Blood gastrin and pepsinogen responses to subclinical infection with Ostertagia ostertagi in adult dairy cattle

Blood gastrin and pepsinogen responses to a single infection with 100,000 Ostertagia ostertagi infective larvae in lactating dairy cows were investigated. None of the infected cows showed signs of clinical ostertagiasis, nor was there any difference in live weight gain, milk yield or faecal egg count between groups. Pepsinogen levels of the infected group were significantly elevated between days 3 and 24 after infection (peak 1041 mU tyrosine; day 14). In contrast, there was no significant difference in blood gastrin levels between infected and control animals suggesting that few adult worms had become established in the former group. These data are compared with the increases in both gastrin and pepsinogen levels recorded in susceptible calves exposed to the same level, pattern and strain of ostertagia infection in a previous experiment. It is suggested that gastrin assay may be of value in adult cattle for indicating when elevated pepsinogen levels are merely associated with a rise in larval intake and not with the establishment of large adult worm burdens.     

Gastrin and pepsinogen changes during an Ostertagia ostertagi challenge infection in calves

Daily changes in serum gastrin and pepsinogen concentration have been studied during two types of infection with Ostertagia ostertagi in calves. In a first experiment two calves were trickle infected (10 times 10,000 L3 Ostertagia) and two animals received a single infection of 100,000 L3 Ostertagia. Gastrin and pepsinogen changes are discussed in relation to adult wormburdens. The second experiment involved 8 calves and was designed to investigate pepsinogen and gastrin changes following a challenge infection in previously sensitized calves. The high dosed group was infected with 5,000 L3 O. ostertagi during 30 days, the low dosed group received 500 L3 O. ostertagi and group 3 served as uninfected control. At day 41 post infection all animals were treated with oxfendazole and on day 61 challenged with 100,000 L3 O. ostertagi. Only in the high dosed group a distinct pepsinogen and gastrin reaction was noticed. Both parameters dropped to almost preinfection levels after treatment. Two days post challenge a moderate rise (+/- 1,000 mU tyr) of the pepsinogen concentration was observed in the previously infected animals and gastrin showed a temporary slight increase in several animals 8 to 10 days post challenge. The effect of treatment and challenge infection is discussed in relation to gastrin and pepsinogen changes and immunity.     

Gastric function in dogs with naturally acquired gastric Helicobacter spp. infection

The association of Helicobacter pylori with gastritis, peptic ulcers, and gastric neoplasia has led to fundamental changes in the understanding of gastric disease in humans. The relationship of Helicobacter spp. infection to gastric disease in dogs is unclear. The objective of this study was to determine if Helicobacter infection affects the gastric secretory axis of dogs. Eight Beagle dogs with naturally acquired Helicobacter spp. infection were studied before and after (4 and 29 days) the attempted eradication of Helicobacter spp. with a combination of amoxicillin, metronidazole, and famotidine (AMF). Six specific-pathogen-free, Helicobacter-free Beagle dogs served as controls. The electron microscopic appearance of spiral organisms in infected dogs indicated coinfection with Helicobacter felis- and H bizzozeronii-like organisms. Unstimulated gastric pH and fasting, postprandial, and bombesin-stimulated plasma gastrin were similar in both infected and uninfected dogs, although a trend (P = .09) toward higher meal-stimulated gastrin was observed in infected dogs at 60 minutes. Pentagastrin-stimulated maximal acid output (mmol HCI/kg0.75/hour) and titratable acidity (mmol HCl/mL) were similar in both infected and uninfected dogs, but gastric pH during maximal acid output was lower (P < .01) in uninfected dogs. Mild gastric inflammation was present in both infected and uninfected dogs. Gastric spiral organisms were undetectable in 6/8 infected dogs 4 days after AMF but had recurred in 8/8 dogs 29 days after AMF. Analysis of gastric DNA with Helicobacter-specific primers indicated persistence of Helicobacter DNA at 4 and 29 days after antibiotic therapy. Acid secretion, plasma gastrin, and mucosal inflammation were not affected by the transient suppression of Helicobacter spp. by AMF. These findings suggest that gastric secretory function in dogs is not markedly perturbed by naturally acquired Helicobacter spp. infection and that treatment with amoxicillin, metronidazole, and famotidine causes suppression rather than eradication of gastric Helicobacter spp. in dogs.     

Effects of Ostertagia ostertagi infection on secretion of metabolic hormones in calves.

Effects of Ostertagia ostertagi infection on secretion of insulin, pancreatic glucagon, cortisol, gastrin, and pepsinogen were studied in calves inoculated with 100,000 (group 1) or 10,000 (group 2) O ostertagi infective larvae weekly for 14 weeks. Plasma insulin concentrations in both inoculated groups were lower than those in a non-infected (group 3) control group. The differences between group 1 and group 3 were significant (P < 0.05) at 2 and 12 weeks after initial inoculation. Plasma pancreatic glucagon and cortisol concentrations of groups 1 and 2 did not differ significantly from those of the control group, although plasma pancreatic glucagon concentration was consistently lower in group-1 calves from 4 weeks to end of the study. Plasma pepsinogen and serum gastrin concentrations also increased significantly (P < 0.05) in both groups that received inoculations. We concluded that decreased plasma insulin concentrations are contributory to changes in postabsorptive protein metabolism, and that serum gastrin concentrations are more representative of the pathologic changes in the abomasum than are plasma pepsinogen concentrations.     

Pathophysiologic effects of Ostertagia ostertagi in calves and their prevention by strategic anthelmintic treatments.

Pathophysiologic effects of Ostertagia ostertagi infection and their prevention by strategic anthelmintic treatments were studied in 3 groups each of 6 steer calves. Group-1 calves were noninfected controls. Group-2 calves were inoculated with 100,000 third-stage larvae on the 1st and 28th days of the experiment and grazed on pasture initially free of contamination. Group-3 calves were on a similar regimen as those in group 2, but were also treated with ivermectin 9 days after each larval inoculation. Group-2 calves had increased plasma pepsinogen and gastrin values and decreased weight gains, and total serum protein and albumin concentrations from the 2nd week of infection onward. They were anemic at 10 to 12 weeks and had lower carcass and meat quality at slaughter. Strategic anthelmintic treatments were effective in preventing these effects and calves in groups 1 and 3 had similar performances. On the basis of our findings, high pepsinogen values were related to worm burdens, whereas high gastrin concentrations were related to gastric lesions.     

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

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 Gcell numbers contributes to the hypergastrinaemia associated with ostertagia infection in the calf.     

Gastric distention and gastrin in the dog

Gastric distention was induced in intact dogs by giving a wide range of volumes (11 to 111 ml/kg) of a liquid test meal resulting in a significant (P less than 0.05) increase in plasma gastrin immunoreactivity at 10 and 25 minutes after distention. There was no significant decrease in gastrin immunoreactivity from 10 to 25 minutes of gastric distention. Pretreatment with atropine abolished the distention-induced gastrin release, indicating that distention-induced gastrin release in the intact dog was partially under cholinergic control. There was no relationship between the distending volume and magnitude of gastrin increase.     

Effects of Ostertagia ostertagi and omeprazole treatment on feed intake and gastrin-related responses in the calf

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 with Ostertagia and/or daily treatment with omeprazole (OMP) at 2mgkg(-1) bodyweight for four consecutive days (experiment days 24-27, inclusive) on voluntary feed intake, blood and tissue gastrin concentrations, abomasal G-cell numbers, gastric pH, and blood cholecystokinin (CCK) and pepsinogen concentrations were investigated in the calf. Ostertagia-infected calves demonstrated a significant drop in feed intake between days 24 and 27 post-infection (38%; P<0.001) and in G-cell numbers (42%; P<0.05) and significant increases in abomasal pH (P<0.001), fundic mucosal weight (99%; P<0.01), and blood gastrin (P<0.05) and pepsinogen (P<0.0001). OMP treatment of worm-free animals resulted in a significant drop in intake between days 24 and 27 (30%; P<0.001) and in G-cell numbers (17%; P<0.05) and significant increases in abomasal pH (P<0.01) and blood gastrin (P<0.001). OMP treatment of Ostertagia-infected animals with an existing hypergastrinaemia had no effect on feed intake, abomasal pH, blood gastrin or pepsinogen or abomasal G-cell numbers. Blood CCK concentrations were also unaffected by either Ostertagia infection or OMP treatment. These data suggest that: (a) the depression in feed intake associated with OMP in worm-free calves was not due to a side effect of drug treatment; (b) inappetance in Ostertagia-infected animals is closely associated with the parasite-induced hypergastrinaemia; and (c) the elevation in abomasal pH was a major factor responsible for the elevated blood gastrin concentrations seen in parasitised and OMP-treated animals.     

睾酮对水牛血清胃泌素水平的影响

选用３头雄性中国海仔水牛,观察了去势及去势后注射睾酮对血清胃泌素水平的影响。结果去势后血清胃泌素水平明显下降（５０１．００±３７．２０ｖｓ,４３３．６±１０３．４ｐｇ／ｍｌ,Ｐ＜０．０５）,去势后水牛注射睾酮（２００μｇ／ｋｇＢＷ·ｄ,持续１２ｄ）血清胃泌素水平明显上升（４０８．１±６４．５ｖｓ,５１９．８±３４．４ｐｇ／ｍｌ,ｐ＜０．０５）。表明睾酮影响反刍动物胃泌素分泌。     

Helicobacter felis infection in dogs: effect on gastric structure and function.

The relationship of Helicobacter felis, an organism that is observed in the stomachs of dogs, to gastric disease in dogs is unclear. The objective of this study was to determine if Helicobacter felis infection alters gastric morphology and gastric secretory function in dogs. Five specific-pathogen-free (SPF), Helicobacter-free Beagle dogs were examined before and for 26 weeks after inoculation with H. felis (ATCC 49179). Three SPF uninfected dogs served as controls. All five dogs became colonized by H. felis as determined by urease activity, histopathology, polymerase chain reaction, and transmission electron microscopic examination of serial gastric biopsies. The degree of colonization ranged from < 1 organism/400 x field to > 10 organisms/400 x field. The fundus, body, and cardia were most heavily colonized. Evaluation of gastric biopsies showed mild gastric inflammation and lymphoid follicles in both infected and uninfected dogs. There was no correlation between the number of organisms observed and the degree of gastric inflammation or number of lymphoid follicles. The gastric secretory axis, assessed by fasting and meal-stimulated plasma gastrin, mucosal gastrin and somatostatin immunoreactivity, fasting gastric pH, and pentagastrin-stimulated gastric acid secretion, was similar in both infected and uninfected dogs. Fasting gastric pH was not a reliable indicator of gastric secretory function. These findings suggest that H. felis may not be a gastric pathogen in dogs. However, the density of colonization and limited duration of infection should be considered when interpreting these findings.     

Serum immunoreactive gastrin activity in horses: Basal and postprandial values

Using commercially available diagnostic reagents, serum immunoreactive gastrin activity was measured in five normal horses that were starved of food and water for 24 hours. Blood samples were taken every 15 minutes for two hours. The horses were then fed a pelleted diet for 15 minutes and samples were taken every 15 minutes for a further two hours. Three further samples were taken at hourly intervals. The total sampling period was seven hours. Basal immunoreactive gastrin activity was lower than that reported in other mammals, ranging from a mean of 7.0 pg/ml to 13.8 pg/ml. At 30, 60 and 75 minutes after feeding, mean gastrin immunoreactivity was significantly elevated at 17.4, 19.8 and 18.2 pg/ml respectively. A late significant elevation occurred also five hours after feeding reading 19.4 pg/ml. This low activity may reflect a lower concentration of serum gastrin in the horse than in other mammals, or the methods used in the study may have failed to detect equine serum gastrins.Supported in part by a grant from the Board of the Veterinary Clinical Center, Michigan State University.     

Molecular forms of gastrin in antral mucosa of the horse

The predominant form of gastrin in the antral mucosa of the stomach of virtually all species previously examined is the 17 amino acid peptide little gastrin (G17). This report describes the occurrence in equine antral mucosa of an immunoreactive form of gastrin with elution properties on Sephadex G-50 superfine similar to human unsulfated big gastrin (G34-I). This putative equine big gastrin was a major component of the gastrin immunoreactivity present. A second peak of activity in equine antral mucosa eluted in an identical manner to human little gastrin (hG17-I). Inhibition curves of equine big and little gastrin, with the gastrin radioimmunoassay utilized in this study, were parallel. This observation indicates that there was no spurious increase in the apparent relative amount of big gastrin due to significant differences in the RIA antibody cross-reactivity to big and little equine gastrin. The equine big gastrin peak was resolved by ion exchange chromatography into unsulfated and sulfated forms in approximately equal amounts. This data implies that posttranslational processing of gastrin in horses may differ from that of species previously studied.     

Relationship of plasma gastrin immunoreactivity and gastroesophageal sphincter pressure in clinically normal dogs and in dogs with previous gastric dilatation-volvulus

Fasting and postprandial gastroesophageal sphincter pressure (GESP) and plasma gastrin immunoreactivity were measured in 6 dogs from 9 through 60 months after treatment for and recovery from gastric dilatation-volvulus (GDV). The GESP was not significantly increased in these dogs, compared with that in clinically normal dogs in either the fasting or postprandial state. Corresponding plasma gastrin immunoreactivity was not significantly increased in dogs of the GDV-recovered group, compared with that in clinically normal dogs (fasting or postprandial). An exaggerated increase in GESP in response to food-induced gastrin release was not observed in dogs of the GDV-recovered group. Exogenously administered pentagastrin (3-micrograms/kg bolus, IV) increased fasting GESP in clinically normal dogs over a 4-minute test period (P = 0.01). Gastric distention in response to oral administration of isosmolar saline solution (500 ml) did not significantly increase GESP or plasma gastrin immunoreactivity in clinically normal dogs. In anesthetized clinically normal dogs, gastric distention in response to use of balloons filled to exert intragastric pressure of 30 mm of Hg also did not cause significant increase in plasma gastrin immunoreactivity. Increased GESP, secondary to hypergastrinemia or gastric distention, is an unlikely cause of eructation failure in dogs with GDV.     

Abomasal bacteria produce an inhibitor of gastrin secretion in vitro

Previously, proliferating microflora transferred with abomasal nematodes, were suspected to be the source of the gastrin inhibitor in some parasite excretory/secretory products. Aerobic cultures in HBSS of abomasal fluid from uninfected sheep became inhibitory during the static growth phase, unless antibiotics were present. Basal gastrin secretion was reduced by up to 90%. Rumen fluid and incubates and medium in which Streptococcus bovis and ovine rumen Actinomycete spp. had been grown also contained the inhibitor. Unlike abomasal cultures, rumen fluid and incubates also reduced the measurement of gastrin standards. Rumen incubates were less potent after exposure to pH 2-3, suggesting that inactivation normally occurs in the unparasitised abomasum. Contaminating bacteria which generate the gastrin inhibitor in parasite ES products are probably rumen organisms which survive in the abomasum and proliferate during subsequent incubation. Significantly, rumen bacteria have been shown to be capable of affecting the secretory activity of the gastric mucosa.     

The sequential development of type I and type II ostertagiasis in young cattle with special reference to biochemical and serological changes

The sequential development of Type I and Type II ostertagiasis over a 2-year period in the same naturally infected cattle is described for the first time. Particular reference is made to biochemical and serological changes. Positive relationships were demonstrated between the clinical signs of both Type I and Type II disease, and marked increases in the levels of plasma pepsinogen, plasma gastrin and antibody titres to adult Ostertagia antigen. At necropsy, there were significant relationships between the combined total of adult and developing 5th stage larvae of Ostertagia spp. and the levels of both plasma pepsinogen and gastrin. By the end of the second grazing season the cattle had acquired an immunity to infection with Ostertagia spp. and had very low burdens of this parasite at necropsy. However some of these cattle maintained elevated plasma pepsinogen levels when under natural challenge by Ostertagia spp. larvae and the aetiology of these changes and the problems of diagnosis using this parameter are discussed. Similar trends of infection were observed for Cooperia oncophora, although resistance to the parasite developed more rapidly.     

Abomasal contents of parasitised sheep contain an inhibitor of gastrin secretion in vitro

Serum gastrin concentrations are typically elevated in parasitised sheep; however, in some animals serum gastrin concentrations may fall abruptly despite a very high abomasal pH. Although proliferating abomasal bacteria in culture generate a potent inhibitor of in vitro gastrin secretion, this inhibitor has not been detected in abomasal contents of unparasitised sheep. In sheep parasitised by O. circumcincta, all abomasal fluid samples of pH 5 and above were inhibitory to gastrin release in vitro. Inhibitory activity and abomasal pH were correlated in two separate experiments; the model best fitting the data being sigmoidal in each case, with zero activity at pH 3.6 and 4.6, respectively. There was no clear evidence that the presence of a gastrin inhibitor in the abomasal contents reduced the serum gastrin concentration in parasitised sheep. Serum gastrin was correlated with abomasal pH (log(10) serum gastrin concentrations conformed to log-linear sigmoidal models).     

The effect of porcine hydrolysed collagen on gastric ulcer scores,gastric juice pH,gastrin and amino acid concentrations in horses

Gastric ulcers are common in horses. The purpose of this study was to test the effect of porcine hydrolysed collagen (PHC) on gastric ulcer scores and gastric juice pH in horses. We hypothesise that PHC-administration will result in improved gastric lesion scores and act synergistically with omeprazole to improve treatment efficacy. Thoroughbred horses (n = 10) were studied in a 2-period, 2-treatment crossover design, where the PHC (45 g) was administered twice daily. Horses were treated for 56 days. Gastroscopy was performed and gastric juice pH measured on Days 0, 14, 28, 42, 49 and 56. Nonglandular gastric ulcer number (NGN) and severity (NGS) and glandular ulcer number (GN) and glandular severity (GS) scores were assigned by an investigator masked to treatment and serum gastrin and amino acid concentrations. By Day 42, 2 weeks after discontinuing omeprazole treatment, NGN and NGS scores returned to pretreatment values and serum gastrin was higher when compared to values measured on Day 28. By Day 49, after the feed-deprivation period, NGN and NGS were similar to pretreatment values. By Day 56, mean NGN score was significantly lower in PHC-treated horses, compared to controls. Mean gastric juice pH significantly increased in both groups on Day 28 and the pH was significantly (P = 0.0127) higher in the PHC-treated horses. Serum amino acid concentrations were not significantly different 2 h after feeding PHC and hydroxyproline was not detected. Serum gastrin concentration did not increase 2 h after feeding in the PHC-fed horses. The PHC fed to horses enhanced the effects of omeprazole on increased gastric juice pH, inhibited gastrin secretion after feeding and resulted in fewer nonglandular ulcers after long-term feeding (56 days) in stall-confined horses undergoing intermittent feeding.     

The influence of a low cobalt intake on the neutrophil function and severity of Ostertagia infection in cattle

Two trials involving housed cattle examined the effect of Co depletion and supplementation on immune status as assessed by the neutrophil function test which measures the ability of isolated neutrophils to kill the yeast Candida albicans. A third trial investigated the extent to which Co status influenced the severity of Ostertagia ostertagi infection. In the first two trials liveweight gains were unaffected until some 40-60 weeks on the low dietary Co intake despite very low serum vitamin B12 values being recorded after 10 weeks. However, the immune status as measured by the neutrophil function test was reduced within 10 weeks of commencing the low Co diet. On administration of Ostertagia ostertagi larvae, Co-depleted cattle showed a greater weight loss than Co-supplemented cattle but showed no difference in the length of the prepatent period, worm egg production or serum gastrin and pepsinogen concentrations. After anthelmintic treatment both groups showed a similar response. It is postulated that the lowered immune response of Co-depleted cattle resulted in the greater severity of the Ostertagia ostertagi infection.     

Validation of a radioimmunoassay for measurement of gastrin in equine serum

A commercial radioimmunoassay kit designed for measuring gastrin in human serum was validated for use with equine serum. This nonextraction, double-antibody procedure uses an antiserum with broad specificity for molecular forms of gastrin. Synthetic human gastrin (G17-I) was added to pooled equine serum, and the observed assay values were compared with the mass added. Recovery was 99 to 115% in the gastrin concentration range of 40 to 640 pg/ml. Dilutions of postprandial serum with serum from fasted horses were assayed, and the inhibition curves were compared with those of the human gastrin kit standards, using a log-logit transformation. The slopes of the sample dilution plots were not significantly different from the slopes of the standard curves. Ethylenediamine tetraacetate and heparin adversely affected the assay, resulting in lower assayed gastrin concentration values. The intra-assay coefficient of variation (n = 10) was 3.8%, and the interassay coefficient of variation (n = 6) was 11.2%. The assay sensitivity, as reported by the manufacturer, is 8 pg/ml. Gastrin concentrations in serum from fasted horses ranged from undetectable values (less than 8 pg/ml) to 17.5 pg/ml, and peaked at a mean value (n = 6) of 70 pg/ml 3 hours after feeding. Serum cortisol values monitored during the postprandial blood collection period were in the normal range for horses.     

Development of a protective immunity against Ostertagia leptospicularis in trickle-infected sheep and parallel changes of serum gastrin, pepsinogen and antibody levels

Nine lambs, approximately 9 months of age were allocated to three groups (A, B, C), with three animals in each. Sheep in Groups A and B were trickle-infected with doses of 1000 third-stage larvae (L3) of Ostertagia leptospicularis (five times per week) over periods of 7.5 and 10.5 weeks, respectively, and were subsequently treated with fenbendazole (7.5 mg/kg). Approximately 3 weeks after anthelmintic treatment, all sheep were challenged with a single dose of 100,000 L3, whereas sheep of Group C received the same dose as a primary infection. Sheep of Groups A and B were almost completely refractory against the challenge infection, as indicated by negative faecal egg counts and adult worm burdens. A relatively high infection level was present in the sheep of Group C. The results indicate that a comparatively short immunization period of 7.5 weeks is sufficient to protect lambs against subsequent larval challenge. During immunization, the pepsinogen-, gastrin- and IgA-responses were similar in the individual sheep. In contrast to parasite-specific IgG1 and IgG2 levels, IgA decreased rapidly after cessation of trickle infection and parallel anthelmintic treatment, and may therefore indicate current exposure to parasite antigen. After challenge, the majority of the immunized sheep exhibited immediate and short-term responses of pepsinogen, gastrin and IgA in the serum. The time course and the level of each of these responses were very similar in the individual sheep, suggesting that the release of pepsinogen, gastrin and IgA into the circulation was influenced by related mechanisms.