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Biomedical subjects

J E Valenzuela

Publications and source records attributed to J E Valenzuela.

71 records · Page 4Linked to original sources
PubMed1980

Studies of pure pancreatic secretions in chronic alcoholic subjects without pancreatic insufficiency.

To determine the role alcohol might play in altering pancreatic function, we have examined pure pancreatic juice, obtained by endoscopic cannulation of the pancreatic duct, from a group of 10 chronic alcoholic subjects without history or clinical or laboratory evidence of pancreatic disease and compared the results with those obtained from 15 healthy, non-alcoholic subjects. These findings confirm observations in experimental animals made by others and support the hypothesis that chronic alcohol abuse may damage the pancreas via a sequence of events involving protein hypersecretion. Increase in concentration was not uniform for all proteins measured. Unexpectedly, chronic alcoholics exhibited a highly significant elevation (two- to three-fold over normal) in trypsinogen, in contrast to statistically insignificant increases of other zymogens and trypsin inhibitor. The strikingly increased ratio of trypsinogen to trypsin inhibitor observed in all our alcoholic patients may indicate a weakening of the defence mechanism provided by the trypsin inhibitor against premature intraductal activation of zymogens and explain the predisposition of these patients to pancreatitis.

Adult↗
PubMed1979

Nonsteroidal antiinflammatory drugs: effect on pyloric sphincter and duodenogastric reflux.

We have investigated the effect of nonsteroidal antiinflammatory drugs on canine pyloric sphincter pressure, mucosal potential difference (PD), and duodenogastric reflux in 5 dogs. Only intragastric aspirin at doses of 30 and 100 mg/kg caused a significant (P less than 0.05) decrease in pyloric sphincter pressure, an increase of duodenogastric reflux, and changed the mucosal PD. Neither intravenous aspirin, intragastric phenylbutazone, or intrarectal indomethacin produced these changes. The mechanism for the aspirin effect may be mediated by local pathways related to changes in mucosal PD. We postulate that increased duodenogastric reflux may be an aggravating factor for the gastric mucosal damage caused by intragastric aspirin.

Animals↗
PubMed1979

Pancreatic polypeptide response in patients with chronic pancreatitis.

We studied the plasma pancreatic polypeptide (PP) response to a meal in patients with pancreatitis and attempted to correlate the PP increment with the degree of pancreatic exocrine insufficiency. Control subjects and patients with recurrent pancreatitis showed significant mean increase (P less than 0.05) in plasma PP concentration in response to food. By contrast chronic pancreatitis patients had no significant increase in plasma PP. However, some subjects with normal pancreatic had no response and some patients with chronic pancreatitis did show a response. In addition, no correlation was observed between the PP response and pancreatic exocrine secretion. We conclude that the PP response to a meal has only limited value in the detection of pancreatic destruction.

Adult↗
PubMed1979

Effect of dopamine on human gastric and pancreatic secretion.

It has previously been shown that dopamine stimulates pancreatic exocine secretion and inhibits acid secretion in the dog. In this study, the authors have investigated the effect of dopamine on human gastric and pancreatic secretions. In 6 subjects, dopamine produced a dose-dependent inhibition of pentagastrin-stimulated acid secretion, an effect that was suppressed when the subjects received haloperidol. In 6 other subjects, dopamine infusion did not modify basal pancreatic secretion, and dopamine inhibited pancreatic enzyme secretion during secretin-cholecystokinin infusion. Dopamine also caused a rise in plasma glucagon and insulin. The effects on pancreatic enzyme secretion and plasma glucagon were not antagonized by haloperidol. The results suggest that dopamine is inhibitory for human gastric secretion. The authors did not observe a stimulatory effect of dopamine on human pancreatic exocrine secretion as has been observed in dogs.

Adult↗
PubMed1978

Cimetidine versus intensive antacid therapy for duodenal ulcer: a multicenter trial.

In a randomized double blind multicenter trial, patients treated with cimetidine (800 or 1200 mg daily) or an intensive regimen of Al-Mg antacid (210 ml daily) had similar rates of duodenal ulcer healing and pain relief. After 4 weeks of treatment, the proportion of patients with ulcer healing by endoscopy were: cimetidine (1200 mg), 21 of 33 (64 percent); cimetidine (800 mg), 19 of 32 (59 percent); and antacids, 15 of 29 (52 percent). These proportions did not differ significantly. Eighty per cent of cimetidine-treated patients became asymptomatic by week 4, as did 63 percent of antacid-treated patients (P greater than 0.1). No untoward effects were observed during cimetidine treatment. Twenty-seven per cent of antacid-treated patients reported diarrhea.

Adult↗
PubMed1976

Pyloric-sphincter studies in peptic-ulcer patients: pylorus in peptic ulcer.

Pyloric pressure was assayed by a manometric procedure in the basal state and after intraduodenal infusion of HCl. 13 control subjects, 11 patients with benign gastric ulcer, 8 with duodenal ulcer, and 2 with coexistent gastric and duodenal ulcers were studied. Mean resting pyloric pressure in gastric-ulcer patients (5.17 +/- 0.71) mm Hg) was significantly lower than controls (9.40 +/- 0.85 mm Hg) and did not increase after HCl perfusion into the duodenum. Mean basal pyloric pressure in duodenal-ulcer patients (11.30 +/- 1.57 mm Hg) did not differ significantly from controls and increased after intraduodenal perfusion of HCl to 15.72 +/- 2.40 mm Hg. The two patients with coexistent ulcers had manometric patterns similar to gastric-ulcer patients. Decreased pyloric-sphincter pressure in gastric-ulcer patients may be the mechanism responsible for the increased duodeno-gastric reflux observed in these patients.

Adolescent↗
PubMed1976

Dopamine as a possible neurotransmitter in gastric relaxation.

In dogs with gastric fistulas, intragastric pressure was measured with a flaccid ballon containing 500 ml of water. Graded doses of dopamine caused graded decreases in intragastric pressure. The effect was blocked by pimozide or by metoclopramide but was not significantly affected by phenoxybenzamine, propranolol, guanethidine, or FLA-63 (a beta-hydroxylase inhibitor). Pretreatment with metoclopramide or with pimozide shifted the volume-pressure diagram of the stomach to the left; that is, at any given volume the pressure was greater after than before these drugs. In dogs with vagally innervated gastric pouches and gastric fistulas, feeding for 1 min (while allowing the food to leave the stomach through the gastric fistula) caused a prompt decrease in pressure in the pouch that lasted for about 5 min. Pretreatment with metoclopramide decreased the magnitude and duration of this receptive relaxation. It is concluded that these findings are consistent with (but do not establish) the hypothesis that dopamine is the neurotransmitter for receptive relaxation of the stomach, because dopamine mimics receptive relaxation, and dopamine antagonists partially block reflexly induced receptive relaxation.

Animals↗
PubMed1976

Manometric studies on the human pyloric sphincter. Effect of cigarette smoking, metoclopramide, and atropine.

Pyloric sphincter pressure was assessed with water-perfused polyvinyl tubes. Smoking one cigarette significantly decreased the basal pyloric pressure, whereas 10 mg of metoclopramide as an intravenous bolus increased the pyloric pressure in normal subjects and in patients with gastric ulcer with low basal pressure. Duodenal acidification with 0.1 N HCl significantly increased pyloric pressure. Atropine 15 mug per kg, subcutaneously prevented the rise of pyloric pressure in response to acid infusion into the duodenum.

Adult↗
PubMed1976

Effect of gastrin on pancreatic enzyme secretion and gallbladder emptying in man.

This study was designed to assess the effect of unsulfated synthetic human little gastrin (HG-17-I) on pancreatic secretion and gallbladder emptying in man. During continuous gastric and duodenal aspiration, 6 male subjects were given, on different days, either HG-17-I (7, 20, 60, 180 AND 540 PMOL KG-1 HR-1), chlecystokinin (0.1, 0.3, and 0.9 UKg hr-1) or 238 pmol kg-1 (500 ng kg-1) of HG-17-I as a rapid intravenous injection. Trypsin output and bilirubin output increased significantly (P less than 0.05) above basal levels during the infusion of both peptides. During HG-17-I infusion the highest trypsin output (2.08 +/- 0.22 Karmen U per 10 min) and bilirubin output (4.66 +/- 0.61 mg per 10 min) occurred during the 60 pmol kg-1 hr-1 dose, whereas highest acid output occurred during the 540 pmol kg-1 hr-1 dose. Rapid intravenous injection of HG-17-I produced a prompt and significant rise in trypsin, bilirubin, bicarbonate, and acid outputs. It is concluded that HG-17-I produced significant pancreatic enzyme secretion and gallbladder emptying at doses that are submaximal for acid secretion, suggesting that this may be a physiological effect of gastrin.

Adult↗
PubMed1976

Effect of intestinal hormones and peptides on intragastric pressure in dogs.

Intragastric pressure was measured in dogs with gastric fistulas by using a flaccid balloon containing 500 ml of water. Intravenous infusion of cholecystokinin (20% pure), the carboxyl-terminal octapeptide of cholecystokinin, secretin, and vasoactive intestinal peptide produced dose-related decreases in intragastric pressure with maximal decreases of 40% or more. Glucagon and gastric inhibitory peptide produced smaller decreases in intragastric pressure. Motilin caused a dose-related increase in intragastric pressure that lasted only about 7 min despite continuing infusion of the peptide. The half-dose of cholecystokinin or of octapeptide of cholecystokinin for pancreatic protein secretion and the half-dose of secretin for pancreatic bicarbonate secretion each produced significant inhibition of intragastric pressure, suggesting that these hormones play a physiological reole in regulating gastric pressure.

Animals↗
PubMed1975

Effect of pentagastrin and caerulein on intragastric pressure in the dog.

When gastric acid was not neutralized, doses of pentagastrin as small as 1 mug kg-1 hr-1 decreased intragastric pressure in dogs. When gastric acid was neutralized the smallest effective dose of pentagastrin was 8 mug kg-1 hr-1 which is 16 times the D50 for acid secretion. Thus the decrease in intragastric pressure by small doses of pentagastrin is mediated at least in part by acid secretion. Even with gastric neutralization, a dose of caerulein as small as 63 ng kg-1 hr-1, which is the D50 for pancreatic protein secretion, decreased intragastric pressure. These findings support the view that inhibition of gastric pressure occurs with physiological doses of the cholecystokinin-like peptide caerulein but only with pharmacological doses of pentagastrin.

Animals↗