Biomedical subjects

G Budillon

Publications and source records attributed to G Budillon.

At least 91 records · Page 5Linked to original sources

PubMed1978

Parietal cell hyperplasia induced by long-term administration of antacids to rats.

Suspension of magnesium and aluminum hydroxide (30--60 mEq/24h) or a comparable volme of water was orally administered by gastric intubation to two groups of 20 male Wistar rats each over 60 days. The antacid treatment led to a significant increase in the height (0.464 +/- 0.02 mm v. 0.318 +/- 0.06) and in the volume (472 +/- 32 mm3v.328 +/- 45) of the fundic mucosa of the stomach, in the average count of parietal cells per unit area of the mucosa (32.37 +/- 1.8 v. 22.3 +/- 1.6), and in the total parietal cell population of the stomach (53.6 +/- 3.5 x 10(6) v. 43.2 +/- 3.7 x 10(6)). Furthermore fasting serum gastrin concentration was significantly higher in the antacid treated rats (81.2 +/- 7.4 pg/ml) than in control animals (56.9 +/- 6.9 pg/ml).

Animals↗

PubMed1978

Prolactin secretion in nonalcoholic liver cirrhosis.

Serum prolactin levels were determined following stimulation by sulpiride in 20 patients with nonalcoholic liver cirrhosis and 10 normal controls. Prolactin response was essentially the same in the two groups. Only 5 cirrhotics, all with ascites, showed a lower prolactin response after sulpiride stimulation. This was interpreted as a consequence of a rapid prolactin escape from blood into the ascitic fluid, as it was shown to be the case in 2 of these patients. It is concluded that prolactin secretion in nonalcoholic liver cirrhosis is essentially normal. The higher prolactin levels found by others in alcoholic cirrhosis could be the result of a direct effect of alcohol on hypothalamic structures involved in prolactin secretion.

Adult↗

PubMed1978

Pattern and concentration of free amino acids in the plasma and liver tissue of phenobarbital-treated rats.

The pattern and concentration of free amino acids in the plasma and liver tissue of phenobarbital-treated rats was investigated. In phenobarbital-treated rats, there was a significant plasma increase of the total concentration of free amino acids. No significant change in liver free amino acid concentration was observed because of the contemporaneous and general increase in liver size which does not allow observation of any percentual variation in amino acid concentration.

Amino Acids↗

PubMed1978

Urinary excretion of D-glucaric acid, total glucuronic acid and total porphyrins in porphyria cutanea tarda.

The urinary levels of D-glucaric acid, which is an index of hepatic microsome induction, and the excretion of glucuronic acid and porphyrins were measured in nine patients with Porphyria Cutanea Tarda (PCT) and twelve normal controls. The excretion of D-glucaric acid and glucuronic acid were respectively 3.5 and two times higher in PCT patients compared to controls. A statistical correlation could be demonstrated between urinary excretion of total porphyrins with that of glucaric and glucuronic acids. These findings indicate that microsomal function and porphyrin metabolic derangement are strictly related in PCT.

Fatty Liver↗

PubMed1977

Brush border peptidases and arylamidases in the experimental blind loop syndrome of the rat.

Peptidase and arylamidase activities were assessed in purified brush borders from jejunum of rats with surgically created blind loops. The blind loop segment and the jejunum proximal and distal to the blind loop were studied. Comparable jejunal segments from control rats were also studied. The blind loop syndrome was documented by presence of macrocytic anemia. Enzyme activities were determined on purified brush borders. In rats with the blind loop syndromes enzymatic activities hydrolizing sucrose, L-Leucyl-beta-naphthylamide, L-lysyl-beta-naphthylamide, alpha-L-glutamyl-beta-naphthylamide, L-phenylalanyl-alanine and L-leucyl-glycine were significantly reduced as compared to controls (P less than 0.001). After a short course of antibiotic therapy enzymatic activities returned to normal. Our findings suggest a reversible intestinal mucosa damage in the rat with blind loop syndrome.

Aminopeptidases↗

PubMed1975

The source of ascitic fluid in experimental cirrhosis in the rat.

In order to disclose the source of ascitic fluid in liver cirrhosis, normal and cirrhotic rats were injected with fluorescein into the paracecal vein. The green fluorescence was then evaluated on the surface of the liver, the intestine and the peritoneum. Among healthy rats and in those with anascitic cirrhosis a very slight fluorescence was detected on the liver capsule whereas among rats with ascitic cirrhosis a distinct fluorescence was shown on the liver surface, the small intestine and the peritoneum. Therefore, the peritoneum is a source of ascitic fluid in cirrhosis of the rat.

Animals↗

PubMed1974