Plasma Corticosteroid Concentrations Research Articles

Penetration of corticosteroids into the lung: Evidence for a difference between methylprednisolone and prednisolone

Little is known about the penetration of corticosteroids, such as methylprednisolone and prednisolone, into the lung, despite their common use in the treatment of inflammatory lung diseases. To compare methylprednisolone and prednisolone concentrations in the bronchoalveolar space, we administered these two corticosteroids in a randomized, crossover fashion to 17 adult rabbits. A loading dose was administered and was followed by a continuous infusion for 180 minutes to achieve steady-state plasma concentrations between 200 to 2000 ng/ml. Serial plasma samples were obtained during the infusions. Bronchoalveolar lavages (BAL) were performed at 180 minutes with sterile saline. Plasma and BAL fluid (BALF) were assayed for methylprednisolone and prednisolone concentration by high-performance liquid chromatography. Corticosteroid concentrations were normalized to urea concentrations in plasma and BALF. Generally, BALF corticosteroid concentration increased as plasma concentration increased. At plasma concentrations >800 ng/ml, BALF methylprednisolone concentrations increased exponentially, whereas the increase for prednisolone remained linear. BALF methylprednisolone was five times as high as that of prednisolone when plasma corticosteroid concentration was in the 2000 ng/ml range. With this continuous infusion technique, methylprednisolone has a higher degree of bronchoalveolar penetration than prednisolone, and these differences are greater at higher plasma concentrations.

Neither chronic exposure to ethanol nor aging affects type I or type II corticosteroid receptors in rat hippocampus

Both chronic exposure to ethanol and aging are reported to result in a loss of hippocampal pyramidal neurons and an elevation in plasma corticosteroid concentration. Aging has also been reported to result in a reduction in corticosterone receptors and corticosterone-concentrating cells in the hippocampus. Since these aging-associated effects have been hypothesized to be due to the cumulative exposure to corticosteroids over the life span, in the present studies, we investigated the hypothesis that corticosteroids play a similar role in the loss of hippocampal neurons during chronic ethanol ingestion. In contrast to our expectations, when a liquid diet containing either ethanol or sucrose was administered to male Long-Evans rats for 20–24 weeks, a period of treatment found previously to result in hippocampal neuronal loss, there were no ethanol-associated effects on the specific binding of [ 3H]-aldosterone to Type I or of [ 3H]dexamethasone to Type II receptors in cytosol derived from either whole hippocampus or dorsal versus ventral hippocampus. Allowing the rats to withdraw from the chronic ethanol exposure for 12 weeks also failed to reveal any ethanol-associated effects on corticosteroid receptor concentrations in the hippocampus. The basal morning concentrations of corticosterone in blood plasma were not affected by any of these treatments. In view of these null findings we next investigated the effects of aging on hippocampal corticosteroid receptors in male Long-Evans and Fischer 344 rats. Again we were surprised to find no aging-associated reductions in [ 3H]aldosterone-Type I, [ 3H]corticosterone-Type I or [ 3H]dexamethasone-Type II receptor concentrations in whole hippocampal cytosol, despite the fact that plasma concentrations of CORT were clearly elevated in the aged Long-Evans rats. Our results, therefore, do not support the hypothesis that corticosteroids play a significant role in the loss of hippocampal neurons associated with chronic ethanol ingestion or aging.

Control of canine ACTH by corticosteroids: an integral feedback effect of steroids

These experiments were designed to test whether the pattern of change in plasma corticosteroid or the total corticosteroid dose is important in determining the degree of inhibition of adrenocorticotropic hormone (ACTH) responses to stress by corticosteroid intermediate-delayed feedback. Five conscious dogs were studied. The ACTH response to induced hypoglycemia was measured after no prior corticosteroid feedback signal or after a corticosteroid feedback signal produced by infusion, two bolus injections, or three bolus injections of cortisol and corticosterone. The total corticosteroid dose (45 micrograms/kg) and the total interval of steroid treatment (60-30 min before hypoglycemia) were the same in all three cases of corticosteroid treatment. Changes in plasma glucose concentration during induced hypoglycemia were not altered by corticosteroid treatment. The plasma ACTH response to hypoglycemia was inhibited by all three patterns of treatment with corticosteroids. The inhibition of ACTH response was not significantly altered among the patterns of treatment with corticosteroids. The data suggest that the integrated (total) or the mean change in plasma corticosteroid concentration over time determines the degree of inhibition of stimulated ACTH in this time domain.

Evidence for rapid inhibition of ACTH by corticosteroids in dogs.

These experiments were designed to determine whether stimulated adrenocorticotropic hormone (ACTH) secretion in dogs can be rapidly inhibited by increases in plasma corticosteroid concentrations. Five dogs were injected with a 2:1 mixture of cortisol to corticosterone (corticosteroids; total doses of 22.5, 45, or 90 micrograms/kg) or vehicle simultaneously with the injection of insulin (0.5 U/kg). These dogs were also injected with corticosteroids (45 micrograms/kg) with ovine corticotropin-releasing factor (oCRF-41; 1 micrograms/kg) or with the same dose of corticosteroids alone. Plasma ACTH and corticosteroid concentrations were measured for 90 min after the injections. The inhibition of ACTH secretion was significant 10 min after injection of oCRF-41 and 40 min after injection of insulin. The first significant increase in ACTH during insulin-induced hypoglycemia does not occur until 30 min, however. Therefore, after both of these stimuli to ACTH, the ACTH response is inhibited within approximately 10 min of its onset. The results suggest that canine ACTH responses to stimuli can be rapidly inhibited and that one site of this inhibition is the pituitary.

Effects of low dose ovine corticotropin-releasing hormone in humans: endocrine relationships and beta-endorphin/beta-lipotropin responses.

The effects of low doses (0.03 and 0.1 microgram/kg) of ovine CRH (oCRH) on plasma beta-endorphin/beta-lipotropin (beta End/beta LPH), ACTH, and corticosteroid levels were studied in normal men. The 0.03 microgram/kg oCRH dose produced a reproducible response, with a rapid increase in plasma oCRH to peak levels between 45 and 95 fmol/mL and an appropriate doubling of plasma peptide and corticosteroid concentrations. The relationship between the corticosteroid rise and the rapid beta End/beta LPH and ACTH declines suggested negative feedback by corticosteroids on the release of these pituitary products. Plasma oCRH levels were proportionate to those reported in studies using much higher oCRH doses, and produced plasma oCRH levels in the reported range for the hypophyseal portal circulation. Molecular sieving of the beta End-immunoreactive materials in basal and post-oCRH (0.1 microgram/kg) plasma samples revealed an average basal beta End to beta LPH ratio of 1:1.5; 15 min after oCRH stimulation the average ratio was 4:1. We conclude that a low (threshold) dose of oCRH can reliably stimulate POMC peptide secretion and may preferentially release beta End from the anterior pituitary.

The Effect of Mating and Agonistic Experience on Adrenal Function and Mortality of Male Antechinus stuartii (Marsupialia)

The effects of agonistic and mating behavior on androgen and total plasma corticosteroid concentrations and the maximum corticosteroid binding capacity (MCBC) were investigated in male Antechinus stuartii. Males were subjected to three experimental conditions: isolated from all conspecifics, in daily physical contact with conspecific males, and in intermittent contact with conspecific estrous females. There were no differences among groups in either androgen concentrations or MCBC. Males in contact with other males and therefore subjected to daily aggressive encounters showed greater mortality and significantly higher total plasma corticosteroid levels in mid-August at the end of the breeding season. Results suggest that interactions with estrous females may lower total corticosteroid concentrations and have an ameliorating effect on the stress caused by competition with other males.

Suppression of plasma aldosterone by chronic ACTH administration is offset by converting enzyme inhibitor.

In order to elucidate the mechanism of suppression of plasma aldosterone by chronic ACTH administration, especially the role of the renin-angiotensin system and dopamine, we administered ACTH with or without MK422, a converting enzyme inhibitor, to reduce the endogenous angiotensin II in rats, and measured the plasma renin activity, plasma corticoid concentrations and urinary dopamine excretion. The plasma aldosterone concentration (PAC) was decreased after chronic ACTH administration. However, in the ACTH + MK422 administered group, aldosterone suppression was not observed. It appeared therefore that the aldosterone suppressing mechanism was independent of the weakened renin-angiotensin system following chronic ACTH administration, since PAC was not decreased in the ACTH + MK422 administered group when angiotensin II might be completely eliminated. The urinary excretion of dopamine was significantly increased in the chronic ACTH + MK422 administered group as well as in the chronic ACTH administered group. This suggested that the inhibitory effect of dopamine on aldosterone did not contribute significantly to the suppression of plasma aldosterone. The present results suggest therefore that the mechanism of suppression of plasma aldosterone following chronic ACTH administration was not dependent on the renin-angiotensin system and dopamine.

Transplacental stimulation of fetal lung maturation: effect of triiodothyronine in the female and male rabbit fetus.

We have recently demonstrated that intramuscular administration of triiodothyronine (T3) or thyroxine (T4) to the rabbit doe results in its transfer across the placenta. In this study we investigated the effect of maternally administered T3 upon the functional and morphologic fetal lung maturation. T3 (175 micrograms/kg) or the vehicle was injected intramuscularly into the New Zealand White rabbit does on days 25 and 26 of gestation. On day 27 of pregnancy, the does were killed and the fetuses were delivered. Maternal and fetal plasma T3, glucose and insulin and fetal plasma corticosteroid concentrations were determined. The functional pulmonary maturity was assessed by performing the pressure-volume hysteresis while morphologic maturity was established by histologic techniques. Enhanced functional as well as morphologic fetal lung maturation was observed in female as well as male fetuses in T3-treated animals. However, there was a significant increase in the fetal mortality after T3 treatment, and the duration of survival in the extrauterine environment on premature delivery was not prolonged.

Adrenocortical functions in a macropodid marsupial Thylogale billardierii.

In a study of adrenocortical functions in macropodid marsupials, measurements were made of the effects of ACTH infusion, ether stress and adrenaline infusion on plasma corticosteroid and glucose concentrations in wallabies (Thylogale billardierii) provided with indwelling venous catheters. The mean plasma total glucocorticoid concentration in undisturbed males and females was 80 +/- 5 (S.E.M.) micrograms/l, of which more than 90% was cortisol. This fraction declined to 68% of the total at the highest ACTH-stimulated concentration of 225 micrograms/l, due to an increase in the contribution by 11-deoxycortisol. Although maximal ACTH stimulation (4.5 i.u./kg per h) caused a five- to sixfold increase in cortisol secretion rate, as measured by isotope dilution during constant-rate tracer infusion, plasma cortisol concentration rose only two- to threefold, due to a marked increase in metabolic clearance. Plasma glucose concentration did not change significantly during either short-term (1 h) i.v. infusion or long-term (8 days) i.m. injection of ACTH, even though plasma cortisol concentration was significantly increased. Ether anaesthesia caused a marked hyperglycaemia that preceded an increase in plasma cortisol concentration and was not sustained while plasma cortisol concentration continued to increase. Infusion of adrenaline i.v. at rates sufficient to cause a similar hyperglycaemia had no significant effect on plasma cortisol concentration. A marked hyperglycaemia during xylazine anaesthesia was not associated with an increase in plasma cortisol concentration and was attributable to suppression of insulin secretion.(ABSTRACT TRUNCATED AT 250 WORDS)

Cardiac receptors, vasopressin, and corticosteroid release during arterial hypotension in dogs.

The relative roles of cardiopulmonary and sinoaortic baroreceptors in the regulation of vasopressin and corticosteroid release were evaluated in conscious dogs. The dogs were prepared with inflatable cuffs around either the ascending aorta, proximal to the brachiocephalic trunk, or the pulmonary artery. Inflation of the cuffs was adjusted to cause a reduction of mean systemic arterial pressure (MAP) of 0, 5, 10, 20, or 30% of control for 1 h in separate experiments. In spite of the profound systemic hypotension caused by constriction of the ascending aorta, plasma vasopressin failed to increase and corticosteroids increased only in response to a 30% decrease in MAP. In contrast, a 5% reduction in MAP during pulmonary arterial constriction increased plasma vasopressin and corticosteroid concentrations significantly. The apparent paradox in these results is correlated with different effects of the two maneuvers on left atrial pressure. Left atrial pressure increased dose dependently during inflation of the ascending aortic cuff but decreased during inflation of the pulmonary arterial cuff. In contrast, graded inflation of the pulmonary arterial cuff caused dose-dependent increases in right atrial pressure, plasma vasopressin, and corticosteroids. Therefore, we conclude that powerful inhibitory signals, arising from the left heart, can inhibit vasopressin and hypotension release in response to systemic hypotension.

The effect of road transportation on the blood constituents and behaviour of calves. III. Three months old

Three-month-old Friesian and Hereford cross-bred calves were transported for either 6 (group J) or 18 h (group K). Blood samples taken before, at intervals during and after the journeys were analysed for haematocrit, total and differential leucocyte count, plasma corticosteroid and glucose, serum non-esterified fatty acids (NEFA), calcium, aspartate amino transferase (AST) and creatine kinase (CK). When values measured in the transported calves were compared with values obtained in six starved control calves (group L), there were no significant changes in haematocrit, lymphocyte numbers, serum calcium, AST and CK estimations. The total leucocyte count and neutrophil numbers rose to a mean maximum about 6 h after the journey started, irrespective of the distance travelled. The plasma corticosteroid concentration rose significantly to a maximum within 10 min of the journey starting. The plasma glucose and the mean serum NEFA concentrations rose gradually throughout the journeys, and remained above pre-transport levels up to 7 h after the 18-h journey. The plasma glucose concentration fell slowly after the 6-h journey, until the calves were fed. The calves lay for about 14% of the 6-h journey and 42% of the 18-h journey; 24% of the 18-h transportation was spent ruminating, of which 34% occurred while the calves were standing. Only one calf (0·3%) ruminated during the 6-h journey. The in-transit weight loss was 4·6 ± 0·6 kg for a 6-h journey (2·6 ± 0·3 kg controls) and 6·5 ± 1·1 kg for the 18-h journey (5·9 ± 0·5 kg).

Interaction between angiotensin II and the baroreceptor reflex in the control of adrenocorticotropic hormone secretion and heart rate in conscious dogs.

The present studies were designed to examine the effect of angiotensin II on baroreflex control of adrenocorticotropic hormone secretion and heart rate in conscious dogs. Baroreflex function was assessed by examining the relationship between blood pressure and plasma corticosteroid concentration (used as an index of adrenocorticotropic hormone secretion) and between blood pressure and pulse interval (the inverse of heart rate). Blood pressure was varied by intravenous infusion of four doses (0.3, 0.6, 1.5, and 3.0 micrograms/kg per min) of the vasodilator nitroprusside. Nitroprusside infusion produced an increase in plasma corticosteroid concentration and a decrease in pulse interval, both of which were linearly related to the fall in arterial blood pressure. During infusion of angiotensin II (10 ng/kg per min), however, the lines relating blood pressure to plasma corticosteroid concentration or blood pressure to pulse interval were shifted to a higher pressure level, suggesting that angiotensin II resets the baroreceptor reflex. Angiotensin II blockade with saralasin, an angiotensin II antagonist, or with captopril, a converting enzyme inhibitor, in sodium-depleted dogs with elevated plasma angiotensin II levels produced a shift in the opposite direction in these relationships. Because baroreflex function in sodium-depleted dogs before angiotensin II blockade was similar to that in sodium-replete dogs, despite the increased plasma angiotensin II levels, and because treatment of sodium-replete dogs with saralasin did not affect baroreflex function, these results suggest that endogenous angiotensin II is necessary for the maintenance of normal baroreflex control of adrenocorticotropic hormone secretion and heart rate during sodium depletion. Previous studies designed to evaluate the physiological significance of angiotensin II in the control of adrenocorticotropic hormone secretion showed that high, perhaps supraphysiological, levels of exogenous angiotensin II are required to increase adrenocorticotropic hormone secretion. An additional finding of the present study was that exogenous angiotensin II produces a larger increase in adrenocorticotropic hormone secretion when the pressor effect of angiotensin II was eliminated with simultaneous infusion of the vasodilators nitroprusside or hydralazine. This result suggests that experiments that evaluate the physiological role of angiotensin II in the control of adrenocorticotropic hormone secretion with infusions of exogenous AII may underestimate the importance of endogenously produced angiotensin II, which is normally released without an increase in pressure.

Plasma Corticosteroid Stress Response of Fourteen Species of Warmwater Fish to Transportation

Plasma corticosteroid concentrations were measured in 14 species of fish immediately after they were electrofished from reservoirs on the Alabama River and after they had been transported for 2 h. There was no corticosteroid response in spotted gars Lepisosteus oculatus. Bowfins Amia calva, longnose gars Lepisosteus osseus, and freshwater drums Aplodinotus grunniens had only small corticosteroid increases (14–39 ng/mL) during transportation. Corticosteroids increased by intermediate amounts (59–184 ng/mL) during transportation in blue catfish Ictalurus furcatus, paddlefish Polyodon spathula, largemouth bass Micropterus salmoides, channel catfish Ictalurus punctatus, river carpsuckers Carpiodes carpio, white bass Morone chrysops, striped bass Morone saxatilis, and crappies Pomoxis sp. The greatest increases were 223 ng/mL in gizzard shad Dorosoma cepedianum and 286 ng/mL in common carp Cyprinus carpio. Spotted and longnose gars, largemouth bass, and common carp also were held in tanks for about 2 months at 21°C and then stressed by confinement in a dip net for 30 min. The confinement caused significant increases (P < 0.01) of plasma corticosteroid concentration in all four species. Dip-net confinement appears to be a useful method for comparing corticosteroid responses among species of warmwater fish.

The effect of road transportation on the blood constituents and behaviour of calves. II. One to three weeks old

Six calves, one to three weeks old, were transported by road for 6 h (group J) and another six for 18 h (group K). Blood samples taken before, during and after the journeys were analysed for haematocrit, total and differential leucocyte count, plasma corticosteroid and glucose, serum non-esterified fatty acids (NEFA), total protein and calcium levels, aspartate amino transferase (AST) and creatine kinase (CK) activities. In comparison with the levels found in a group of six calves only starved for 18 h (group L) there were no significant changes in haematocrit, total leucocyte count, serum NEFA, total protein, calcium, AST and CK estimations of transported calves (group J & K). The plasma corticosteroid concentration rose significantly only after loading and, in group K, immediately after unloading. A decrease in plasma glucose occurred after the 6-h journey when calves were not fed for a further 12 h. There was a significant increase in neutrophil numbers and decrease in lymphocyte numbers in both transported groups of calves. The mean loss of weight resulting from 6-h transportation was 1·95 kg (1·5 kg starvation only) and for 18 h 2·95 kg (2·36 kg). Calves lay down for 0 to 55% of the journey and ruminated for 2·9 to 35% of the time.

Characteristics of the receptors which mediate the stimulation of ACTH secretion by vasopressin in conscious dogs.

In order to characterize the receptors which mediate the adrenocorticotropic hormone (ACTH) response to vasopressin in conscious animals, plasma 11-hydroxycorticosteroid concentration was measured in conscious dogs during the infusion of vasopressin or structural analogs of vasopressin which exhibit selective antidiuretic or vasoconstrictor activity. Vasopressin (1.0 ng/kg/min for 60 min) increased mean arterial pressure, decreased heart rate and increased plasma corticosteroid concentration from 1.0 +/- 0.2 to 2.2 +/- 0.2 micrograms/dl (p less than 0.001). A specific antagonist of the vasoconstrictor activity of vasopressin, d(CH2)5MeTyrAVP (10 micrograms/kg), completely blocked the cardiovascular and corticosteroid responses to vasopressin. A selective vasoconstrictor (V1) agonist, PheOrnOT (1.0 ng/kg/min), which produced the same cardiovascular responses as vasopressin, increased plasma corticosteroid concentration from 1.1 +/- 0.1 to 2.9 +/- 0.9 micrograms/dl (p less than 0.005). In marked contrast, a selective antidiuretic (V2) agonist, dDAVP (1.0 ng/kg/min) had no effect on blood pressure, heart rate or plasma corticosteroid concentration. These results indicate that the stimulation of ACTH release by vasopressin in conscious dogs is mediated by receptors which resemble vasoconstrictor-type (V1) receptors rather than antidiuretic-type (V2) receptors.

Effects of dibutyryladenosine 3',5'-monophosphate on steroid biosynthesis in humans.

The effects of dibutyryladenosine 3', 5'-monophosphate (DBcAMP), a nucleotide analogue, on blood pressure, serum electrolytes and plasma corticoid concentrations were investigated in 10 normotensive healthy subjects who received a constant diet containing 5-8 g sodium chloride in hospital. The systolic blood pressure did not change after infusion of 0.25 or 0.33 mg/kg/min of DBcAMP for 20 min. On the other hand, the diastolic blood pressure was significantly decreased after the infusion of DBcAMP. The levels of serum sodium and potassium were significantly decreased after the infusion of DBcAMP. After infusion of 0.25 mg/kg/min of DBcAMP for 20 min, the changes in plasma levels of 6 corticoids [progesterone, deoxycorticosterone (DOC), 18-hydroxy-deoxycorticosterone (18-OH-DOC), corticosterone, cortisol and dehydroepiandrosterone sulfate (DHEA-S] revealed no significant changes. After infusion of 0.33 mg/kg/min of DBcAMP for 20 min, the plasma levels of cortisol, corticosterone and 18-OH-DOC were significantly increased and the changes in plasma levels of aldosterone showed a tendency to increase but this was not significant. The plasma levels of DOC and DHEA-S were not appreciably changed, while the plasma levels of progesterone were significantly decreased after the infusion of 0.33 mg/kg/min of DBcAMP. It is speculated therefore that DBcAMP may act to enhance the activity of the sodium-potassium pump and to promote steroid biosynthesis dose-dependently in humans.

Behavioural, physiological and immunological consequences of social status and aggression in chronically coexisting resident-intruder dyads of male rats

The behavioural and physiological consequences of social status and reciprocal fighting in resident-intruder dyads of Long Evans male rats were evaluated. Before a chronic cohabitation of 10 days, residents and intruders were individually housed for one month to increase their aggressiveness. Control animals included isolates, i.e., animals kept individually housed throughout the experiment and pair-housed rats, i.e., pairs of rats housed together from their rats in the laboratory. In 19 out of 20 dyads, a clear dominance relationship developed with an advantage to the resident in 68% of the cases. Dominants showed more exploratory activity than subordinates in an open-field test at the end of the cohabitation period; subordinates groomed longer than animals from other experimental groups. Dominants had lower pain thresholds than individually and pair-housed animals. Both dominants and subordinates had higher tyrosine hydroxylase enzymatic activities in the left adrenal than isolated and pair-housed rats. Subordinates lost body weight and had higher plasma corticosteroid concentrations than animals from the other experimental groups. In addition, they had smaller thymus glands and reduced spleen lymphocyte responses to mitogenic stimulation in vitro, in comparison to dominant animals. These results show that subordination in the dyadic resident-intruder paradigm leads to a complex syndrome of behavioural and physiological changes, some of which may be modulated by the intensity of aggressive interactions.

Effect of bromocriptine treatment on the aldosterone response to angiotensin II and adrenocorticotropin in idiopathic hyperaldosteronism.

Bromocriptine can prevent an increase in plasma aldosterone during the infusion of angiotensin II in normal subjects and during upright posture in some patients with idiopathic hyperaldosteronism. To determine if bromocriptine prevents the increase in plasma aldosterone concentration during angiotensin II infusion in idiopathic hyperaldosteronism, we infused angiotensin II in five patients with idiopathic hyperaldosteronism, before and after treatment with bromocriptine (2.5 mg, three times daily for 5 days), and measured the resulting plasma aldosterone and angiotensin II concentrations. We also determined the adrenal response to ACTH infusion before and after bromocriptine treatment in four of these patients. Bromocriptine treatment did not significantly change the plasma concentrations of aldosterone before or during the infusions of angiotensin II and ACTH. It did significantly decrease mean blood pressure and increase the plasma corticosteroid concentrations in the preinfusion periods, but it did not alter the response of blood pressure to angiotensin II or of plasma corticosteroid concentrations to the ACTH infusions.

Corticosteroid Levels in White Leghorn Hens as Affected by Handling, Laying-House Environment, and Genetic Stock

Correlation coefficients between handling time and plasma corticosteroid concentration of White Leghorn hens were minimal when times varied from 43 to 161 sec (r=.17; P<.05, df=244), and no association was found when blood collection times exceeding 90 sec were omitted (r=−.02, df=219). Handling times carried to specific endpoints of 30 and 60 sec indicated no difference, but times of 60, 120, 180, and 600 sec were associated with highly significant differences in corticosteroid levels that were inconsistent between genetic stocks. Strains selected for increased part-year egg mass responded less rapidly to handling than did unselected control strains. Confinement of hens for 4 to 6 hr in nests within their own pens caused increases of >30% in corticosteroids as compared to samples obtained from hens caught directly from the floor.Neither floor pen vs. colony cage nor genetic stock differences were found for plasma corticosteroid levels of hens at a mean age of 55 weeks. Adrenocorticotropic hormone stimulation of 63-week-old hens caused an 8.5-fold increase in corticosteroids above basal but failed to elicit differential effects associated with environments or genetic stocks. Nevertheless, hens kept in floor pens had 10.8% higher survival in the laying house and exceeded colony-cage hens by more than 40% in hen-day egg mass for the final 10 weeks of a 40-week laying period.

Confinement and Water Quality-Induced Stress in Largemouth Bass

Plasma values of corticosteroids, glucose, chloride, and osmolality were determined in largemouth bass Micropterus salmoides under various environmental conditions. No differences were observed in quiescent fish due to sex, size, time of day, or the types of holding facilities tested (tanks, raceways, ponds). Differences were observed in plasma glucose, chloride, and osmolality values among fish acclimated to 10, 16, and 23 C. Abrupt temperature changes caused elevations in plasma corticosteroid and glucose concentrations and reduced plasma chloride and osmolality. Confinement in a net, for up to 48 hours, caused elevated glucose and corticosteroids and reduced chloride and osmolality values. After 48 hours of confinement, fish required up to 14 days to recover normal plasma characters. Generally, short-term exposure to poor water quality (high concentrations of CO2 and NH3, and low concentrations of dissolved oxygen) altered plasma corticosteroids and glucose but had little effect on plasma chloride or osmolality. Net confinement plus poor water quality caused additional stress. Plasma glucose and corticosteroid values were good indicators of stress during application of acute stressors whereas chloride and osmolality were useful indicators of long-term stress and patterns of recovery after stressors were removed. Received October 14, 1983 Accepted August 23, 1984