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D G Gall

Publications and source records attributed to D G Gall.

At least 55 records · Page 3Linked to original sources
PubMed1992

Evidence of a physiological role for bombesin in the postnatal development of the rabbit pancreas.

The effect of chronic administration of bombesin (BBN) on the development of the pancreas and the role of endogenous BBN in the postnatal development of exocrine pancreatic function were investigated in suckling New Zealand White rabbits. BBN administered intraperitoneally (i.p) at various doses (1.25, 12.5 and 30 micrograms/kg body weight) to suckling rabbits for 13 days starting on day 4 of life induced pancreatic growth as characterized by dose-dependent increases in pancreatic wet weight, total protein content and total DNA content compared to littermate controls. The maximum effect was observed using bombesin at 30 micrograms/kg. This increase represented hyperplasia since there was no BBN-induced change in the protein:DNA ratio. Pancreatic amylase activity was significantly increased by all doses of BBN, with a maximal effect at 1.25 micrograms/kg. The specific BBN receptor antagonist [Leu13-psi(CH2NH)Leu14]-BBN, given i.p for 9 days at 30 micrograms/kg body weight starting on day 20 of life, significantly reduced the development of pancreatic amylase and lipase activities compared to controls (48 and 36% reductions, respectively). Our findings confirm the trophic effect of BBN on the neonatal pancreas and provide evidence of a physiological role for endogenous BBN-peptides in the development of pancreatic exocrine function.

Aging↗
PubMed1992

A role for phospholipid-derived inflammatory mediators in intestinal anaphylaxis in the rat.

This study investigated the role of phospholipid-derived inflammatory mediators in electrolyte transport in the normal rat jejunum and during intestinal anaphylaxis to a food protein in a rat model. In a standard Ussing chamber preparation, the leukotrienes (LTs) C4 and D4 both significantly stimulated an increase in short-circuit current in a concentration-dependent manner. The responses to both LTC4 and LTD4 were significantly reduced by the LTD4 receptor antagonist, MK-571. The 5-lipoxygenase products, LTB4, 5-hydroxyeicosatetraenoic acid and 5-hydroperoxyeicosatetraenoic acid did not significantly alter short-circuit current. The thromboxane mimetic, U-46619, had a small, but significant stimulatory effect on short-circuit current. Platelet-activating factor (PAF) caused a significant, concentration-dependent increase in short-circuit current, with effects at concentrations as low as 2 nM and with a maximum effect of 69 +/- 14 microA/cm2. The stimulatory effect of 0.2 microM PAF was significantly reduced by the PAF receptor antagonist WEB 2086. Exposure of sensitized jejunum to ovalbumin caused a biphasic increase in short-circuit current which was reduced by pretreatment with the 5-lipoxygenase inhibitor, L651,392, and the PAF receptor antagonist, WEB 2086. The response to ovalbumin was not significantly affected by pretreatment of the tissue with the LTD4 receptor antagonist, MK-571, at concentrations which inhibited the responses to exogenous LTC4 and LTD4. The thromboxane/endoperoxide receptor antagonist, L670,596, had no significant effect on the short-circuit current response to ovalbumin.(ABSTRACT TRUNCATED AT 250 WORDS)

Anaphylaxis↗
PubMed1991

The effect of atrial natriuretic peptide on intestinal electrolyte transport.

The effect of atrial natriuretic peptide (ANP) on rat small intestinal electrolyte transport was examined. In vivo, intravenous administration of rat ANP(99-126) induced diuresis and natriuresis in conjunction with a significant decrease in intestinal water (basal, 37.1 +/- 5.7 versus ANP 28.5 +/- 6.0 microliters/cm per 20 min, P less than 0.05) and Na+ (4.0 +/- 0.7 versus 2.8 +/- 0.9 mumol/cm per 20 min, P less than 0.05) absorption (n = 9). In vitro, in Ussing chambers, in both jejunum and ileum, addition of 1.0 microM ANP to short circuited, stripped tissue produced a maximal increase in short circuit current and stimulated net Cl- secretion due to a significant increase in the unidirectional serosal to mucosal flux (JCl-sm: jejunum 17.4 +/- 1.3 versus 19.8 +/- 1.3 microEq/cm2 per h, P less than 0.01, n = 6; ileum 13.4 +/- 0.5 versus 17.2 +/- 0.6, P less than 0.01, n = 6) which was inhibited by the calcium channel antagonist verapamil (82 +/- 26%, P less than 0.05) and by the 5-HT2 receptor antagonist cinanserin (72 +/- 44%, P less than 0.05). Guanylate cyclase activity was stimulated by ANP in intact epithelium, but not in isolated crypt and villus enterocytes.

Animals↗
PubMed1991

Mechanisms of platelet-activating factor-induced electrolyte transport in the rat jejunum.

Platelet-activating factor (PAF) is known to cause chloride secretion in the small and large intestine in vitro. The present study investigated the mechanism of action of PAF-induced electrolyte transport in stripped rat jejunal segments mounted in standard Ussing chambers. Short circuit current was monitored as the indicator of active transport. PAF caused a concentration-dependent increase in short circuit current, whereas its precursor, lyso-PAF, did not. The response to 0.2 microM PAF was inhibited by 92% when chloride ion in the bathing solution was replaced. The response was also significantly inhibited by the PAF receptor antagonist, WEB 2170, the cyclooxygenase inhibitor, indomethacin, the phospholipase A2 inhibitor, mepacrine, and the calcium channel blocker, verapamil. In other in vitro experiments, PAF was shown to stimulate jejunal synthesis of prostaglandin E2, but not 6-keto-prostaglandin F1 alpha or the peptidoleukotrienes C4, D4 or E4. In similar experiments, 0.2 microM PAF enhanced the depletion of jejunal mucosal free arachidonic acid as measured by gas chromatography. These results show that platelet-activating factor stimulates chloride transport in the rat jejunum in vitro, and that the response is dependent upon extracellular calcium, the stimulation of phospholipase A2 and the cyclo-oxygenase catalyzed metabolism of arachidonic acid to prostaglandin E2.

Animals↗
PubMed1991

Distribution and function of brain natriuretic peptide in the stomach and small intestine of the rat.

The distribution and function of brain natriuretic peptide (BNP) was studied in the rat stomach and jejunum. BNP-like immunoreactive nerves were found in the myenteric plexus, circular muscle, submucosa and in the crypt region of the jejunum. In the stomach, BNP-like immunoreactivity was found in the myenteric plexus, circular muscle, submucosa and at the base of the gastric glands. In the submucosa, BNP-like immunoreactivity was often associated with blood vessels. In segments of rat jejunum mounted in Ussing chambers, serosal exposure to rat BNP caused a concentration-dependent increase in short circuit current. A maximal effect of 18 +/- 4 microA/cm2 was observed with 1 microM BNP. The effect was quantitatively and qualitatively similar to that elicited by serosal exposure to equimolar atrial natriuretic peptide. The response to BNP was reduced by 88% in chloride free Kreb's buffer, by 83% in tissues pretreated with cinanserin, an antagonist of the 5-HT2 subtype of the 5-hydroxytryptamine receptor, and by 96% in tissues pretreated with tetrodotoxin, a blocker of axonal conduction. These results are consistent with a physiological role for BNP as a neuromodulator of gastrointestinal electrolyte transport.

Animals↗
PubMed1991

Growth, activities of enzymes in the small intestine, and ultrastructure of microvillous border in gerbils infected with Giardia duodenalis.

The aim of this study was to assess and correlate changes in weight gain, food intake, small intestinal disaccharidase activities and microvillous border surface area over the course of a primary Giardia duodenalis infection in weanling Mongolian gerbils (Meriones unguiculatus). Weight gain in infected animals was significantly impaired between days 8 and 20 postinoculation when compared to age- and weight-matched controls. No difference in food intake was observed between groups. Trophozoite population in the small intestine was maximal on day 4 and 6 of infection, and colonization persisted in the duodenum throughout the experiment (30 days). In infected gerbils, mucosal sucrase and maltase activities were significantly depressed in the duodenum and jejunum on day 4 and in all areas of the small intestine by day 6. Eight and 25 days postinoculation, disaccharidase activities had recovered in the jejunum and distal small intestine but remained depressed in the duodenum, the area where trophozoite colonization persisted. Diffuse loss of microvillous border surface area was observed in the duodenum and jejunum after 6 days of infection. Eight days postinoculation, microvillus surface area had returned to normal in the jejunum, but not in the duodenum. Our findings demonstrate that acute giardiasis in weanling gerbils impairs weight gain, depresses disaccharidase activities, and diffusely reduces mucosal microvillous border surface area.(ABSTRACT TRUNCATED AT 250 WORDS)

Animals↗
PubMed1991

The role of gastroesophageal reflux in pediatric dysphagia.

The history, physical examination, and the results of the upper gastrointestinal series, esophageal manometry, 24-h pH recording, endoscopy, and biopsy are reviewed in 16 children (mean age of 10.6 years, range of 3 years 5 months to 15 years 3 months) who presented to the Alberta Children's Hospital with dysphagia ("food-sticking") without previously identified provocative disorders since January 1985. Of the 16 patients, 11 had had intermittent obstruction, and 7 had had intervention to relieve obstruction (2 Heimlich maneuvers, 1 intravenous glucagon, and 4 endoscopy after failure of intravenous glucagon). Although only five children had a recent history suggestive of gastroesophageal reflux, 12 had histologic evidence of reflux esophagitis (including 1 with a peptic stricture, 1 with "nutcracker" esophagus, and 1 with esophageal dysmotility characteristic of Down's syndrome) and all responded clinically to antireflux therapy. Of the remaining four patients, one had extrinsic esophageal compression from a vascular ring (right aortic arch with left ligamentum arteriosum), one had a single and another had recurrent episodes of food-sticking without any identified abnormality, and one declined investigation. In childhood, dysphagia may be the presenting symptom of reflux esophagitis in the absence of a history suggestive of gastroesophageal reflux and without evidence of a peptic stricture.

Adolescent↗
PubMed1991

Effects of Yersinia enterocolitica infection on rabbit intestinal and colonic goblet cells and mucin: morphometrics, histochemistry, and biochemistry.

The effects of Yersinia enterocolitica on intestinal goblet cells were investigated in New Zealand white rabbits. Animals infected with Y enterocolitica were compared with weight matched and pair fed controls. Goblet cell hyperplasia developed in the distal small intestine of infected rabbits on day 1, in the mid small intestine on day 3, and in the upper small intestine on day 6. In all regions hyperplasia persisted throughout the 14 day study. The degree of hyperplasia was greater in the distal small intestine than the upper and mid regions. Goblet cells in the proximal colon of infected animals seemed to respond as those in the distal small intestine. Thus goblet cell hyperplasia developed more rapidly and to a greater extent in the ileocaecal region where mucosal injury was most severe. These changes resulted directly from Y enterocolitica infection since goblet cell numbers did not increase in pair fed controls. Histochemically, goblet cell mucins from infected rabbits were unchanged at either six or 14 days. Biochemical analysis, however, established that purified mucins from animals on day 6 after infection were less sialylated (in the small intestine) and more sulphated (in the small intestine and proximal colon). In addition, mucins from the distal small intestine and the proximal colon seemed to contain fewer but longer oligosaccharide chains.

Amino Acids↗
PubMed1991

Epidermal growth factor upregulates intestinal electrolyte and nutrient transport.

The role of epidermal growth factor (EGF) in the acute regulation of intestinal transport of electrolytes and glucose was examined. In vivo transport studies were performed in New Zealand White rabbits (500-900 g) using a single-pass perfusion technique. In vitro net fluxes were determined under short-circuited conditions in Ussing chambers. Kinetic parameters of glucose transport in the presence and absence of EGF were measured in brush-border membrane vesicles. In vivo studies showed that the addition of 60 ng/ml EGF to the perfusate resulted in increased absorption of H2O, Na+, Cl-, and glucose from the jejunum. In Ussing chambers, the presence of EGF caused an increase in jejunal net fluxes of glucose-stimulated Na+ and 3-O-methylglucose due to an increase in mucosal-to-serosal movements. Verapamil abolished the EGF effect. In the absence of glucose, net fluxes of Na+ and Cl- were enhanced in the presence of EGF due to a decrease in the serosal-to-mucosal movement of both ions. Verapamil had no effect on this decrease. The incubation of EGF with brush-border membrane vesicles had no effect on either the maximal flux or the Michaelis constant of glucose transport. These results indicate that EGF is capable of regulating absorption of electrolytes and nutrients from the small intestine and suggest a role for this peptide in the control of intestinal transport.

Animals↗
PubMed1991

Refeeding enhances intestinal repair during an acute enteritis in infant rabbits subjected to protein-energy malnutrition.

We examined the effects of refeeding during an acute bacterial enteritis on small intestinal repair in infant rabbits subjected to protein-energy malnutrition and in noninfected and infected dietary controls. Malnutrition was induced by litter expansion at 7 d of age. Randomly selected litters from both dietary groups were infected on d 17 with Yersinia enterocolotica. Inflammation and intestinal damage were observed in the jejunum and ileum at the "acute stage" of infection in 23-d-old animals from both dietary groups, as evidenced by an inflammatory infiltrate, blunted villi, and reduced disaccharidase activities. In addition, ileal glucose-stimulated Na+ absorption was depressed. On d 24, a 7-d period of ad libitum refeeding of breast milk and rabbit feed was initiated in randomly selected litters of infected-malnourished animals and all dietary controls. Mucosal repair was nearly complete at 31 d of age in infected dietary controls and in the infected-malnourished animals that were refed, as demonstrated by the recovery of segmental mucosal mass and ileal glucose-stimulated Na+ transport in association with the resolution of inflammation and diarrhea. Only mucosal disaccharidase activities remain depressed. In contrast, in 31-d-old infected-malnourished animals subjected to ongoing nutrient deprivation, severe intestinal damage persisted as evidenced by increased mortality, ongoing intestinal inflammation, mucosal hypoplasia, depressed disaccharidase activities, and reduced glucose-stimulated Na+ transport. We conclude that a refeeding regimen introduced during an acute bacterial enteritis is well tolerated and promotes recovery of intestinal mass, structure, and function in malnourished infant rabbits and dietary controls.

Animals↗
PubMed1991

Epidermal growth factor and postnatal development of intestinal transport and membrane structure.

The effects of epidermal growth factor (EGF) on postnatal development of intestinal transport and the physical composition of the microvillus membrane were examined. New Zealand White rabbits received EGF (40 micrograms/kg/d) from d 3 of life to d 17 either intraperitoneally or orogastrically. Intestinal H2O, Na+, and glucose absorption expressed per cm of intestine were significantly increased in animals receiving EGF by either route. When EGF was given by the orogastric route, nutrient absorption rates normalized to mucosal DNA were not elevated; thus, increased absorption induced by orogastric EGF appeared to be secondary to mucosal hyperplasia. In contrast, systemic EGF up-regulated cellular nutrient transport. To evaluate at which membrane level these changes occurred, brush border membrane vesicles were isolated from both the jejunum and ileum of control and EGF-treated animals. Rates of Na(+)-dependent glucose transport into the vesicles revealed that in the ileum systemic EGF up-regulated maximal rates of glucose transport by 54% without affecting the Km. These observations were associated with alterations in the lipid composition and physical properties of the microvillus membrane. EGF-treated animals had significant reductions in membrane cholesterol content and altered ratios of phospholipid subclasses. The net result of these variations was that the microvillus membrane isolated from EGF-treated animals was significantly more fluid than membrane from controls. Thus, these results suggest that EGF modulates development of transport function during the postnatal period both by stimulating mucosal growth and by inducing specific transport processes. Furthermore, these changes are associated with alterations in the physical composition of the microvillus membrane.

Animals↗
PubMed1990

Effect of acute Yersinia enterocolitica infection on small intestinal ultrastructure.

The purpose of this study was to assess the jejunal and ileal brush border injury caused by Yersinia enterocolitica and to correlate these alterations with functional abnormalities. Weanling rabbits infected with 10(10) organisms of a human pathogenic Y. enterocolitica strain were compared with control and pair-fed, sham-treated animals. On day 6, infection resulted in a diffuse decrease in brush border enzyme activities in the small intestine and villus atrophy and crypt hyperplasia in the ileum. By day 14, ileal architecture and jejunal disaccharidases had returned to normal, but enzyme abnormalities persisted in the ileum. Ultrastructural studies showed decreased brush border surface area in the jejunum and ileum on day 6 and in the ileum on day 14 of infection. Abnormalities of brush border function caused by infection correlated with the changes in microvillus surface area. In pair-fed animals on day 6, brush border surface area was slightly decreased in the ileum but increased in the jejunum, suggesting that the brush border injury resulted from infection rather than from malnutrition alone. The findings indicate that Y. enterocolitica inflicts a diffuse brush border injury that is in keeping with the generalized defect in brush border enzyme activity and transport function.

Abscess↗
PubMed1990

Intestinal anaphylaxis in the rat. Effect of chronic antigen exposure.

The effect of chronic dietary antigen challenge on the intestine was examined in sensitized rats. Three groups of Hooded-Lister rats were studied: animals sensitized to egg albumin; sham-sensitized animals; and unmanipulated controls. In sensitized rats, serum immunoglobulin E titers to egg albumin were greater than or equal to 1:64, whereas control and pair-fed rats showed no response. Sensitized rats received egg albumin 1 mg/ml in drinking water and rat chow ad libitum. Pair-fed animals also received egg albumin but were pair-fed with sensitized animals. Controls received water and rat chow ad libitum. Chronic antigen challenge resulted in reduced food intake and weight gain in sensitized animals. When the rats were killed after 9 days of antigen exposure, proximal intestine from experimental animals showed decreased disaccharidase activity, brush-border microvillus surface, area, and villus height. Crypt depth and enterocyte migration rate were increased. Mucosal mast cell involvement was suggested by mast cell proliferation, evidence of mast cell degranulation, and increased serum rat mast cell protease II levels. At the time of death, only sensitized jejunum demonstrated an increase in short-circuit current in Ussing chambers in response to antigen challenge. The findings indicate that chronic antigen exposure leads to intestinal injury, reduced food intake, and diminished weight gain.

Anaphylaxis↗
PubMed1990

Intestinal protozoa and epithelial cell kinetics, structure and function.

Intestinal protozoa are not only common enteric pathogens in the tropics but also the high incidence of infection among immunocompromised patients in northern countries has evoked an increased interest in these parasites. Although enteric protozoa are a major cause of diarrhea and malabsorption in humans and other animals, the pathophysiology of gut disturbances caused by them remains poorly understood. Clinical signs related to enteric protozoan disease commonly involve malabsorption, diarrhea, weight loss or retarded weight gain and anorexua. Since these infections are most prevalent and most severe in the young, this may translate into considerable illness among children and significant loss to the agricultural economy where domestic animals are prone to infection. In this review we describe the effects of intestinal protozoan diseases on the structure, kinetics and function of absorptive intestinal cells and other epithelial cells, and correlate morphological injury with physiological alterations in the parasitized gut. Some of the interactions between immune responses and pathophysiology will be discussed, but in-depth discussion of intestinal immunity has recently been undertaken by other authors.

Journal Article↗
PubMed1990

Mediation of food protein-induced jejunal smooth muscle contraction in sensitized rats.

Alterations in myoelectric and motor activity are important features of food protein-induced intestinal anaphylaxis. To determine the mediator(s) involved, rats were sensitized by injection of egg albumin (10 micrograms ip), and controls were sham sensitized with saline. Fourteen days later the contractility of longitudinally oriented jejunal segments (mucosa intact) was examined in standard tissue baths in response to antigen (Ag) or other agents. Although control and sensitized tissues similarly contracted to stretch, bethanechol, histamine, or 5-hydroxytryptamine (5-HT), Ag contracted only sensitized segments. Contractile response 1) was specific to the sensitizing Ag, as bovine serum albumin did not induce contraction, and 2) could be passively transferred with serum containing specific IgE antibody. Mast cell degranulation after Ag challenge was suggested by a significant loss of granulated mast cells in sensitized compared with control rats challenged with Ag. Concanavalin A, which degranulates mucosal and connective tissue-type mast cells, and compound 48/80, which degranulates only connective tissue-type mast cells, produced a contractile response. Ag-induced contraction was significantly inhibited by the mucosal and connective tissue-type mast cell stabilizer doxantrazole (P less than 0.001) and the connective tissue mast cell stabilizer disodium cromoglycate (P less than 0.05). Diphenhydramine and cimetidine together blocked histamine-induced contraction but failed to affect Ag-induced contraction in sensitized tissues.(ABSTRACT TRUNCATED AT 250 WORDS)

Animals↗
PubMed1990

Impact of refeeding on intestinal development and function in infant rabbits subjected to protein-energy malnutrition.

The impact of early postnatal protein-energy malnutrition and of 4, 7, and 14 d of nutritional rehabilitation on small intestinal growth, development, structure and function was examined in 28-, 32-, 35-, and 42-d-old infant rabbits. Malnutrition was induced by litter expansion 7 d postpartum and, in randomly selected malnourished animals, refeeding was begun at weaning, 28 d. Results are compared to ad libitum fed dietary controls. Malnutrition altered the small intestine of the developing rabbit, as evidenced by: 1) reduced jejunal and ileal mass as shown by decreased mucosal wt, protein, and DNA content; 2) depressed epithelial proliferation and enterocyte migration along the crypt-villus axis; 3) delayed epithelial maturation as measured by mucosal enzyme activities; and 4) enhanced glucose-stimulated Na+ transport. Refeeding stimulated rapid and complete recovery, as evidenced by: 1) restoration of jejunal and ileal mucosal mass within 4 d; 2) enhancement of epithelial renewal and enterocyte migration by 7 d; and 3) complete return of the normal pattern of mucosal enzymes by 14 d. With 7 d of refeeding, glucose-stimulated Na+ transport was down-regulated to the level of dietary controls. We conclude that early postnatal protein-energy malnutrition has a severe impact on small intestinal growth, development, structure, and function. Furthermore, a brief period refeeding induced a rapid and complete recovery of these parameters.

Animals↗
PubMed1990

Effects of murine giardiasis on growth, intestinal morphology , and disaccharidase activity.

The aim of this study was to assess the effects of Giardia muris on host growth and food intake, small intestinal morphometrics, mucosal enzyme activities, and brush border ultrastructure. Weanling mice infected with 1,000 G. muris cysts were compared to control and pair-fed sham-treated animals. Infection with G. muris resulted in decreased food intake and retarded growth. In infected animals, villus atrophy was observed in the duodenum throughout the study period and in the jejunum on days 8 and 50. On day 30, whereas jejunal architecture returned to normal in infected animals, malnourished pair-fed animals exhibited a compensatory increase in villus height. Sucrase and maltase were depressed in infected animals on days 2-24. On day 8 jejunal disaccharidases in pair-fed animals were also decreased but to a lesser extent than in infected animals. On day 24, disaccharidase values for control and infected mice were similar, whereas values in pair-fed animals were increased. On day 8, jejunal microvilli were shorter in infected animals than in control and pair-fed animals. This brush border injury was present throughout the jejunum and was also observed in pair-fed animals, but to a lesser extent. These findings suggest that G. muris retards growth in weanling mice, results in small intestinal injury, and interferes with the compensatory response to malnutrition of the infected host. Villus atrophy and brush border enzyme deficiencies associated with the disease mainly occur in the duodenum and jejunum, where trophozoites are most numerous. In infected and in pair-fed animals, the decrease in jejunal disaccharidase activities correlated with a diffuse shortening of brush border microvilli.

Animals↗