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Biomedical subjects

G A Castro

Publications and source records attributed to G A Castro.

At least 73 records · Page 4Linked to original sources
PubMed1979

Influence of enteric parasitism on hormone-regulated pancreatic secretion in dogs.

The objective of this study was to test the hypothesis that enteric parasites affect pancreatic secretion in their host. Pancreatic bicarbonate and protein outputs were studied in dogs with gastric and pancreatic fistulas to determine the secretory response to exogenously administered secretin and cholecystokinin and to intraduodenal stimulation with hydrochloric acid and sodium oleate to release endogenous hormones. Bicarbonate and protein concentrations in pancreatic juice were measured prior to infection with Trichinella spiralis and at various periods during primary and secondary infections. Dose-related increases in secretory activity were observed in uninfected hosts in response to all stimuli. Infected dogs responded like controls to exogenous hormones, but showed reduced secretion under duodenal stimulation during the 1st wk of primary infection. This altered response returned to normal 3 wk after primary infection and did not occur following secondary infection. Results support the conclusion that reduced pancreatic secretion is associated with enteric parasitism and is due to a defect in hormone release or in the supply of hormone available for release.

Animals↗
PubMed1979

Enteral and parenteral feeding to evaluate malabsorption in intestinal parasitism.

General evidence of malnutrition such as loss in body weight associated with intestinal parasitism has been attributed to decreased food intake, to intestinal malabsorption, and to change in host basal metabolism. To establish the relative importance of these factors in this regard, rats with trichinosis were studied. The weights of infected and uninfected animals were followed after being placed on one of three feeding regimens for 1 week--stock diet ad libitum, intraduodenal nutrition, and intravenous nutrition. Infected rats on a stock diet lost weight whereas those on the other two regimens maintained the same weight pattern as uninfected counterparts. The maintainance of body weight occurred despite alterations at the level of the intestinal brush border as indicated by a depression of intestinal disaccharidase activities (sucrase and lactase) and by reduction of monosaccharide absorption (measured as accumulation of beta-methyl glucoside) in the proximal, heavily infected region of the small intestine. There was no compensatory increase in enzyme activity nor in the absorptive capacity in the distal gut. Results support the conclusion that inadequate oral food intake rather than changes in basal metabolism or intestinal pathophysiology accounts for weight loss during the intestinal phase of infection.

Animals↗
PubMed1979

Influence of parasitism on secretin-inhibited gastric secretion.

This study tested the hypothesis that the inhibitory action of secretin on gastrin-stimulated gastric acid and pepsin secretion is comprised in animals harboring intestinal stages of the parasite Trichinella spiralis. Pentagastrin-stimulated acid and pepsin secretion, and the influence of secretin on these processes, were measured in dogs prepared with gastric fistulas and Heidenhain pouches. Dogs were studied before and after infection with 10(4) T. spiralis larvae/kg body weight. Gastric secretion was stimulated by constant intravenous infusion of pentagastrin, 1 microgram/kg per hour. Exogenous secretin inhibited pentagastrin-stimulated acid and pepsin output from both the main stomach and Heidenhain pouch in infected as well as in the uninfected dogs. Identical inhibition was observed in uninfected dogs during duodenal infusion with HCl to release endogenous secretin. In contrast, duodenal stimulation with HCl did not inhibit acid and pepsin secretion in dogs tested during the 1st week following infection. Results support the conclusion that the regulatory effect of secretin on gastrin-stimulated gastric secretion is impaired during the early phase of infection, and is due to depressed synthesis or release of secretin from duodenal mucosa.

Animals↗
PubMed1976

Response to immunized, parenterally nourished rats to challenge infection with the nematode, Trichinella spiralis.

Experiments were desinged to test the hypothesis that structural and chemical changes in the small intestine associated with total parenteral nutrition (TPN) alter relationships between hosts and enteric parasites. Parenteral feeding of rats immunized to Trichinella spiralis (nematoda) led to a decrease in gut mass. This was reflected by a significant drop in gut wet weight and reductions in mucosal dry weight, DNA, protein, carbohydrate and lipid. These changes were accompanied also by lowered brush border enzyme activity. When challenged orally with 8 X 10(3) T. spiralis larvae and switched immediately to oral feeding, more worms became established in the small intestines of these rats than in rats given similar doses of larvae, but maintained by oral feeding throughout the experiment. Despite the significant difference in initial worm burden, both enterally fed and parenterally fed rats completely expelled their parasites by 7 and 8 days postinfection, respectively. Results indicated that factors involved in preventing establishment of T. spiralis in immunized rats were suppressed by the prolonged absence of food from the GI tract, whereas factors responsible for expelling worms that were able to gain residence in the mucosa appeared to be unaltered or at least functionally reversible.

Animals↗
PubMed1976

Serum and antral gastrin levels in rats infected with intestinal parasites.

Serum and antral gastrin were measured in rats infected with either Trichinella spiralis or Hymenolepis diminuta as a step in testing the hypothesis that parasites change certain aspects of host physiology by altering gastrointestinal (GI) hormone levels or responses to GI hormones. Parasitism with T. spiralis was associated with inflammatory changes in the small bowel mucosa and with a significant increase in serum gastrin. Neither changes in hormone level nor inflammation were induced in tapeworm-infected rats. These results reveal the capacity of tissue penetrating parasites to alter the level of circulating gastrin. This finding coupled with considerable indirect evidence suggests that some of the pathologic changes induced in hosts by enteric parasites may be due to changes in functions that are regulated by GI hormones.

Animals↗
PubMed1976

Course of infection with enteric parasites in hosts shifted from enteral to total parenteral nutrition.

UNLABELLED: Two groups of rats were kept on an oral diet after infection with 10(4) Trichinella spiralis or 10 Hymenolepis diminuta larvae. Sixteen days and 2 days after infection with H. diminuta and T. spiralis, respectively, 8 rats from each group were switched to intravenous (iv) alimentation, while the remaining animals were retained on oral nutrition as controls. Rats were killed during the following 21 days. The number of T. spiralis recovered from iv-fed rats was significantly higher than in controls, whereas the sex ratio and worm size were similar. Disaccharidase deficiencies normally associated with either infection or parenteral feeding were additive in the infected, parenterally nourished rats. The rise in peroxidase activity normally associated with intestinal trichinosis was not as great (P less than 0.05) in iv-fed rats. Intravenous feeding did not affect tapeworm number, but caused destrobilization. This was followed by secondary proglottization that led to development of worms of normal length and with gravid segments, but with an increased length: weight ratio. CONCLUSIONS: oral food deprivation in the host does not adversely affect development of established T. spiralis. The larger worm burden in iv-fed rats may be due to reduced inflammation normally involved in worm expulsion. Exogenous food in the gut is not necessary for maintaining established H. diminuta; factors necessary for sustenance and growth can be acquired by the worm entirely from the exocrino-enteric circulation.

Animals↗
PubMed1976

Altered small bowel propulsion associated with parasitism.

Experiments were designed to test the hypothesis that alterations of intestinal motility accompany enteric helminth infections. Motility was measured in rats during the intestinal phase of infection with the nematode Trichinella spiralis by following the transit of radioactive chromium through the gut. Intraduodenal catheters were surgically implanted in rats. One week after the operation one group of animals was infected with 8 x 10(3) T. spiralis larvae and a second group was infected with 16 x10(3) larvae. A third group of uninfected rats served as controls. Three, four, or five days postinfection, Na2 51CrO4 was injected through the catheter into the duodenum or fasted animals and its propulsion through the small bowel was allowed to progress for 15 min. The distribution of radioactivity throughout the small intestine and cecum was then plotted as a function of gut length. Intestinal transit was increased significantly by infection. The leading edge of radioactivity transversed 100% of the gut length in infected rats and 70% in controls. The amount of injected radioactivity transversing the midpoint of the small intestine was estimated by regression equations to be 38% of the injected dose for control rats and 59 and 57% for infected groups. Increased propulsive activity in parasitized rats was associated with inflammatory changes and a significant reduction in disaccharidase levels in the gut mucosa. The latter conditions were most marked in the proximal small bowel where the majority of worms resided.

Animals↗
PubMed1975

Intestinal disaccharidase and peroxidase activities in parenterally nourished rats.

The importance of the presence of food in the gastointestinal (GI) tract in maintaining normal enzyme activity in the small intestine was investigated in rats that were kept from eating for as long as 2 weeks. During this time animals were sustained on a nutrient solution administered intravenously. Enzyme activity and small bowel mass in these animals and similiar parameters in rats that were administered the same solution orally were compared with control groups fed an essentially isoenergetic diet of stock rat food and water. Disaccharidase and peroxidase levels in mucosal scrapings expressed as activity/milligram protein, activity/intestine, and activity/100 g body weight, were significantly reduced in intravenously nourished rats but not in rats receiving the solution orally. In addition to changes in enzyme activities, parenteral feeding was accompanied by a significant reduction in the small bowel weight:body weight ratio as compared with that of rats fed the stock diet or nutrient solution orally. Results support the conclusion that normal activity of intestinal enzymes spatially distributed with regard to depth within the mucosa depends on the presence of food in theGI tract and cannot be maintained at normal levels by total intravenous nutrition.

Animal Nutritional Physiological Phenomena↗
PubMed1975

Alcohol and dietary factors in cirrhosis. An epidemiological study of 304 alcoholic patients.

Alcohol intakes and dietary habits of 304 alcoholic, hospitalized patients were evaluated. There were 195 patients with hepatic cirrhosis, 40 precirrhotics, and 69 noncirrhotics. Alcohol contributed 50% to 58% of total calories. Two thirds of the patients drank excessively for more than 20 years. There were no statistically significant differences between the three groups in the duration or degree of alcohol excess. Dietary intakes were assessed for a period of at least two years before the presenting illness. Noncirrhotics had higher food caloric intakes and higher protein intakes than the cirrhotics (P less than .05). The findings suggest that dietary factors may be involved in the pathogenesis of the disease.

Adult↗