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Biomedical subjects

S Harvey

Publications and source records attributed to S Harvey.

At least 217 records · Page 12Linked to original sources

The effect of immunization against somatostatin on growth rates and growth hormone secretion in the chicken.

The effect of both active passive immunization against somatostatin on growth rate and growth hormone levels was studied in chickens. Passive immunization against somatostatin by administration of antiserum had no effect on rate of growth of chickens and no persistent effect on circulating growth hormone (GH) levels. In acute experiments, administration of anti-somatostatin serum caused a marked elevation of GH levels in chickens at both 4 and 8 weeks of age, but the relative stimulation was greater in the older birds. Active immunization against somatostatin significantly stimulated growth rate in chickens, but was not shown to have a clear effect on circulating GH levels. These data suggest that somatostatin control over GH secretion may not be fully developed in the chicken at 4 weeks of age, but that immuno-neutralization of somatostatin can produce an increase rate of growth in chickens similar to that seen in mammals.

Aging↗

Promotion of the Whitten effect in female mice by synthetic analogs of male urinary constituents.

Two volatile constituents of male mouse urine, 2-(sec-butyl)-4,5-dihydrothiazole and dehydro-exo-brevicomin, were synthesized and tested for their ability to induce estrous cycle in female mice (the Whitten effect). The suppression of ovarian cycling activity that resulted from grouping the females was abolished by exposure to normal male urine. The synthetic compounds, when added together in appropriate concentrations to the (previously inactive) urine of castrated males, or even to water, were found to be as effective as normal male urine. The action of the synthetic compounds appears attenuated for singly caged females.

Animals↗

Plasma concentrations of corticosterone and thyroid hormones in laying fowls from different housing systems.

Plasma concentrations of corticosterone, thyroxine (T4) and triiodothyronine (T3) were measured in representative mature female domestic fowls from three housing systems: cages, covered strawyard and range. There were no between-system differences for T4 but T3 was lower in birds from range than in those from cages. Corticosterone concentrations were lower in birds from strawyards than in those from range and cages. In the strawyards there were no differences in corticosterone concentrations between normal and low-ranking hens. The latter were selected on the basis that they remained apart from the flock, were under-weight, poorly feathered and unable to feed at will. Low-ranking hens had significantly higher plasma concentrations of T3 and T4 than normal birds. This was attributed mainly to the poor feather covering of most low-ranking birds. It was concluded that, in the assessment of different housing systems, plasma corticosterone and thyroid hormones were not useful measures of long-term stress or welfare. Different factors relevant to welfare may have contrary effects on the plasma concentrations of these hormones.

Animals↗

Seasonal changes in concentrations of plasma hormones in the male ring dove (Streptopelia risoria).

Seasonal changes in concentrations of plasma LH, prolactin, thyroxine (T4), GH and corticosterone were measured in captive male ring doves exposed to natural lighting at latitude 56 degrees N. Plasma LH levels decreased steeply in autumn when the daylength fell below about 12.5 h but increased in November as the birds became short-day refractory. In comparison with plasma LH concentrations in a group of short-day refractory birds exposed to 6 h light/day from the winter solstice, plasma LH levels in birds exposed to natural lighting increased further in spring after the natural daylength reached about 12.5 h. There were no seasonal changes in plasma prolactin concentrations and plasma T4 concentrations were at their highest during December, January and February, the coldest months of the year. The seasonal fall in plasma LH levels in September was associated with a transitory increase in plasma T4, a transitory decrease in plasma corticosterone and a sustained increase in plasma GH. It is suggested that in the ring dove, short-day refractoriness develops rapidly in November to allow the bird to breed when the opportunity arises, during the winter and early spring. The annual breeding cycle is synchronized by a short-day induced regression of the reproductive system in the autumn, the primary function of which may be to enable the birds to meet the energy requirements for the annual moult. The changes in plasma T4, corticosterone and especially of GH at this time of year are probably concerned with the control of moult or the associated changes in energy requirements.

Animals↗

Stimulation of in-vivo growth hormone secretion in young chickens by rat hypothalamic growth hormone-releasing factor and synthetic analogues.

Rat hypothalamic GH-releasing factor (rhGRF), at doses between 0.1 and 10 micrograms/kg, increased plasma GH concentrations in immature domestic fowl 5-10 min after i.v. injection. Sodium pentobarbitone anaesthesia blunted the GH responses to rhGRF, although in both conscious and anaesthetized chicks the maximal responses were induced by a dose of 1 microgram rhGRF/kg. The stimulatory effect of rhGRF on in-vivo GH secretion was less than that provoked by corresponding doses of human pancreatic GRF, but greater than that elicited by two rhGRF analogues, (Nle27)-rhGRF(1-32) and (Nle27)-rhGRF(1-29). These results demonstrate that the chicken pituitary is responsive to mammalian GRF and provide evidence of structure-activity relationships of GRF in the domestic fowl.

Animals↗

Somatostatin immunoneutralization stimulates thyroid function in fowl.

The influence of somatostatin on thyroid function has been examined in immature domestic fowl passively immunized with somatostatin antiserum. Plasma thyroxine (T4) and tri-iodothyronine (T3) concentrations were markedly increased within 10 min of antisomatostatin administration and remained raised for at least 5 h. The increases in the T3 and T4 concentrations following somatostatin immunoneutralization were directly related to the volume of antisera administered. The increase in the T3 concentration exceeded the increase in the T4 concentration, resulting in a T3 : T4 ratio greater than unity. While the raised T4 concentration began to decline 30 min after antisomatostatin administration, raised T3 concentrations were sustained for at least 2 h, and further increased the plasma T3 : T4 ratio. These results demonstrate that somatostatin immunoneutralization stimulates thyroid function in fowl. The magnitude and rapidity of the thyroidal responses to somatostatin immunoneutralization suggests that they occur independently of the hypothalamic-pituitary-thyroid axis. Somatostatin appears to exert a tonic inhibitory control on avian thyroid function, possibly by effects mediated at the thyroid gland to inhibit T4 release and by peripheral effects to suppress the conversion of T4 and T3.

Animals↗

Serotoninergic inhibition of LH secretion in the domestic fowl.

Immature cockerels were injected with drugs known to affect serotoninergic activity. The receptor agonist quipazine as well as pargyline, an inhibitor of serotonin breakdown, both reduced plasma LH concentrations in a time-dependent fashion. The effect of pargyline was also dose-related. The serotonin precursor, tryptophan, reduced plasma LH levels. Tryptophan and pargyline were as effective in pubertal cockerels as in 3-week-old birds. Responses to quipazine were attenuated by the antagonist, methysergide, although another antagonist, cyproheptadine, also reduced plasma LH levels. Serotonin itself had no effect on plasma LH levels. Parachlorophenylalanine, which blocks serotonin synthesis, had no effect on plasma LH by itself, but attenuated the tryptophan-induced inhibition of LH. These data indicate that serotoninergic mechanisms inhibit secretion of LH in domestic fowl. This mechanism probably operates through the central nervous system.

Animals↗

In-vitro conversion of thyroxine to tri-iodothyronine by chicken hepatic 5'-deiodinase: kinetic studies.

In-vitro studies with chicken liver homogenates demonstrate that the conversion of thyroxine (T4) to tri-iodothyronine (T3) is dependent upon tissue concentration, time of incubation, pH, temperature, the presence of dithiothreitol (DTT) and the concentration of substrate (T4), and is heat-labile. The generation of T3 is inhibited by iopanoic acid and 6-n-propyl-2-thiouracil. The kinetics of conversion of T4 to T3, determined by Lineweaver-Burke analysis, indicated an apparent Michaelis-Menten constant (Km) of 1.16 mumol/l with a maximum velocity (Vmax) of 44.57 pmol T3 generated/mg protein per min from T4. Dithiothreitol appears to behave as a co-substrate for this system with an apparent Km of 98.5 mumol/l and a Vmax of 1.41 pmol T3 generated/mg protein per min at a T4 concentration of 5 mumol/l. These data suggest that the conversion of T4 to T3 in fowl proceeds by means of an enzymatic system, probably 5'-monodeiodinase, and is responsible for maintaining T3 levels in vivo.

Animals↗

Somatostatin tonically inhibits growth hormone secretion in domestic fowl.

Passive immunization of immature chickens with sheep somatostatin (SRIF) antiserum promptly increased the basal plasma GH concentration and augmented TRH-induced GH secretion. Although exogenous SRIF had no inhibitory effect on the basal GH concentration in untreated birds or birds pretreated with non-immune sheep serum, it suppressed the stimulatory effect of SRIF immunoneutralization on GH secretion. These results suggest that SRIF is physiologically involved in the control of GH secretion in birds, in which it appears to inhibit GH release tonically.

Animals↗

Plasma levels of luteinizing hormone, growth hormone, and estradiol from six weeks of age to sexual maturity in two lines of chickens selected for low or high abdominal fat content.

An experiment was conducted to investigate possible differences in plasma hormone levels between females of two lines of chickens selected for high (FL) or low (LL) abdominal fat content. Blood was taken at weekly intervals from 6 weeks of age to sexual maturity, and assays were performed for luteinizing hormone (LH), growth hormone (GH), and estradiol (E2). Age-related increases in the plasma titers of LH and estradiol were found while GH remained low apart from initial and final fluctuations. There was no difference between the strains in plasma E2, only minor differences in plasma GH, but a clear-cut difference was observed in plasma LH during the prepubertal period. Plasma LH tended to be higher in the LL, but the reason for this remains unclear.

Adipose Tissue↗

Endocrine changes associated with fat deposition and mobilization in svalbard ptarmigan (Lagopus mutus hyperboreus).

Plasma concentrations of Triiodothyronine (T3), thyroxine (T4) and growth hormone (GH) have been measured in blood samples taken from Svalbard ptarmigans (Lagopus mutus hyperboreus), shot throughout 1 whole year at Svalbard (79 degrees N). Plasma T3 levels varied in a monophasic pattern with low levels in winter and a peak in August, whereas plasma T4 levels remained constant throughout the year. High plasma T3 levels coincide with molt and a large food intake while low plasma levels of T3 coincide with molt arrest and a low food intake. Plasma GH levels were highest in winter and lowest in May and September. The low plasma GH levels in early autumn coincide with elevated liver weights and maximum rate of fat deposition. High GH levels in midwinter coincide with low liver weights and the mobilization of fat stores. A possible relationship between molt, food intake, fat deposition/mobilization, and plasma levels of T3 and GH is discussed.

Adipose Tissue↗

Calcium control of growth hormone release from chicken pituitary glands in vitro.

The influence of calcium on the basal and stimulated release of growth hormone (GH) from chicken pituitary glands has been determined in vitro. Basal GH release occurred in Ca2+ deficient media, although it was increased in proportion to the medium Ca2+ concentration. Growth hormone release was stimulated by 10(-7)-10(-9) M thyrotrophin-releasing hormone (TRH), maximal stimulation being observed in the presence of 10(-8) M TRH and 1.5 mM Ca2+. Decreases in the Ca2+ concentration (to 0.75, 0.375, or 0 mM) suppressed the GH response to 10(-8) M TRH, as did increases (to 3.0 and 6.0 mM) in the Ca2+ concentration. These results suggest that GH release in chickens is regulated by Ca2+-dependent mechanisms.

Animals↗

Food intake regulation of circulating thyroid hormones in domestic fowl.

The relationship between food intake and thyroid function has been investigated in immature domestic fowl. Starvation delayed, but did not suppress, the triiodothyronine (T3) response to intravenously administered thyrotropin-releasing hormone (10 micrograms/kg). This probably resulted from a suppression of monodeiodinase activity, since the conversion of thyroxine (T4) to T3 in thyroidectomised birds following an intramuscular injection of T4 (10 micrograms/kg) was markedly reduced by starvation. Starvation, for 24 or 48 hr, lowered the circulating T3 level but increased the T4 concentration. When fasted birds were refed the T4 concentration was initially enhanced but subsequently declined as the T3 concentration progressively increased. The accompanying decline in the T4:T3 ratio in fasted-refed birds indicated that the rise in the T3 level resulted from the peripheral monodeiodination of T4. The increase in T3 concentration could be induced solely by carbohydrate; the intraperitoneal administration of glucose (2.0 g/kg) to fasted birds resulting in a slight, transient rise in the T3 concentration and a fall in the T4:T3 ratio. The generation of T3 was also energy dependent, in that the magnitude of the T3 response of fasted birds to refeeding was proportional to the amount of food consumed and to the metabolisable energy (ME) content of the diet. Moreover, when exogenous T4 (100 micrograms/kg) was intramuscularly administered to thyroidectomised birds fed a diet with a high ME content, the conversion of T4 to T4 was greater than that in birds fed a diet of lower ME content. These results demonstrate that nutritional stimuli are involved in the regulation of thyroid function in birds, particularly in the peripheral generation of T3.

Animals↗

Haemorrhage and adrenocortical activity in the fowl (Gallus domesticus).

Plasma aldosterone concentrations were markedly elevated in chickens by the removal of 10-30% of their total blood volume. This aldosterone response to haemorrhage was delayed and of reduced magnitude in birds pretreated for 48 hr with dexamethasone (100 micrograms/kg every 12 hr), in which the basal aldosterone level was also suppressed. Corticosterone concentrations were elevated in both haemorrhaged and nonhaemorrhaged birds, although these responses were completely abolished by dexamethasone pretreatment, which also reduced the basal corticosterone concentration. Prolactin concentrations were unaffected by haemorrhage. These results demonstrate that haemorrhage specifically affects adrenocortical function by increasing aldosterone release and suggests that factors other than the pituitary-adrenal axis are responsible for this stimulation of secretion.

Adrenal Cortex↗

Independence of salt gland function and adrenocortical activity in ducks (Anas platyrhynchos).

In immature ducklings injected with hypertonic saline the volume of extrarenal salt gland secretion was unaffected by prior treatment (immediately or 4 hr before salt loading) with long-lasting adrenocorticotrophin (ACTH 100 iu/kg, im) or exogenous corticosterone (1.0 mg/kg, im). Pretreatment with metyrapone, an 11-beta-hydroxylase blocker, (80 mg/kg, im) 4 hr before salt loading did not effect the volume of salt gland secretion but delayed the onset of extrarenal excretion. Salt gland function was suppressed in birds pretreated with metyrapone immediately prior to salt loading. The intravenous administration of metyrapone after salt loading immediately reduced salt gland activity, which remained suppressed for at least 40-50 min thereafter. The inhibitory effect of metyrapone on salt gland activity was not counteracted by the subsequent or simultaneous administration of exogenous corticosterone to salt-loaded ducks. These results suggest that acute alterations in adrenocortical activity are not causally responsible for changes in salt gland function.

Adrenal Cortex↗