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C Vaillant

Publications and source records attributed to C Vaillant.

At least 37 records · Page 2Linked to original sources
PubMed2000

Quantitative morphological analysis of embryonic cockroach (Periplaneta americana) brain neurons developing in vitro.

Neurons dissociated from the brain of embryonic cockroaches (Periplaneta americana) can be maintained in culture for several weeks. The survival as well as the progressive organization of the neurons into a complex network was studied during a 5-week period under different culture conditions. About 10% of the dissociated cells adhered to the culture dish. This figure remained constant throughout the culture. The cell diameter ranged from 10 to 20 microns and did not change significantly over time in culture. Whereas only a few cells exhibited neurites at the start of the culture, the number of cells exhibiting neurites increased to reach about 99% after 2 weeks. The different cells were then connected to each other, forming a network, which became more and more complex. The number of cells per cluster as well as the length and the diameter of the "connectives" that linked the different clusters were found to increase with time. The morphology of individual neurons within the network was visualized after intracellular injection of biocytin. Labeling with antibodies raised against serotonin or GABA indicated that neurons were able to differentiate and to acquire specific neurotransmitter fates. The serotonergic phenotype was found to appear progressively throughout the culture, in parallel with the formation of the network. Cell density, addition of fetal calf serum, and ecdysone were shown to influence the development of the network.

Animals↗
PubMed2000

Time-dependent effects of endothelin-3 on enteric nervous system development in an organ culture model of Hirschsprung's disease.

BACKGROUND/PURPOSE: Terminal colonic aganglionosis (Hirschsprung disease) results from incomplete rostrocaudal colonisation of the embryonic gut by neural crest cells (NCC). Mutations in the genes encoding endothelin-3 (EDN3) or its receptor (EDNRB) have been shown to result in a similar aganglionosis. This article describes the development of an organ culture model using embryonic murine gut to determine how endothelin-3 regulates development of the enteric nervous system. METHODS: Gut explants from mice of different gestational ages were cultured for up to 3 days in the presence or absence of 5 micromol/L of the specific endothelin-B receptor antagonist BQ788. EDN3 and EDNRB mRNA expression were analysed by reverse-transcription polymerase chain reaction (RT-PCR) and whole-mount in situ hybridisation. NCC were localised using immunoreactivity for PGP 9.5, a specific neuronal marker. RESULTS: EDN3 mRNA continued to be expressed by caecal mesenchymal cells and EDNRB mRNA by the migrating NCC in culture. Embryonic day (E)11.5 explants were already colonised by NCC up to the terminal ileum. Complete colonisation occurred in organ culture over the next 72 hours (equivalent to E 14.5). Explants of E 12.5 and E 13.5 showed complete colonisation after 48 and 24 hours culture, respectively. Terminal aganglionosis resulted from treatment of E 11.5 and E 12.5 gut explants with 5 micromol/L BQ788, whereas there was no inhibitory effect on E 13.5 explants. CONCLUSIONS: An organ culture model has been developed in which NCC colonisation of embryonic gut mirrors that described in vivo. Blockade of the EDN3/EDNRB receptor pathway shows that the interaction of endothelin-3 with its receptor is only necessary for NCC colonisation at early time-points, despite the continued expression of endothelin-3 mRNA in the gut.

Animals↗
PubMed1999

Spatiotemporal expression patterns of metalloproteinases and their inhibitors in the postnatal developing rat cerebellum.

Matrix metalloproteinases (MMPs) are proteolytic enzymes that degrade the components of the extracellular matrix (ECM). The balance between MMPs and their inhibitors [tissue inhibitors of metalloproteinases (TIMPs)] in the pericellular environment determines the most significant proteolytic events in tissue remodeling. In vitro evidence is accumulating that these molecules may be crucial in the maturation of neural cells. Here, we investigated the in vivo expression of MMPs 2, 3, and 9 and TIMPs 1, 2, and 3 in the developing and adult rat cerebellum using immunohistochemistry and in situ hybridization. During postnatal development, all Purkinje (PK) cell somata expressed all the MMPs and TIMPs studied, whereas their growing dendritic trees expressed only MMP 3 and TIMP 3. In the adult, MMP 3 was confined to PK cell bodies, whereas TIMP 3 was expressed in PK cell somata and processes. Irrespective of the developmental stage, Bergmann glial processes contained only MMP 9, but their somata contained both TIMP 1 and MMP 9. In granular cells, MMPs 3 and 9 and TIMPs 1, 2, and 3 were chiefly detected at a time when migration is known to be maximal; except for that of TIMP 1, their expression persisted in the internal granular layer in the adult. The functional relevance of MMP expression was verified by gelatin zymography. MMP 9 activity was maximal on postnatal day 10 (P10) and was detectable at a low level on P15 and in the adult, whereas MMP 2 activity remained similar throughout postnatal development. Regional and cell-specific expression of MMPs and TIMPs closely reflects the successive stages of cerebellar development, thereby suggesting a pivotal role for ECM proteolysis in brain development and plasticity.

Age Factors↗
PubMed1999

Hormone-induced secretory and nuclear translocation of calmodulin: oscillations of calmodulin concentration with the nucleus as an integrator.

Many important enzyme activities are regulated by Ca2+-dependent interactions with calmodulin (CaM). Some of the most important targets for CaM action are in the nucleus, and Ca2+-dependent CaM translocation into this organelle has been reported. Hormone-evoked cytosolic Ca2+ signals occur physiologically as oscillations, but, so far, oscillations in CaM concentration have not been described. We loaded fluorescent-labeled CaM into pancreatic acinar cells and monitored the fluorescence in various regions by confocal microscopy. Sustained high concentrations of the hormone cholecystokinin or the neurotransmitter acetylcholine evoked a transient movement of cytosolic CaM from the basal nonnuclear area into the secretory granule region and, thereafter, a more substantial and prolonged translocation of CaM into the nucleoplasm. About 50% of the CaM that bound Ca2+ translocated. At a lower hormone concentration, evoking Ca2+ oscillations, regular spikes of increased CaM concentration were seen in the secretory granule region with mirror image spikes of decreased CaM concentration in the basal nonnuclear region. The nucleus was able to integrate the Ca2+ spike-evoked pulses of CaM translocation into a sustained elevation of the nucleoplasmic concentration of this protein.

Acetylcholine↗
PubMed1999

Ontogeny of interstitial cells of Cajal in the human intestine.

BACKGROUND/PURPOSE: Interstitial cells of Cajal (ICC) recently have been identified as intestinal pacemaker cells. Abnormalities in ICC are increasingly recognized in a number of neonatal disorders such as infantile hypertrophic pyloric stenosis, Hirschsprung's disease, and transient intestinal pseudo-obstruction. The aim of this study was to determine the fetal and postnatal differentiation and development of ICC in the human gastrointestinal tract to aid interpretation of pathological specimens. METHODS: Specimens of human gastrointestinal tract from (1) fetuses (9 to 17 weeks' gestation; n = 12), (2) premature and full-term neonates with non-gut motility-related disorders, (age 26 to 59 weeks' gestation; n = 13), and (3) children (age 4 months to 13 years; n = 7) were immunohistochemically stained with antibodies to c-kit(a marker for ICC) and protein gene product 9.5 (PGP9.5, a marker for neural tissue). RESULTS: (1) C-kit-positive ICC were present throughout the gut in all specimens including those from the earliest gestational ages. C-kit and PGP9.5 immunoreactivities were present in different cell populations. (2) The distribution of ICC varied with gestational age and with region of the gut. (3) Maturation of ICC networks continues postnatally in a region-specific manner. CONCLUSIONS: ICC are present from an early stage in human gut development. Interpretation of apparent abnormalities in ICC distribution as being of pathological significance should be tempered by the knowledge that ICC networks continue to develop postnatally and that ICC development varies throughout the gut.

Child↗
PubMed1998

Abnormal colonic interstitial cells of Cajal in children with anorectal malformations.

BACKGROUND/PURPOSE: Constipation is a frequent functional problem in children after operation for all types of anorectal malformations. Although this has been assumed to be caused by hypomotility of the rectosigmoid colon, recent studies have demonstrated generalized colonic hypomotility in children with high or intermediate anomalies. The cause of this disorder is unknown. The aim of this study was to determine whether the observed colonic hypomotility seen in patients with anorectal malformations was caused by defects in distribution or density of interstitial cells of Cajal (ICC), recently identified as 'intestinal pacemaker cells'. METHODS: Colostomy specimens from 12 patients with high anorectal anomalies (ARM group; age 0 to 14 months) were compared with colostomy specimens from five control patients with nonmotility-related gastrointestinal pathology (age, 1 to 4 months). Specimens were immunohistochemically labelled with antibodies to PGP9.5, a marker for neural tissue, and antibodies to c-kit, a recently characterized marker for interstitial cells of Cajal (ICC). RESULTS: Ganglion cells were present in all histological specimens. Abnormalities in distribution and density of c-kit-positive ICC were present in 7 of 12 ARM patients. In two ARM patients, ICC were completely absent, and in five patients, ICC density was markedly reduced in circular muscle and at the submucosal border of circular muscle. Only five ARM patients had a distribution of ICC similar to that of control patients. CONCLUSION: Defects in the population of intestinal pacemaker cells may underlie the colonic hypomotility seen in high anorectal malformations and hence may contribute to refractory constipation.

Anus, Imperforate↗
PubMed1997

Regulation by gastric acid of the processing of progastrin-derived peptides in rat antral mucosa.

1. Inhibition of gastric acid secretion by proton pump inhibitors like omeprazole increases the synthesis and secretion of the pyloric antral hormone gastrin. We report here how omeprazole influences the conversion of the gastrin precursor to its final products, and the abundance of mRNAs encoding proteins associated with progastrin processing in rat antral mucosa. 2. Progastrin processing was studied using a pulse-chase protocol in antral mucosa, incubated in vitro, from rats treated with omeprazole for up to 5 days. Labelled peptides were detected by on-line scintillation counting after immunoprecipitation and HPLC. The mRNAs encoding prohormone-processing enzymes were identified by Northern blot, polymerase chain reaction or ribonuclease protection assay, and their cellular origins identified by immunocytochemistry. 3. Cleavage of [3H]- and [35S]-labelled progastrins at Arg-94-95 or Arg-57-58, and amidation at Phe-92 were not influenced by pretreatment with omeprazole. In contrast, cleavage of G34 (the thirty-four amino acid amidated gastrin) at Lys-74-75 to give G17 (the seventeen amino acid amidated gastrin), and of G34-Gly to G17-Gly (G34 and G17 with COOH-terminal glycine), was increased 3-fold after treatment with omeprazole for either 1 or 5 days. 4. Approximately 20% of newly synthesized amidated and Gly-extended gastrins were secreted within 240 min of the labelling period in omeprazole-treated samples, but secretion of labelled gastrins from control tissue was undetectable over a comparable period. 5. The amidating enzyme, peptidyglycine alpha-amidating mono-oxygenase (PAM), the prohormone convertases PC1/3, PC2, PC5 and the PC2 chaperone 7B2 were localized to rat antral gastrin cells by immunocytochemistry. The relative abundance of mRNA species encoding 7B2, PC5 and PAM were unchanged after treatment with omeprazole for 5 days, whereas gastrin, PC1/3 and PC2 mRNAs are known to increase at this time. 6. The main consequence of increased cleavage at Lys-74-75 is the production of G17 and G17-Gly at the expense of G34 and G34-Gly, respectively. The latter have longer plasma half-lives, and so their increased cleavage may serve to limit the rise in plasma gastrin concentration after inhibition of acid secretion. Changes in the abundance of mRNAs encoding prohormone-processing enzymes cannot account for the rapidity of the changes in cleavage of progastrin at Lys residues after omeprazole.

Animals↗
PubMed1997

Amine precursor uptake and decarboxylation: significance for processing of the rat gastrin precursor.

1. Conversion of prohormone precursors to smaller active products occurs in secretory granules, which also have the capacity to concentrate biogenic amines. We have examined how processing of the gastrin precursor, progastrin, in rat antral mucosa is influenced by modulation of the biogenic amine content of secretory granules. 2. Newly synthesized progastrin-derived peptides in rat antral mucosa were labelled in vitro with 35SO4(2-) using a pulse-chase protocol and detected after immunoprecipitation by HPLC with on-line liquid scintillation counting. Secretory granule morphology was examined by electron microscopy. The effects of experimentally manipulating secretory granule pH and amine content were examined. 3. The dopamine precursor L-beta-3,4-dihydroxyphenylalanine (L-DOPA) inhibited cleavage of 35S-labelled thirty-four amino acid amidated gastrin, i.e. [35S]G34, and of [35S]G34 with COOH-terminal glycine, i.e. [35S]G34-Gly, at a pair of lysine residues, but did not influence cleavage of progastrin at pairs of arginine residues. The effect of L-DOPA was reversed by reserpine, which inhibits the amine-proton exchangers VMAT1 and VMAT2, and by carbidopa, which inhibits aromatic L-amino acid decarboxylase. 4. Treatments that raise intragranular pH, e.g. the weak base chloroquine, the ionophore monensin and the vacuolar proton pump inhibitor bafilomycin A1, had similar effects to L-DOPA. 5. Electron microscopical studies showed that the electron-dense aggregrates in gastrin cell secretory granules were lost after inhibition of the vacuolar proton pump. Treatment with L-DOPA produced reserpine-sensitive dissipation of the electron-dense aggregates, compatible with the idea that increased amine delivery raised intragranular pH. 6. The data suggest that the processes of amine precursor uptake, decarboxylation and sequestration in secretory granules are associated with selective modulation of progastrin cleavage, possibly by raising intragranular pH and thereby inhibiting pH-sensitive prohormone convertases.

Adrenergic Uptake Inhibitors↗
PubMed1997

Effects of Ostertagia ostertagi on gastrin gene expression and gastrin-related responses in the calf.

1. Infection with the bovine abomasal nematode Ostertagia ostertagi results in a loss of acid-secreting parietal cells and an increase in gastric pH. The effects of an experimental infection on gastrin mRNA expression, blood and tissue gastrin concentrations, the different molecular forms of gastrin in each, and pyloric mucosal chromogranin A-derived peptides were investigated in the calf. 2. An increase in blood gastrin concentrations in the infected group reached a peak by day 28 postinfection (635 pg ml-1; P < 0.01). Gel chromatography analysis of blood samples revealed that the hypergastrinaemia comprised largely gastrin-34 (G-34) in parasitized calves while gastrin-17 (G-17) predominated in control animals. 3. An 11-fold increase in gastrin mRNA expression was recorded in the parasitized animals which was accompanied by a 23.8% reduction in pyloric mucosal gastrin content and an apparent drop of 24.7% in the number of gastrin-producing G cells detected. There was no major change in the relative abundance of G-17 and G-34 in the pyloric mucosa of infected calves. No significant differences in the concentration of pyloric mucosal chromogranin A-derived peptides were recorded between infected and control groups. 4. These data suggest that the hypergastrinaemia seen in parasitized calves results largely from an increase in gastrin synthesis and that depletion of previously stored peptide makes virtually no contribution to elevated blood gastrin concentrations.

Animals↗
PubMed1997

Gastrin biosynthesis in the antrum of patients with pernicious anemia.

BACKGROUND & AIMS: The gastrin precursor progastrin produces multiple alternative active products, but the pathways of posttranslational processing in human antral mucosa have not yet been studied directly. The aim of this study was to investigate the biosynthetic relationships and release kinetics of newly synthesized progastrin-derived peptides in the antrum of patients with pernicious anemia. METHODS: Antral mucosal explants were incubated with [35S]sulfate and [3H]tyrosine to label progastrin and its derivatives, which were detected by online scintillation counting after immunoprecipitation and high-performance liquid chromatography. RESULTS: [35S]- and [3H]progastrin were detected within 2.5 hours, and labeled G34Gly and G34 were readily detected after 5-hour incubation. Pulse-chase studies indicated conversion of progastrin to G17 via G34Gly and G34. Secretion of newly synthesized G34, but not G34Gly, was routinely detected; G17Gly was present only in trace quantities in cell extracts and media. In control samples, progastrin synthesis was about 10 times lower than in pernicious anemia samples, although the proportions of different labeled amidated gastrins after 5-hour incubation were similar. CONCLUSIONS: In the antrum of patients with pernicious anemia, Gly-gastrins, particularly G34Gly, are biosynthetic intermediates and not major secretory products. Some G34 is secreted preferentially under basal conditions.

Aged↗
PubMed1997

Relation between cholecystokinin and antral innervation in the control of gastric emptying in the rat.

BACKGROUND: Antral motility and the hormone cholecystokinin (CCK) are major determinants of the rate of gastric emptying. The relation between CCK and antral neurons in regulating gastric emptying is uncertain. Benzalkonium chloride (BAC) causes selective lesions in gut myenteric neurons after serosal application. AIM: To develop a model of antral denervation using BAC to enable the study of the relation between CCK and antral neurons in regulating gastric emptying. METHODS: BAC, vehicle or the afferent neurotoxin capsaicin were applied to the serosal surface of the rat antrum or corpus; neurochemical markers of intrinsic and afferent neurons were detected by using immunohistochemistry and radioimmunoassay. Gastric retention of solids was determined after fasting, and emptying of liquids was measured in rats with gastric fistulae. RESULTS: In BAC treated rats radioimmunoassay of tissue extracts revealed a dose related specific loss of gastrin releasing peptide, substance P, and vasoactive intestinal polypeptide immunoreactivities from the treated region, and immunohistochemistry revealed loss of the neuronal marker PGP 9.5 and the afferent neuropeptide calcitonin gene related peptide (CGRP). Adjacent untreated regions were unaffected by BAC, with the exception that CGRP was depleted in both corpus and antrum after antral treatment. After antral BAC treatment fasted rats retained solids for over 48 hours. Moreover, in antrally denervated rats with gastric fistulae, the emptying of saline, acid and peptone was delayed substantially. The CCK dependent inhibition of gastric emptying of peptone was preserved after antral treatment with BAC. CONCLUSIONS: Serosal BAC causes lesions in the innervation of the treated region of the stomach. The innervation of the antrum is essential for normal emptying of both liquids and solids, but the inhibition of gastric emptying produced by CCK is not dependent on antral neurons.

Animals↗
PubMed1995

Subcellular pathologic features of glucocorticoid-induced hepatopathy in dogs.

Dogs are particularly susceptible to development of glucocorticoid-induced hepatopathy, but the mechanisms are not well understood. We investigated the pathogenesis of glucocorticoid hepatopathy by examining sequential morphologic and biochemical changes in the liver of dogs during steroid administration. Six adult Beagles were given prednisolone acetate (4mg/kg of body weight, once daily for 24 days IM). Serum samples and percutaneous liver biopsy specimens were obtained before the start of the study (treatment day [TD] 0) and at TD 5, 10, 15, and 25. There were significant (P < 0.05) and progressive increases in serum activities of alkaline phosphatase, gamma-glutamyltransferase, and alanine transaminase. Light microscopic changes in liver biopsy specimens included progressive hepatocellular swelling and vacuolation. Electron microscopy revealed glycogen accumulation, peripheral displacement of organelles, and prominent dilatation of bile canaliculi, compared with findings at TD 0. Liver biopsy specimens taken at TD 25 had significantly (P < 0.05) increased activities of the plasma membrane enzymes, alkaline phosphatase and gamma-glutamyltransferase, and 5'-nucleotidase was significantly (P < 0.001) decreased. Subcellular fractionation on reorientating sucrose density gradients revealed high-density peaks of alkaline phosphatase and gamma-glutamyltransferase, compatible with a specific increase in the biliary canalicular component of the enzyme activities. Neutral alpha-glucosidase activity was shifted to the denser fractions, indicative of an increase in the proportion of rough to smooth endoplasmic reticulum and consistent with enhanced synthesis of plasma membrane proteins. There also was evidence for progressive increase in fragility of intracellular organelles, particularly lysosomes. These findings indicate that glucocorticoid hepatopathy in dogs is associated with progressive alterations not only to the plasma membrane, but also to other subcellular organelles.

Alanine Transaminase↗
PubMed1994

Discrimination between temperature- and brefeldin A-sensitive steps in the sulfation, phosphorylation, and cleavage of progastrin and its derivatives.

Maturation of the acid-stimulating hormone gastrin involves precursor cleavage, tyrosine sulfation, serine phosphorylation, and COOH-terminal amidation. We have used brefeldin A and incubation at 22 degrees C to determine where and when these modifications occur. Immunogold studies of gastrin cells incubated at 22 degrees C revealed swollen Golgi cisternae, the terminal regions of which were associated with an accumulation of progastrin immunoreactivity. At 22 degrees C, [3H]tyrosine and [35S]sulfate were incorporated into progastrin, but Arg94-Arg95 cleavage, and Ser96 phosphorylation, were inhibited. When pulse labeling at 22 degrees C for 120 min was followed by a chase at 37 degrees C, [35S]progastrin was cleaved at Arg94-Arg95 with a t1/2 of about 10 min, compared with about 20 min for [3H]progastrin. Approximately 60% of the COOH-terminal cleavage fragment was phosphorylated, but there was little or no incorporation of [32P]phosphate into progastrin. Addition of brefeldin A during the chase substantially inhibited cleavage of [3H]progastrin, but not [35S]progastrin. However, when pulse labeling was limited to 20 min at 22 degrees C, the presence of brefeldin A in a subsequent chase at 37 degrees C completely inhibited cleavage of [35S]progastrin. The data indicate that progastrin sulfation occurs in the trans-Golgi network, exit from which involves passage through first a brefeldin A-sensitive and then a temperature-sensitive step. Cleavage at Arg94-Arg95 and Ser phosphorylation are closely linked, occur distal to the temperature-sensitive step, and are followed by amidation in secretory granules. It is known that mature secretory granules do not phosphorylate progastrin-derived peptides, and so phosphorylation appears to coincides with, and may provide a marker for, delivery of peptide from trans-Golgi work to immature secretory granules in gastrin cells.

Amides↗
PubMed1993

Diagnosis of grass sickness by ileal biopsy.

Ileal biopsies were obtained from 18 horses with grass sickness, 15 horses with other alimentary disease and three horses without gastrointestinal disease. Samples of small intestine were also obtained from nine cases of obstruction due to small intestinal strangulation. Histological examination revealed that severe enteric neuropathy in the absence of other significant morphological changes was confined to the horses with grass sickness.

Animals↗
PubMed1993

Enteric neuropathy in horses with grass sickness.

The degeneration of enteric neurones has been recorded in grass sickness, but the distribution of the lesions in the gut and their possible relationship with the severity of the clinical signs has not been established. Samples obtained from 11 anatomically defined sites along the gastrointestinal tract of eight control horses without gastrointestinal disease, five horses with acute grass sickness and three horses with chronic grass sickness were examined histologically. The organisation of the enteric ganglia was similar to that in other large mammalian species. Minor exceptions included the presence of fundic mucosal nerve cell bodies and blood vessels within submucosal ganglia. All the horses with grass sickness had severe enteric neuropathy, widespread in the acute cases but localised to the distal small intestine in the chronic cases. These neuronal lesions are consistent with, and may explain the intractable gastrointestinal propulsive deficit that characterises grass sickness.

Acute Disease↗
PubMed1993

Calcitonin- and somatostatin-positive cells in thyroid gland of pigs at different ages.

Immunohistochemical studies were carried out on calcitonin-, somatostatin- and serotonin-reactive cells in newborn pigs and pigs at 3 weeks and 7 months old. The aim of these studies was to examine if the expression of various bioactive substances by parafollicular cells in the pig thyroid varied during development. The volume density of the follicular epithelium was nearly the same in newborn and 3-week-old piglets and significantly lower in 7-month-old animals. The volume density of calcitonin-positive cells, expressed as a percentage of the follicular epithelium density, was similar in young animals, being 12.10% and 13.03% in newborn and 3-week-old piglets, respectively. A small but significant increase to 14.40% was seen in 7-month-old pigs. Somatostatin-positive cells formed a much smaller population at all time points, but these also showed a significant increase with age (0.13%, 0.17% and 0.52% of follicular epithelium density in newborn, 3-week- and 7-month-old pigs, respectively). However the changes in the volume density of somatostatin-positive cells correlated inversely with thyroid activity, the density being highest when the activation index was lowest, suggesting that thyroid activity may be regulated by an increase in the synthesis of this inhibitory peptide. Serotonin-positive cells were extremely rare at all time points and their volume density was not calculated.

Age Factors↗
PubMed1993

Gastrin and gastrin-related responses to infection with Ostertagia ostertagi in the calf.

The effects of a single challenge with 60,000 infective Ostertagia ostertagi larvae on blood and gastrointestinal mucosal gastrin concentrations, gastrin-producing G-cell numbers in the pyloric mucosa and growth of different parts of the gut were investigated in 16, two-and-a-half-month-old calves. Infected calves exhibited a rise in abomasal pH which was accompanied by a 145 per cent increase in wet weight of the fundic mucosa (P < 0.05) and a significant rise in blood total gastrin concentrations (P < 0.01). Circulating little gastrin (G-17) was unaffected. Pyloric mucosal total gastrin concentrations remained unaltered in the infected calves until day 28 when levels fell to 36.9 per cent of control group values (P < 0.01). Pyloric mucosal G-cell numbers declined during the experiment in the infected group. It is suggested that release of previously stored tissue gastrin and not a change in G-cell numbers contributes to the hypergastrinaemia associated with ostertagia infection in the calf.

Animals↗