Effect of fermented soya beans on diarrhoea and feed efficiency in weaned piglets.

AIMS: To evaluate anti-diarrhoeal and growth enhancing properties of fermented soya beans in weaned piglets. METHODS AND RESULTS: In a first phase piglet diet, toasted full-fat soya beans (20%) were replaced with either cooked soya beans or Rhizopus microsporus or Bacillus subtilis fermented soya beans. The effect on the incidence, severity and duration of diarrhoea in enterotoxigenic Escherichia coli (ETEC)-challenged weaned piglets was determined (pen trial, 24 piglets per treatment). Severity of diarrhoea was significantly less on the diet with Rhizopus-fermented soya beans compared with the control diet containing toasted soya beans. Piglets fed fermented soya beans showed increased feed intake (13 and 12%), average daily weight gain (18 and 21%) and feed efficiency (3 and 8%) (for Rhizopus and Bacillus-fermented soya beans, respectively). However, in the treatment groups an unequal mortality and a potential unequal distribution of receptor-positive piglets were observed. CONCLUSIONS: Cooked and fermented soya beans could be beneficial in the control of diarrhoea in ETEC-challenged weaned piglets (particularly Rhizopus fermented) and significantly improved weight gain and feed intake (particularly Bacillus fermented). SIGNIFICANCE AND IMPACT OF THE STUDY: Fermented soya beans could offer benefits with respect to the control of diarrhoea and feed efficiency in piglets.

[Euthanasia of piglets: gas or injection?]. / Euthanasie bij jonge biggen: gas of injectie?

Methods for the humane killing of animals are watched critically by both the public and the veterinary community. Evaluation of such methods requires assessment of efficacy as well as emotional and ethical aspects. Rapidity of loss of consciousness is a crucial factor in such evaluations. In the present study, four methods for piglet euthanasia were compared with regard to presence of indicators of discomfort (pain, anxiety, stress) and rapidity of onset of death, defined as the absence of breathing, heart beats and reflexes, combined with isoelectricity of the electro-encephalogram (EEG). The study was performed on piglets, which had to be destroyed on account of preventive measures against swine fever. The following methods were applied: CO2 98%, CO2/O2 65/35%, T61 and pentobarbital (Euthesate) injected intracardially. Intracardial injections of T61 and pentobarbital provide fast unconsciousness and death with minimal discomfort to the animal.

Pubertal development in the male pig: effects of treatment with a long-acting gonadotropin-releasing hormone agonist on plasma luteinizing hormone, follicle stimulating hormone and testosterone.

The effects of a long-acting gonadotropin-releasing hormone (GnRH) agonist, [D-Trp6]-GnRH (GnRH-A) on developmental profiles of plasma luteinizing hormone (LH), follicle stimulation hormone (FSH) and testosterone (T), and pituitary responsiveness to exogenous GnRH were studied in male Dutch Landrace x Large White crossbred pigs from 1 to 30 wk of age. Group 1 control animals (control; n = 12) were injected subcutaneously in the neck with vehicle at 1 and 16 wk of age. Group 2 animals (early treatment; n = 10) were injected with 600 micrograms [D-Trp6]-GnRH at 1 wk and with vehicle at 16 wk. Group 3 animals (late treatment; n = 8) were injected with vehicle and 3 mg GnRH-A at 1 and 16 wk, respectively. Group 4 animals (early plus late treatment; n = 9) were injected at both 1 and 16 wk with GnRH-A. Blood was collected by brachiocephalic puncture at weekly or biweekly intervals, and through brachiocephalic cannulae, to determine longitudinal profiles of LH, FSH and T, and plasma gonadotropin responses to intravenous injection of GnRH (0.1 microgram/kg), respectively. In control animals, LH and FSH declined over the first 5 wk of postnatal life and peaked again at 10-14 wk. Levels of both hormones were basal from 18 to 30 wk. Plasma T was high in the first week, declined progressively over the next few weeks and remained low until 24 wk when a transient increment was noted. The LH and FSH responses to acute GnRH stimulation were similar at 7 and 14 wk and declined significantly at 23 wk of age.(ABSTRACT TRUNCATED AT 250 WORDS)

Total ligation of the left renal vein in the dog: an inappropriate model for varicocele.

Induction of varicocele was attempted by ligation of the left renal vein (LRV) in male dogs (Group I). Before the operation and in the 4-month post-operative period, sperm count, sperm motility, and sperm morphology of Group I (n = 8) dogs were compared to sham operated animals (Group II, n = 5). Furthermore, haemodynamics as well as testicular and vascular morphology were studied. In Group I, changes in diameter and consistency of the spermatic cord were temporary. Semen quality was reduced significantly during the second month after ligation of the LRV, but improved thereafter. Haemodynamic studies revealed that LRV blood pressure was increased significantly in Group I dogs. An extensive venous collateral network replaced the occluded LRV. Retrograde blood flow in the left testicular vein (LTV) was observed only in the proximal part of the LTV of Group I dogs. In Group II dogs numerous pairs of sufficient valves prevented reflux into the LTV. Histological examination revealed that spermatogenesis was not impaired and that the left pampiniform plexus had not changed. The number of Leydig cells was decreased slightly in Group I dogs. Sufficient valves in the LTV prevented formation of a permanent varicocele.

Plasma thyrotropin concentration in the male pig: profile from birth to puberty and the effect of season and social environment in the young adult.

Plasma thyrotropin (TSH) secretion was studied in crossbred (Landrace x Large White) immature and young adult Landrace male pigs. Levels of TSH were low over the first 9 wk post-natally and were maximal at 12 wk of age. Thereafter, hormone levels declined and by 16 wk returned to values similar to those at 7 wk. In addition, a transient increase in TSH was noted at 22 wk. A second experiment involved 2 groups of young adult boars housed either in a socially non-restrictive environment (adjacent to estrual females) or a socially restrictive environment (not in direct physical contact with females). TRH stimulated secretion of TSH and the magnitude of this response was affected by month; minimum and maximum responses were found in May and August respectively. There was an effect of social environment on TRH-induced TSH secretion; during February and August, the magnitude of the TSH response to TRH was lower in socially restricted than in socially non-restricted boars.

Absence of direct effects of GnRH on testicular steroid secretion in the ram.

Effects of GnRH, administered via the testicular artery, on testicular steroidogenesis were studied in rams during the non-breeding season. Concentrations of testosterone and 17-hydroxyprogesterone in testicular venous blood showed similar profiles which were identical for GnRH-treated (0.5 ng infused over 60 min or 25 ng injected) and control testes. Increases of testicular venous concentration of both hormones were only marginally reflected in peripheral venous concentrations. Peripheral administration of hCG (200 i.u., i.v.) stimulated testosterone secretion to a larger extent than 17-hydroxyprogesterone secretion in 10/11 rams, GnRH-treated and control testes showing identical responses. High testicular venous concentrations of both hormones after administration of GnRH were paralleled by increased concentrations of endogenous LH. These LH peaks were evoked by 25 ng GnRH in 7/8 rams. The observed effects of GnRH treatment on testicular steroid secretion thus cannot be considered to be the result of direct stimulation of steroidogenesis by GnRH.

[Use of a dental health education center]. / Het Amsterdamse TIP-project. Deel I. Het gebruik.

In the year 1986 1910 persons made use of the services of a dental health education center in Amsterdam. One day a week a dentist could be consulted. The rest of the week other members of the team were available for answering questions. Almost 30% of the questions concerned dental treatment, diagnosis of treatment plan, 20% dental fees and other financial aspects of treatment and questions for folders, posters et cetera accounted for another 20%. Only 5% of the questions referred to preventive matters. A quarter of the dentist's interventions consisted of giving a second opinion. More women than men, and more privately insured than sick fund insured contacted the center.

Effects of morphine and naloxone on plasma levels of LH, FSH, prolactin and growth hormone in the immature male pig.

The effects of acute i.v. administration of gonadotrophin-releasing hormone (GnRH; 0.1 micrograms/kg), morphine (3 mg/kg) and/or naloxone (0.5 mg/kg) on LH and FSH secretion was evaluated in young male pigs (approximately 6 weeks old) with venous brachiocephalic cannulae. The effects of morphine and/or naloxone treatments on prolactin and GH were also evaluated. The influence of morphine on hypophysial hormone secretion was also examined 2 days after castration. Animals treated with morphine and/or naloxone were compared with saline-injected control animals. Injection of GnRH induced 400 and 50% increases in LH and FSH respectively. Morphine and/or naloxone did not influence LH secretion in intact or castrated animals. Morphine suppressed (P less than 0.01) FSH levels 40-60 min after injection whereas naloxone had no effect. Castration eliminated morphine-induced suppression of FSH. Injection of morphine followed by naloxone resulted in acutely raised (P less than 0.05) FSH concentrations. Morphine induced a threefold increase (P less than 0.01) in prolactin within 30 min of injection and naloxone inhibited the effect of morphine. Levels of GH were increased (P less than 0.01) 20 min after morphine treatment and this increase was delayed when naloxone was given immediately after morphine. Naloxone alone did not affect prolactin or GH secretion. Castration caused increases in LH (P less than 0.05) and FSH (P less than 0.01), did not influence prolactin or GH, and reduced plasma testosterone to undetectable (less than 1.0 nmol/l) levels. These results suggest that in young male pigs the hypothalamic-hypophysial axis is responsive to GnRH and gonadal negative feedback.(ABSTRACT TRUNCATED AT 250 WORDS)

Prolactin in the developing pig.

Prolactin (PRL) was determined in plasma of fetal pigs from 40 days post coitum (d.p.c.) onwards. Values increased in the last 3 wk of the gestational period and reached 10 ng/ml at term. Immunoreactive lactotropes could be identified as early as 31 d.p.c. Lactotrope development appeared to be biphasic, with no apparent increase in cell number in the 51-75 d.p.c. period. Sex differences in volume percentage of lactotropes and plasma PRL levels were observed in the 71-75 d.p.c. period. Pituitary PRL content increased 20-fold between 95 d.p.c. and term and 10-fold between birth and 6 wk. Volume percentage of lactotropes did not change from birth to 6 wk. In the postnatal period, plasma PRL concentrations were high in the first 1-2 wk and they decreased thereafter. Lower stable values were observed until about 10 wk, when PRL concentrations began to increase. Prepubertal peak levels were observed in the 10- to 16-wk period and a pubertal peak was observed at 20-22 wk. No significant differences between plasma PRL profiles of males and females were observed in the postnatal period. Castrated males, however, had consistently lower plasma PRL concentrations than intact boars. Cryptorchid boars had PRL concentrations comparable to intact boars. The PRL profile, in relation to the pattern of gonadal development, suggests a role for PRL in gonadal development of the pig.

Feedback regulation of gonadotropic hormone secretion in neonatal pigs.

The effect of castration and of administration of charcoal-treated porcine follicular fluid (pFF) containing inhibin-like activity on plasma concentration of gonadotropic hormones was studied in neonatal pigs. Plasma follicle-stimulating hormone (FSH) concentration averaged 25.1 +/- 1.5 ng/ml (mean +/- SEM) in 1-wk-old females and gradually declined to 20.2 +/- 0.7 ng/ml 6 wk later. Ovariectomy did not significantly influence plasma FSH concentration. In males, concentration averaged 8.0 +/- 0.7 ng/ml before castration but rose significantly within 2 days after castration. Injection of luteinizing hormone-releasing hormone (LHRH) did not influence plasma FSH concentrations in intact males, but did in females and in 7-wk-old males castrated at 1 wk. Plasma luteinizing hormone (LH) concentrations in 1-wk-old females (2.2 +/- 0.4 ng/ml) gradually declined and were not influenced by castration. Concentrations of plasma LH in 1-wk-old male piglets (2.8 +/- 0.7 ng/ml) were not significantly influenced by castration within 2 days but were significantly higher 6 wk later. LHRH induced a significant rise in plasma LH concentrations in all animals. Injection of pFF resulted in a decline of plasma FSH concentrations in intact and castrated males and in intact females, but did not influence plasma LH concentrations. These data demonstrate a sex-specific difference in the control of plasma FSH, but not in plasma LH concentration in the neonatal pig. Plasma FSH concentrations, but not plasma LH concentrations, are suppressed by testicular hormones in 1-wk-old piglets. Plasma FSH concentrations can be suppressed in both neonatal male and female pigs by injections of pFF.

Effect of somatostatin and thyrotrophin-releasing hormone on the levels of growth hormone in the circulation of the chronically catheterized pig fetus in utero.

The effects of i.v. administration of thyrotrophin-releasing hormone (TRH) and of somatostatin on circulating plasma levels of porcine GH in the chronically catheterized pig fetus have been examined. Growth hormone levels increased markedly (P less than 0.01) following TRH administration, but there was no change in thyroxine levels by 1 h after treatment. Administration of somatostatin caused a significant (P less than 0.05) decrease in mean GH levels, but the response was variable between pigs. Saline administration had no significant effect on GH levels. These results suggest that the mechanisms regulating postnatal GH release are present in the fetal pig, but may not be fully developed 8-12 days before delivery.

Development of pituitary gonadotropic cells in the pig fetus and the effect of luteinizing hormone-releasing hormone administration.

Pituitary gonadotropic development in fetal pigs has been studied immunocytochemically. From 50 days postcoitum (p.c.) until 90 days p.c. the volume density of luteinizing hormone (LH) immunoreactive cells increased from 0.12% to 0.61% of the glandular mass of the anterior part of the pituitary gland. From 90 to 100 days p.c. a steep increase to 4.5% was found. A single injection of long-acting luteinizing hormone-releasing hormone (LHRH) to the fetus at 75 days p.c. inhibited this developmental pattern. Pulsatile administration of LHRH agonist to fetuses from 70 to 73 days p.c. had no significant effect on the volume density of LH immunoreactive cells, whereas pulsatile administration from 70 to 80 days p.c. and from 95 to 105 days p.c. inhibited the normal increase of this parameter. It is concluded that from 70 days p.c. onwards the development of fetal gonadotropic cells can be manipulated by exogenous LHRH.

Urinary corticoids in the diagnosis of canine hyperadrenocorticism.

In 20 healthy experimental dogs the 24 hour urinary corticoid excretion as measured by cortisol radioimmunoassay on two consecutive days varied from 0.5 to 3.3 nmol/kg/24 hours and from 0.3 to 3.6 nmol/kg/24 hours. In 20 dogs with otherwise proven spontaneous hyperadrenocorticism these values varied from 4.4 to 35.7 nmol/kg/24 hours and from 3.6 to 26.8 nmol/kg/24 hours respectively. Corticoid/creatinine ratios in morning urine samples of 28 healthy pet dogs were 1.2 to 6.9 X 10(-6). In 27 dogs with spontaneous hyperadrenocorticism all ratios exceeded the range observed in the healthy pet dogs.

Development of nervous tissue in the heart of the fetal and neonatal pig and the effect of decapitation in utero.

The development and distribution of the nerves in the heart of the pig was studied macroscopically and by light microscopy. Hearts were collected from 86 fetuses between 31 and 114 days of gestation (term = 114 days), from 12 neonatal pigs aged 9 and 20 days and from 6 adult sows of the Dutch Landrace breed. The effect of vagotomy produced by decapitation in utero at 40-43 days was studied in an additional 24 hearts from fetuses aged between 51 and 114 days of gestation. The amount of acetyl-thiocholine reactive fibres increases in the atria, A-V node and ventricles throughout gestation. At every age the amount of nervous tissue is highest in the A-V node and lowest in the ventricles. Hearts from decapitated fetuses have smaller amounts of nerve tissue than those from intact fetuses at every age studied. Ganglia are present in both intact and decapitated fetuses. Fluorescent cells containing catecholamines are observed in hearts from fetuses as young as 35 days gestation. Although fluorescent nerve fibres are rarely seen in hearts at 70 days gestation, more fibres are present near birth and thereafter there appears to be a considerable increase in the number of fibres and in the intensity with which they fluoresce. These results show that there is substantial nerve growth into the heart of the pig during gestation and that catecholamine containing nerve fibres develop later than those reactive to acetyl-thiocholine.

Plasma cortisol response to thyrotrophin releasing hormone and luteinizing hormone releasing hormone in healthy kennel dogs and in dogs with pituitary-dependent hyperadrenocorticism.

The change in the plasma concentration of cortisol after the administration of thyrotrophin releasing hormone (TRH) and LH releasing hormone (LH-RH) was studied in normal dogs and in dogs with pituitary-dependent hyperadrenocorticism (PDH). The normal dogs showed a small but significant increase in the plasma concentration of cortisol 15 min after intravenous injection of TRH and LH-RH. In ten of the dogs with PDH the response to TRH was not significantly different from that in the normal dogs, but in 13 the response was significantly greater. In 15 of the dogs with PDH the response to LH-RH administration was within or below the range of responses in the normal dogs and in only one dogs was the response to LH-RH greater than that in the normal dogs. These findings are discussed in relation to the pathogenesis of PDH.

Hypothalamic catecholamine levels in dogs with spontaneous hyperadrenocorticism.

Hypothalamic norepinephrine (NE) and dopamine content was studied in dogs with spontaneous and iatrogenic hypercortisolism and in untreated normal dogs. The concentration of NE in the hypothalamus was subnormal in 4 of 8 dogs with pituitary-dependent hyperadrenocorticism (PDH), whereas long-term administration of corticotropin or cortisone acetate did not result in low hypothalamic NE content. In dogs with hyperadrenocorticism due to adrenocortical tumor subnormal as well as normal and high hypothalamic NE levels were found. Hypothalamic as well as striatal dopamine content did not differ among groups of dogs with PDH, adrenocortical tumor, corticotropin treatment, cortisone treatment and in untreated normal dogs. The subnormal hypothalamic NE levels in dogs with PDH may be involved in the hypersecretion of ACTH found in this disease. The normal hypothalamic dopamine levels in dogs with PDH are not consistent with a dopaminergic-depletion as the cause of PDH.

The determination of cortisol in human plasma: evaluation and comparison of seven assays.

In a comparative study, seven different methods for the determination of cortisol in human plasma were evaluated, using routine patient samples. Four of these methods used radioactive steroids (125I- or 3H-labelled) and in three no radioactivity was needed. For the statistical evaluation a direct 3H-radioimmunoassay was arbitrarily taken as the independent variable. It was found that all other methods correlated well with this assay. However, the simplest method, the fluorimetric, cannot be recommended mainly because of its non-specific fluorescence and troublesome interference from some widely-used drugs. Of the methods evaluated a radioimmunoassay is recommended. For laboratories having no equipment for measurements of radioactivity, the more elaborate and time-consuming fluorometric method of Clark may represent a good alternative.

Adrenocortical function tests in dogs with hyperfunctioning adrenocortical tumours.

The response has been studied in nine dogs with hyperadrenocorticism due to adrenocortical tumours to the administration of dexamethasone, insulin, lysine-vasopressin and tetracosactide by measuring the changes in plasma cortisol concentration. Administration of dexamethasone did not produce a decrease in the plasma concentration of cortisol in any of these dogs. Administration of insulin caused slight increases in the plasma concentration of cortisol in four out of eight dogs. Lysine-vasopressin increased the plasma concentration of cortisol in eight out of nine dogs, three responded supranomally. Eight out of the nine dogs responded to tetracosactide administration, three responded supranormally, It is concluded that in the dog, in contrast to man, the lysine-vasopressin test cannot be used to differentiate between pituitary-dependent hyperadrenocorticism and hyperadrenocorticism due to an adenocortical tumour. Apparently pituitary ACTH is not completely depleted in dogs with hyperfunctioning adrenocortical tumours.

Hypothalamic corticotrophin releasing factor activity in dogs with pituitary-dependent hyperadrenocorticism.

Hypothalamic corticotrophin releasing factor (CRF) activity was determined in five dogs with spontaneous hyperadrenocorticism and in three control animals (one untreated, one treated with high doses of ACTH for 2 months and one treated with high doses of cortisone for 2 months). Hypothalamic CRF activity was low or undetectable in four dogs with Cushing's syndrome due to an adrenocortical tumour. The results are compatible with a pituitary origin for pituitary-dependent hyperadrenocorticism in the dog but are not conclusive; direct information about the rates of hypothalamic CRF secretion is required.