect of hypercalcemia on pancreatic secretion is prevented by pretreatment with cholecystokinin and cholinergic agonists.

Recently, we demonstrated that hypercalcemia causes marked stimulation of feline exocrine pancreatic secretion, and that this effect is absent when a large dose of cholecystokinin (CCK) is infused prior to induction of hypercalcemia. To investigate this effect in more detail, anesthetized cats were given calcium i.v. after preadministration of CCK or urecholine (a cholinergic agonist) at specific doses, or of saline as a control. We found that the hypercalcemia-induced stimulation of pancreatic protein secretion was abolished after preadministration of CCK at large doses. After the prestimulus dose was decreased or the calcium dose was increased, however, the pancreatic secretory response to hypercalcemia was preserved. In contrast, the response to a submaximal dose of CCK was unchanged after prestimulation with a large dose of CCK. Similar results were obtained when urecholine instead of CCK was used as prestimulus. These findings indicate that loss of pancreatic responsiveness to hypercalcemia following prestimulation with CCK is dependent on doses of both prestimulus and calcium used, and that it is not specific for prestimulation with CCK but also inducible by cholinergic agonists. They further suggest that this phenomenon is not due to exhaustion of pancreatic secretory capacity, but may reflect decreased sensitivity to the hypercalcemic stimulus instead.

Animals↗
PubMed1986

Duodenal calcium in chronic pancreatitis: is it of diagnostic value?

Chronic pancreatitis has been reported to be associated with an increased secretion of calcium in pancreatic juice. To determine whether estimation of duodenal calcium may be useful for diagnosing chronic pancreatitis, we compared duodenal calcium output in patients with chronic pancreatitis and in subjects without pancreatic disease, during intravenous infusion of secretion alone, with calcium, or with cholecystokinin-pancreozymin (CCK-PZ). Duodenal calcium output increased during infusion of both calcium and CCK-PZ to a similar extent in chronic pancreatitis and controls. Overall, duodenal output of chymotrypsin was markedly lower in chronic pancreatitis; however, chymotrypsin output increased in response to both intravenous calcium and CCK-PZ in both groups. Bilirubin output increased in both groups during calcium infusion, but this increase was significantly reduced in chronic pancreatitis; in contrast, CCK-PZ caused a similar increase in both groups. The high calcium output observed in hypercalcemia in the presence of low enzyme output suggests increased pancreatic secretion of enzyme-independent calcium in chronic pancreatitis. However, the difference is obscured by biliary calcium, which is secreted in much higher concentrations. Thus, duodenal calcium determination does not appear to be a useful diagnostic test in chronic pancreatitis.

Bilirubin↗
PubMed1986

Pancreatic exocrine secretion in response to intraduodenal infusion of different detergent agents in anesthetized cats.

Bile salts, when instilled into the intestine at pH 6, stimulate pancreatic exocrine secretion in man and cat. We investigated if the surface tension as a major physicochemical property of bile acids might be responsible for this effect. In anesthetized cats, either conjugated taurocholate (TC) or unconjugated ursodesoxycholate (UDC) as steroidal detergents or oleate as nonsteroidal detergent were perfused into the duodenum. The critical micellar concentration (CMC) and the surface tension (gamma) were as follows: for oleate 18.6 mmol/l and 27.7 dyn . cm-1, for UDC 10.75 mmol/l and 46.5 dyn . cm-1, for TC 14.5 mmol/l and 58.6 dyn . cm-1. The intraduodenal perfusion of the three solutions at 30 mmol/l and pH 8 evoked an equal pancreatic flow (about 300 mg/15 min) and bicarbonate secretion. It is suggested that the free ionized form of TC perfused intraduodenally is responsible for stimulation of the pancreatic exocrine secretion. We show that the stimulatory effect seems to be independent of the detergency of these molecules.

Animals↗
PubMed1986

Bile-stimulated secretin release in cats.

Duodenal perfusion with sodium taurocholate (TC), pH 10.5 (60 mM, made isotonic with NaCl, 30 ml/h for 90 min), increased the plasma immunoreactive secretin level (IRS) from 2.1 +/- 1.0 to 19.1 +/- 6.0 pM (p less than 0.025; n = 6) in anaesthetized cats. Dose-response studies with TC, pH 7.2 (0-60 mM, made isotonic with NaCl, 45 ml/h for 20 min), demonstrated a threshold concentration of TC for IRS release between 10 and 15 mM (p = 0.05; n = 6). Instillation of gallbladder bile from the same animal (1.5 +/- 0.1 ml, pH 7.0 +/- 0.1, over 12 min) increased the IRS concentration from 1.5 +/- 0.4 to 8.1 +/- 3.4 pM (p less than 0.025; n = 6). IRS concentrations also increased when gallbladder bile was mixed with either saline (from 3.4 +/- 1.7 to 11.6 +/- 2.5 pM; p less than 0.05; n = 5) or feline pure pancreatic juice (PPJ) (from 3.1 +/- 0.7 to 5.7 +/- 1.1 pM; p less than 0.025; n = 6). The peak value was significantly lower when bile was mixed with PPJ than with saline (p less than 0.05). We conclude that TC, the dominating bile salt in feline bile, can release IRS also above pH 7, that physiological concentrations of TC can elicit this response, that the response is also produced by gallbladder bile from the same animal, and that PPJ inhibits the bile-induced IRS release. Thus secretin release by bile is likely to be a physiological principle in the regulation of the pancreatic secretion.

Animals↗
PubMed1986

Action of intragastric ethanol on pancreatic exocrine secretion in relation to the interdigestive gastrointestinal motility in humans.

On different days, fasted volunteers were given either 100 ml of ethanol (40% v/v), glucose (isocaloric to ethanol) or distilled water intragastrically; the instillations always starting during the first observed duodenal phase I of the interdigestive migrating complex (IMC). Both ethanol and glucose produced a fed pattern of motility but only glucose significantly (P less than 0.05) delayed the reappearance of a new duodenal phase III of the IMC when compared to water. Ethanol and glucose significantly increased the 1-h duodenal bicarbonate output 7- and 16-fold, respectively. Glucose, but not ethanol, stimulated the duodenal amylase output when compared to water. Glucose, but not ethanol, caused a significant rise in plasma gastrin concentration; plasma secretin levels not being altered by both substances. We conclude that in non-alcoholic humans, an intragastric administration of ethanol in a concentration present in whisky and in an amount that is consumed in ordinary social drinking has a weak stimulatory action on pancreatic bicarbonate secretion and that this action is not mediated by release of secretin.

Adult↗
PubMed1986

Effect of calcitonin on the interdigestive motility and on gastric and pancreatic secretion in humans.

Calcitonin given in doses (0.2 and 1 MRC U/kg-1h-1) reproducing the levels observed in medullary carcinoma of the thyroid, induced the appearance of phase III type activity and reduced the duration of the IMC in the small intestine from 123 to 87 min with 0.2 MRC U kg-1h-1 and from 123 to 43 min with 1 MRC U kg-1h-1 but not in the stomach of young volunteers. This increase in phase III-like activity occurred despite a sharp reduction in motilin levels. Only the highest dose of calcitonin reduced significantly acid secretion (by more than 90%) while both doses reduced amylase secretion by respectively 65 and 71% when compared to the control levels. These changes in motility and secretion could partly explain the diarrhea observed in patients with the medullary carcinoma of the thyroid.

Adolescent↗
PubMed1985

[Therapy of stomach ulcer with low-dose antacid gel and cimetidine. A multicenter double-blind study].

In a multi-centre double-blind (double-dummy) trial the effectiveness of low-dose antacid gel (6 X 12 ml/d; neutralisation capacity 120 mmol) was compared with that of a standard dose of cimetidine (1 g/d) in the curative treatment of gastric ulcer. Antacid gel was given to 65 patients, cimetidine to 60. Diagnosis was confirmed by endoscopic biopsy, which was also employed in a serial follow-up. After 4 weeks antacid gel and cimetidine produced cures in 43% and 52%, respectively; after 8 weeks 76% and 89%, respectively, the difference between the two methods not being statistically significant. There was also no statistically significant difference with regard to ulcer pain. In one case each in the antacid and cimetidine groups, the treatment had to be stopped because of side effects. Diarrhoea was more common on cimetidine than on antacid gel. It is concluded that both low-dose antacids gels and cimetidine are suitable in the treatment of gastric ulcers.

Adult↗
PubMed1985

Effects of acute hypercalcemia on exocrine pancreatic secretion in the cat.

To investigate the effects of acute hypercalcemia on exocrine pancreatic secretion, anesthetized cats were given calcium intravenously. Increasing hypercalcemia (3.7-6.3 mmol/L) evoked a dose-dependent increase in enzyme output that was 12 times greater than in normocalcemic controls (p less than 0.001) and was 60% of subsequent maximal stimulation with intravenous cholecystokinin (CCK). The effect of hypercalcemia on enzyme secretion was abolished when CCK was administered 60 min before calcium and at a dose to cause maximal enzyme output. Atropine did not prevent the calcium-induced increase in enzyme secretion. Pancreatic fluid and bicarbonate outputs were not influenced by hypercalcemia during intravenous administration of small amounts of secretin, but were increased by addition of CCK to the secretin infusion. Hypercalcemia did not induce macroscopic or light-microscopic changes in pancreatic morphology. Plasma levels of both CCK and gastrin were increased (p less than 0.01) during hypercalcemia, with and without precalcium administration of CCK; atropine significantly inhibited (p less than 0.05), but did not abolish the calcium-induced releases of both peptides. These data suggest that in the anesthetized cat, acute hypercalcemia induced by intravenous calcium infusion stimulates pancreatic secretion of enzymes, but not fluid and bicarbonate. Acute hypercalcemia also causes release of CCK and, as shown previously, gastrin. The findings suggest that the stimulatory effect of hypercalcemia on pancreatic enzyme secretion is not dependent on intact cholinergic pathways and is probably not exclusively mediated by release of CCK or gastrin.

Acute Disease↗
PubMed1985

Different actions of intravenous ethanol on basal (= interdigestive) secretion of gastric acid, pancreatic enzymes and bile acids and gastrointestinal motility in man.

The action of an intravenous infusion of ethanol (10% v/v; given in a dose of 300 mg kg-1 body weight for 30 min followed by 3 mg kg-1 min-1 for 2 hr) on the basal (= interdigestive) gastrointestinal motor activity and the basal gastric acid, pancreatic amylase and bile acid secretion was determined in 6 healthy human volunteers. Ethanol did not affect the duration of the interdigestive motor complex and the output of bile acids into the duodenum. Ethanol significantly (P less than 0.05) stimulated the gastric acid output by about 2.2-fold and inhibited the pancreatic amylase output by about 43% as compared to control experiments in which an intravenous infusion of 0.15 M NaCl was given. Ethanol did not alter the mean plasma levels of gastrin and pancreatic polypeptide as compared to prestimulatory values and to control experiments. In conclusion, these results show that intravenous ethanol given in a moderate dose stimulates gastric acid output and inhibits pancreatic amylase output in fasting non-alcoholic human beings. The mechanism(s) of these different actions of ethanol is unknown since release of gastrin or pancreatic polypeptide by ethanol does not account for the observed effects of intravenous ethanol.

Adult↗
PubMed1984

[Etiology of hyposiderinemia and anemia in Crohn's disease].

UNLABELLED: In a prospective study the frequency of anaemia and serum iron deficiency was investigated in 373 patients with Crohn's disease. Anaemia was present in 52% of patients, hyposiderinaemia in 37%. Involvement of the colon resulted in more pronounced anaemia and hyposiderinaemia than in pure ileitis. For further assessment of iron metabolism serum ferritin or iron binding capacity as well as intestinal iron absorption were determined in 34 patients both anaemic and hyposiderinaemic. In 22 patients sideroachrestic anaemia due to inflammation was found, 5 patients showed iron deficiency due to bleeding. In 6 patients simultaneously lowered serum iron and ferritin or increased latent iron binding capacity with non-increased iron absorption indicated relative iron absorption defects. In one case also the absolute intestinal iron absorption was decreased. However, in only one of these 7 patients typical microscopic changes of Crohn's disease were demonstrable in the upper intestine. CONSEQUENCES: 1. Anaemia in Crohn's disease is most frequently caused by inflammation (sideroachrestic anaemia). 2. In colonic involvement the anaemia can be aggravated by iron deficiency due to bleeding. 3. In rare cases part of the anaemia can be due to iron absorption defects which need not necessarily be associated with macroscopic recognizable mucosal damage.

Adolescent↗
PubMed1984

Interdigestive gastrointestinal motility and secretion of gastric acid and pancreatic enzymes in young cigarette smokers.

The basal (interdigestive) gastrointestinal motor activity and the interdigestive gastric acid and pancreatic amylase secretion were determined in 10 young smokers (mean age 23 years) and 7 nonsmokers (mean age 26 years). There was no significant difference in the length of the interdigestive motor complex between smokers and nonsmokers, but the speed of transmission of the activity front (phase III) in the upper intestine was significantly (p less than 0.05) greater in smokers than in nonsmokers. No significant overall changes in the interdigestive gastric acid and pancreatic amylase outputs were observed between the two groups studied.

Adult↗