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L Bustos Fernández

Publications and source records attributed to L Bustos Fernández.

12 recordsLinked to original sources
PubMed1994

Influence of pirenzepine on colonic serotonin changes induced by short chain fatty acid.

In this work we have demonstrated the influence of a short chain fatty acid (acetate) on the number of enterochromaffin (EC) cells containing serotonin (5HT), at two different pH (pH 6.9 absorptive stimuli, and pH 2.9 secretory stimuli), infused into the colon during one hour. The number of EC cells decrease significatively, specially in the cecum with a solution of low pH (2.9). The action of piprenzepine in preventing this reduction demonstrated that was partly mediated by a cholinergic receptor mechanism. On the other hand, a decrease on the release of 5HT to the lumen was a observed under the influence of pirenzepine. We conclude that the short chain fatty acid acetate, at a low pH induces the release of serotonin through a cholinergic mechanisms indicated by the inhibition observed with antimuscarinic drug.

Acetates↗
PubMed1994

[Do the physical characteristics of radiopaque markers modify the results of the measurement of colonic transit time?].

UNLABELLED: This study was performed in 15 healthy control subjects (8 males- age 23-70 and 7 females age 20-74) as a way to compare the total and segmental colonic transit time with two different type of radiopaque markers. One type of markers was 3 mm cut sections of a radiopaque polietilene 14 French Levine tube, with a medium weight of 64.3 mg and a specific gravity (SG) of 1.28. The other type were 7 mm lenticular insoluble barium (lentils) with medium weight of 231 mg and a SG of 1.87. Each subject ingested 20 markers of each type with the breakfast and front and profile plain films of the abdomen were taken 24 and 48 hs after. The total colonic transit time for the polietilene markers was 17.7 hs and 27.3 hs for the barium type (BM) (p < 0.001). The segmental transit time for right colon was 2.4 hs (PM) and 9.7 hs (PM) and 9.7 hs (BM) (p < 0.001) in the left colon 9.5 hs (PM) and 11.3 hs (BM) and in rectoanun 5.9 hs (BM) with no statistical significance. CONCLUSION: the physical characteristics of the radiopaque markers can modify the results of the colonic transit times.

Adult↗
PubMed1993

[The effect of different lactic acid isomers in the colon of rats].

Depending on quantity and/or quality, the presence of lactic acid in the colonic lumen may be associated with metabolic damage of the colon. The influence exerted on the rat colon by the different isomers and racemic of the lactic acid, used at two extreme dilutions (20 and 100 mEq/l), has been the subject of study in this paper. The modifications on pH, water and electrolytes are associated with the absorptive/secretory action of the colonic wall. In addition, a study has been made on the influence of lactic acid on the colonic mucus and albumin permeation. Histopathologic studies of the caecum and left colon have been performed. There is a different colonic wall behaviour for each of the different isomers of the lactic and its racemic; a larger absorption of water, Na+ and Cl- for the D (-) isomer at a low concentration; its behaviour is completely opposite at high concentration. The final pH is higher when the D (-) isomer takes part; comparing the different isomers, there are small variations as far as albumin permeation is concerned. At high concentration there is a decline in Cl- absorption. The high percentage of erosions that take place especially in the caecum, where L (+) isomer can be found at high concentration, it is remarkable. The present observations suggest that the presence of lactic acid in (the) ulcerative colitis deserves great attention, especially in about the quantity and quality in which the acid can be found.

Animals↗
PubMed1993

[Influence of sodium butyrate intake on murine colonic carcinogenesis].

The role of short chain fatty acids (SCFA) in murine colonic carcinogenesis (MCC) has not yet been clarified. In rats, Freeman et al have reported an increased number of colonic tumors induced with dimethylhydrazine (DMH) and sodium butyrate in drinking water. On the other hand, Deschner et al showed that tributyrin intake did not increase MCC induced with azoxymethane. Both of them have reported high levels of fecal butyric acid with sodium butyrate and tributyrin intake. Although salt intake has been positively associated with colorectal cancer some authors do not support this association. We have evaluated the influence of right hemicolectomy (RH) (right colon as main source of SCFA) and the intake of 2%-pH 7 sodium butyrate (S.BUT) and 4 g/l sodium chloride (S.CHL) in drinking water, in MCC. Forty eight male Wistar rats weighing 150 g were divided into 4 groups: RH, S.BUT, S.CHL, control (C). Half of the animals received weekly DMH 20 mg/kg subcutaneously for 12 weeks. Necropsy was performed after 6 months. We have determined fecal SCFA content by gas chromatography. Neoplasm was present in 70% of rats treated with DMH. The number of animals with tumors was: RH 4/6, S.BUT 4/6, S.CHL 3/5, C 6/6. Tumor frequency was: RH 1.17 +/- 0.48, S.BUT 1.50 +/- 0.76, S.CHL 1.20 +/- 0.49, C 1.50 +/- 0.22. S.BUT group, treated with DMH, presented a lower butyric acid concentration (p < 0.05) in comparison with other groups. We have no explanation for this finding; gastric absorption of sodium butyrate may be an important factor.(ABSTRACT TRUNCATED AT 250 WORDS)

Animals↗
PubMed1992

Volatile fatty acids, lactic acid, and pH in the stools of breast-fed and bottle-fed infants.

We measured fecal pH, volatile fatty acids (VFA), and lactic acid concentrations in 67 healthy infants ranging in age from 1 to 5 months. The babies were divided into five groups according to their diet: group 1: human milk, with subgroups of 1 month of age (n = 8), and 2-5 months (n = 12); group 2: formula milk, with subgroups of 1 month of age (n = 9) and 2-5 months (n = 10); group 3: cow's milk, one group of 2-5 months of age (n = 12); group 4: human milk supplemented with formula milk, 2-5 months of age (n = 8); and group 5: human milk supplemented with cow's milk, 2-5 months of age (n = 8). Fecal VFA concentration and pH of bottle-fed infants (groups 2 and 3) were significantly higher and lactic acid concentrations significantly lower than those of the breast-fed group. Groups 4 and 5 showed significantly higher pH and propionic acid concentration, and lower lactic acid concentration than Group 1 did. There were no significant differences in the data on pH, VFA, and lactic acid concentrations between the feces of formula and cow's milk groups. On the other hand, the addition of formula or cow's milk to the human milk was sufficient to alter the profile of VFA, the pH, and the lactic acid concentration of breast-fed infants stools. Low pH, low VFA, and high lactic acid concentrations make the colonic content of breast-fed babies an environment favorable for Bifidobacteria growth, and this is probably the main protective factor against gastrointestinal infections.

Acetates↗
PubMed1991

Effect of loperamide and bisacodyl on intestinal transit time, fecal weight and short chain fatty acid excretion in the rat.

We analyzed the effect of drugs that modify the colonic motility on rat intestinal transit time (ITT) (measured with radiopaque markers), fecal weight (FW) and fecal concentration of short chain fatty acids (FSCFA) (assayed by gas liquid chromatography), over a four-week period. Bisacodyl was used to accelerate and Loperamide to retard the intestinal transit in rats maintained on a conventional diet. The first and 3rd week were drug-free control periods. The mean values of these periods were: ITT = 28.9h +/- 1.9 FW: 9.2 +/- 1.2 g/24 h and FSCFA = 60.6 +/- 17.9 mmol/g. After loperamide administration, we observed an increase in the mean ITT as compared to the control period (40.4 +/- 8.0h) and decrease in FW (4.8 +/- 3.6 g/24h) and in FSCFA = 32.2 +/- 5.6 mmol/g). After bisacodyl administration, we found a shorter ITT in relation to controls (24.8 +/- 2.5h), and increases in FW (27.5 +/- 3.6g/24h) and in FSCFA (108.2 +/- 39.9 mmol/g). There was a negative correlation between ITT and FW (R = 0.67 p less than 0.01) and a positive correlation between total SCFA concentration and FW (R = 0.71 p less than 0.01). The concentration of acetic, propionic and butyric acids increased with progressive increments in fecal weight, whereas concentrations of isovaleric and caproic acids decreased. The results of this study show that the FW and the FSCFA may be influenced by modifications in the intestinal transit time.

Animals↗
PubMed1988

[Post-sectional antral peptic ulcer and antrofundic re-anastomosis in rats (manifestation of a probable antrofundic neuroendocrine center)].

The antrum-fundic section and re-anastomosis (AESR), liberates, in Wistar male rats, genuine antral peptic ulcers. They start within 20 days. They are progressive evolution, penetrating into all gastric walls. Between 7 and 8 months, they involve near organs (spleen, liver, pancreas) and produce a great inflammatory reaction of the peripancreatic ganglions. The antral peptic ulcer is induced if the gastric lesser curvature's nerves are sectioned and a concomitant pyloroplasty is done or not. The gastric hemisection, if anterior or posterior, break out the peptic ulcer only on the same side of the antrum-fundic interruption. In all this situations, except in cases of concomitant pyloroplasty, it is proved a pronounced and significantly increase of the gastric (g/kg), but not pancreatic index. In the AFSR series with nervous section on the lesser curvature and without pyloroplasty, the percentage of antral peptic ulcers in 56%. It is postulated the probably existence, at an antrum-fundic level, of a neuroendocrine center. Its nullification or disturbance by the section and re-anastomosis procedure could generate the antral ulcer and other histologic changes (increase of the "G" cells, hyperplasia of the parietal, ECL and "A like" cells) by one or various hypothetical ways: 1. Direct action, nullifying the normal blocking function of somatostative over the "G" cells and or parietal cells. 2. Disturbing or nullifying the motor pump effect of the gastric antrum, and on this way, enhancing the duodenum-gastric reflux with all know deleterious effects of the bile in the antrum particularly in an acid milieu. 3. Modifying, in the opposite direction, the sensitivity by one hand, of the "G" cells mass and by the other one, of the parietal, ECL and "A like" cells. The depression of the fundic sensitivity will induce the hyperplasia of the "G" cells, the hypersecretion of gastrin and, "a posteriori", all the secretory effects and trophic characteristic of it. 4. Disturbing the prostaglandins secretion, perhaps through a deficit of the nervous innervation, with the resulting epiphenomenon of a cytoprotection deficit mediated through the mucus and bicarbonate production. It is probably that the proposed physiopathogenic mechanism are associated and that the final result, the antral peptic ulcer is the consequence of an increase of the aggressive factors (acid, bile) and a concomitant depression of the defensive factors (cytoprotection), starting normally by the prostaglandins through the mucus and bicarbonate secretion.

Anastomosis, Surgical↗