Lower Plasma Cortisol Concentrations Research Articles

The relationship between hypoxia exposure and circulating cortisol levels in social and solitary African mole-rats: An initial report

Hypoxemia from exposure to intermittent and/or acute environmental hypoxia (lower oxygen concentration) is a severe stressor for many animal species. The response to hypoxia of the hypothalamic–pituitary-adrenal axis (HPA-axis), which culminates in the release of glucocorticoids, has been well-studied in hypoxia-intolerant surface-dwelling mammals. Several group-living (social) subterranean species, including most African mole-rats, are hypoxia-tolerant, likely due to regular exposure to intermittent hypoxia in their underground burrows. Conversely, solitary mole-rat species, lack many adaptive mechanisms, making them less hypoxia-tolerant than the social genera. To date, the release of glucocorticoids in response to hypoxia has not been measured in hypoxia-tolerant mammalian species. Consequently, this study exposed three social African mole-rat species and two solitary mole-rat species to normoxia, or acute hypoxia and then measured their respective plasma glucocorticoid (cortisol) concentrations. Social mole-rats had lower plasma cortisol concentrations under normoxia than the solitary genera. Furthermore, individuals of all three of the social mole-rat species exhibited significantly increased plasma cortisol concentrations after hypoxia, similar to those of hypoxia-intolerant surface-dwelling species. By contrast, individuals of the two solitary species had a reduced plasma cortisol response to acute hypoxia, possibly due to increased plasma cortisol under normoxia. If placed in perspective with other closely related surface-dwelling species, the regular exposure of the social African mole-rats to hypoxia may have reduced the basal levels of the components for the adaptive mechanisms associated with hypoxia exposure, including circulating cortisol levels. Similarly, the influence of body mass on plasma cortisol levels cannot be ignored. This study demonstrates that both hypoxia-tolerant rodents and hypoxia-intolerant terrestrial laboratory-bred rodents may possess similar HPA-axis responses from exposure to hypoxia. Further research is required to confirm the results from this pilot study and to further confirm how the cortisol concentrations may influence responses to hypoxia in African mole-rats.

Necroptosis Contributes to LPS-Induced Activation of the Hypothalamic-Pituitary-Adrenal Axis in a Piglet Model.

Stressors cause activation of the hypothalamic-pituitary-adrenal (HPA) axis and a systemic inflammatory response. As a newly proposed cell death manner in recent years, necroptosis occurs in a variety of tissue damage and inflammation. However, the role of necroptosis in HPA axis activation remains to be elucidated. The aim of this study was to investigate the occurrence of necroptosis and its role in HPA activation in a porcine stress model induced by Escherichia coli lipopolysaccharide (LPS). Several typical stress behaviors like fever, anorexia, shivering and vomiting were observed in piglets after LPS injection. HPA axis was activated as shown by increased plasma cortisol concentration and mRNA expression of pituitary corticotropin-releasing hormone receptor 1 (CRHR1) and adrenal steroidogenic acute regulatory protein (StAR). The mRNA expression of tumor necrosis factor α (TNF-α), interleukin-1β (IL-1β) and IL-6 in the hypothalamus, pituitary gland and adrenal gland was elevated by LPS, accompanied by the activation of necroptosis indicated by higher mRNA expression of necroptosis signals including receptor-interacting protein kinase (RIP) 1, RIP3, and phosphorylated mixed-lineage kinase domain-like protein (MLKL). Furthermore, necrostatin-1 (Nec-1), an inhibitor of necroptosis, inhibited necroptosis indicated by decreased mRNA levels of RIP1, RIP3, MLKL, and phosphoglycerate mutase family member 5 (PGAM5) in the hypothalamus, pituitary gland and adrenal gland. Nec-1 also decreased the mRNA expression of TNF-α and IL-β and inhibited the activation of the HPA axis indicated by lower plasma cortisol concentration and mRNA expression of adrenal type 2 melanocortin receptor (MC2R) and StAR. These findings suggest that necroptosis is present and contributes to HPA axis activation induced by LPS. These findings provide a potential possibility for necroptosis as an intervention target for alleviating HPA axis activation and stress responses.

PSIV-13 Effects of oral administration of vitamin E and selenium on stress indicators and oxidative biomarkers in road- transported pregnant Holstein heifer

Abstract We investigated the effects of oral administration of vitamin E and selenium (ESe) on oxidative stress biomarkers in road-transported pregnant heifers. Thirty-six pregnant Holstein heifers (body weight 515 ± 48.3 kg and age 524 ± 42.4 days) were assigned to four treatments: no transportation with no administration of ESe (NTR-NESe, n = 10); no transportation with oral administration of ESe (70 IU DL-alpha-tocopheryl acetate/kg of DM and 0.3 mg sodium selenite/kg of DM; NTR-ESe, n = 10); transportation with no administration (TR-NESe, n = 8); transportation with oral administration of ESe (TR-ESe, n = 8). Two trucks (8 heifers/truck) were used for the 200 km transportation. Blood was collected h 1 before, immediately after transportation (h 0), h 6, h 24 and h 48 after transportation. The TR × time and ESe × time effects were observed (P < 0.01) for plasma cortisol concentration, indicating that TR heifers had higher plasma cortisol concentrations than NTR heifers and that ESe-administrated heifers had lower plasma cortisol concentrations than NESe heifers at h 0 after transportation. The TR and ESe effects were observed (P < 0.01) for plasma haptoglobin (Hp) concentration. The TR increased Hp concentration at h 6 and h 24 after transportation, and ESe decreased Hp concentration in the transported heifers. The ESe (P = 0.02) and ESe × time interaction (P < 0.01) effects were observed for plasma total oxidative status (TOS) concentrations. The TR increased plasma TOS concentrations at h 0, and the ESe decreased plasma TOS concentrations in transported heifers. In contrast, the TR decreased (P < 0.05) plasma TAS concentrations at h 6 and h 24 after transportation, and the ESe increased (P < 0.05) plasma TAS concentrations in the transported heifers. These results suggest that transportation induces oxidative stress and the ESe may alleviate oxidative stress in the transported heifers.

Tissue Distribution and Immunomodulation in Channel Catfish (Ictalurus punctatus) Following Dietary Exposure to Polychlorinated Biphenyl Aroclors and Food Deprivation.

Although most countries banned manufacturing of polychlorinated biphenyls (PCBs) over 40 years ago, PCBs remain a global concern for wildlife and human health due to high bioaccumulation and biopersistance. PCB uptake mechanisms have been well studied in many taxa; however, less is known about depuration rates and how post-exposure diet can influence PCB concentrations and immune response in fish and wildlife populations. In a controlled laboratory environment, we investigated the influence of subchronic dietary exposure to two PCB Aroclors and food deprivation on tissue-specific concentrations of total PCBs and PCB homologs and innate immune function in channel catfish (Ictalurus punctatus). Overall, we found that the concentration of total PCBs and PCB homologs measured in whole body, fillet, and liver tissues declined more slowly in food-deprived fish, with slowest depuration observed in the liver. Additionally, fish that were exposed to PCBs had lower plasma cortisol concentrations, reduced phagocytic oxidative burst activity, and lower cytotoxic activity, suggesting that PCBs can influence stress and immune responses. However, for most measures of immune function, the effects of food deprivation had a larger effect on immune response than did PCB exposure. Taken together, these results suggest that short-term dietary exposure to PCBs can increase toxicity of consumable fish tissues for several weeks, and that PCB mixtures modulate immune and stress responses via multiple pathways. These results may inform development of human consumption advisories and can help predict and understand the influence of PCBs on fish health.

Black and white autoimmunity: early warning colours of adrenal crisis

A 31-year-old woman was admitted to the Department of Endocrinology, University Hospital of Nancy, with abdominal pain and vomiting that had been ongoing for 3 days. She had noticed a darkening of her skin colour, with some areas spared, over the previous 3 months and reported having asthenia, episodic diarrhoea, and weight loss for more than 12 months. Physical examination showed a non-segmental acrofacial vitiligo with an intense black and white contrast (figure A, D) and a cervical thyroidectomy scar as a result of surgery to treat Grave's disease (figure C). Both low plasma cortisol (19·2 nmol/L [normal range 185–624]) and high adrenocorticotropic hormone (74·1 pmol/L [1–10·7]) concentrations confirmed a primary adrenal insufficiency. This diagnosis was supported by visualisation of atrophy of the adrenal glands on abdominal CT (figure E, arrows).

Quantitative Trait Loci Affecting Response to Crowding Stress in an F2 Generation of Rainbow Trout Produced Through Phenotypic Selection

Selective breeding programs for salmonids typically aim to improve traits associated with growth and disease resistance. It has been established that stressors common to production environments can adversely affect these and other traits which are important to producers and consumers. Previously, we employed phenotypic selection to create families that exhibit high or low plasma cortisol concentrations in response to crowding stress. Subsequent crosses of high × low phenotypes founded a multigenerational breeding scheme with the aim of dissecting the genetic basis for variation underlying stress response through the identification of quantitative trait loci (QTL). Multiple methods of QTL analyses differing in their assumptions of homozygosity of the causal alleles in the grandparental generation yielded similar results in the F1 generation, and the analysis of two stress response phenotype measurement indexes were highly correlated. In the current study, we conducted a genome scan with microsatellites to detect QTL in the F2 generation of two families created through phenotypic selection and having larger numbers of offspring than families screened in the previous generation. Seven suggestive and three significant QTL were detected, seven of which were not previously detected in the National Center for Cool and Cold Water Aquaculture germplasm, bringing the total number of chromosomes containing significant and suggestive stress response QTL to 4 and 15, respectively. One significant QTL which peaks at 7 cM on chromosome Omy12 spans 12 cM and explains 25 % of the phenotypic variance in family 2008052 particularly warrants further investigation. Five QTL with significant parent-of-origin effects were detected in family 2008052, including two QTL on Omy12. The 95 % confidence intervals for the remaining QTL we detected were broad, requiring validation and fine mapping with other genotyping approaches and mapping strategies. These results will facilitate identification of potential casual alleles that can be employed in strategies aimed at better understanding the genetic and physiological basis of stress responses to crowding in rainbow trout aquaculture production.

Comparison of the neurobiological effects of attribution retraining group therapy with those of selective serotonin reuptake inhibitors

The aim of this study was to compare the effectiveness of attribution retraining group therapy (ARGT) with selective serotonin reuptake inhibitors (SSRIs) in the treatment of major depressive disorder (MDD), generalized anxiety disorder (GAD), and obsessive-compulsive disorder (OCD). Subjects were sequentially recruited and randomized into two groups, one receiving ARGT (n = 63) and the other SSRIs (n = 66) for 8 weeks. Fifty-four ARGT outpatients with MDD (n = 19), GAD (n = 19), and OCD (n = 16) and 55 SSRI outpatients with MDD (n = 19), GAD (n = 19), and OCD (n = 17) completed the study. All subjects were assessed using the Hamilton Depression Scale and Hamilton Anxiety Scale before and after treatment. The 10-item Yale-Brown Obsessive Compulsive Scale was employed only for OCD subjects. Plasma levels of serotonin, norepinephrine, cortisol, and adrenocorticotropic hormone were also measured at baseline and 8 weeks after completion of treatment. Symptom scores were significantly reduced (P < 0.001) in both the ARGT and SSRI groups at the end of treatment. However, MDD, GAD and OCD patients in the ARGT group had significantly lower plasma cortisol concentrations compared to baseline (P < 0.05), whereas MDD and OCD patients receiving SSRIs showed significantly increased plasma levels of serotonin (P < 0.05). These findings suggest that ARGT may modulate plasma cortisol levels and affect the hypothalamus-pituitary-adrenal axis as opposed to SSRIs, which may up-regulate plasma serotonin levels via a different pathway to produce an overall improvement in the clinical condition of the patients.

145. Temporal associations between IL-6 and cortisol production in response to acute psychosocial stress

Objective Although it is known that there is a temporal, regulatory relationship between cortisol and IL-6, it has not yet been established that such a relationship extends to the neuroendocrine and immune responses to acute psychosocial stress. Methods Healthy adult participants underwent the Trier Social Stress Test. IV blood samples were collected before and after the test (time points 0, +15, +30, +45, +60, +75, +90), and emotional ratings were completed. Results Lower plasma cortisol concentration at time point 0 was correlated with higher IL-6 concentrations at time points +60 and +75 (p = 0.001; p = 0.001). Lower plasma cortisol at time point +15 was also correlated with higher IL-6 at time points +60 and +75 (p Conclusion Subjects with lower baseline plasma cortisol concentrations generated a greater IL-6 response one hour after initiation of the TSST. Greater change in depressive mood, higher BMI, and female gender also contributed to elevated IL-6 response to the TSST. These results suggest that the temporal regulatory relationship between cortisol and IL-6 persists even in the context of acute psychosocial stress.

Effects of stray voltage on the physiology of stress, growth performance and carcass parameters in Romane male lambs

The effects of permanent or random exposure to stray voltage on a water trough were evaluated in growing–finishing Romane male lambs between the age of 13 and 19 weeks. Ninety lambs were assigned during two 6-week experimental periods to one of three treatments, with 30 animals in each treatment (15 per experimental period). The treatments were permanent exposure to voltage (PERM, 3.5 V) on the water trough, random exposure to voltage (RAND, 3.5 V, 34 h/week) and no voltage exposure for the control group (CONT). No effects of voltage exposure were observed on production parameters: growth, average daily gain and water intake. The stress physiology seemed to be slightly modified with a lower plasma cortisol concentration at slaughter in PERM lambs compared to CONT lambs ( P < 0.05) and a higher adrenal medulla weight in PERM lambs compared to CONT lambs ( P < 0.05). However, no differences were observed between treatments in heart-rate, basal plasma cortisol concentration and tyrosine hydroxylase and phenylethanolamine-N-methyl transferase activities. Carcass yield, temperature and the pH of the M. longissimus dorsi were not modified by voltage exposure during rearing. In the good carcass conformation class (R class in EUROP grading scheme), there were fewer fat carcasses (grade 4 of 5) in the PERM and RAND compared to the CONT group ( P < 0.05). In conclusion, no major effects of voltage exposure were observed in male lambs on production, carcass parameters and stress physiology. Stray voltage could be considered as a mild stressor in growing–finishing lambs.

A randomized study of the effects of perioperative i.v. lidocaine on hemodynamic and hormonal responses for cesarean section

Intravenous infusion of lidocaine attenuates the stress response to surgery. We aimed to evaluate the effects of perioperative lidocaine on the hemodynamic and hormonal responses for cesarean delivery. After the gaining of ethical approval, 90 patients scheduled for elective cesarean delivery were randomly allocated to receive either lidocaine 1.5 mg x kg(-1) i.v. bolus 30 min before induction, followed by an infusion of 1.5 mg x kg(-1) x h(-1) until 1 h after surgery (n = 45), or saline placebo (n = 45). Anesthesia was maintained with 50% nitrous oxide in oxygen with 0.7% isoflurane. Hemodynamic variables, plasma cortisol, maternal and neonatal lidocaine concentrations, Apgar scores at 1 and 5 min, neonatal acid-base status, and the neurologic and adaptive capacity score (NACS) were recorded. After induction, patients receiving lidocaine had a smaller increase in heart rate and mean arterial blood pressure (P < 0.02) and lower plasma cortisol concentrations (31.1 +/- 9.91 vs 45.6 +/- 8.43 microg x dL(-1); P < 0.001). There were no differences between the two groups in Apgar scores, NACS, or neonatal acid-base status. After delivery, maternal and umbilical venous concentrations and umbilical vein-to-maternal vein ratios of lidocaine were 2.05 +/- 0.42 microg x mL(-) and 1.06 +/- 0.31 microg x mL(-1), and 0.52 +/- 0.07, respectively. Perioperative lidocaine is safe and effective in attenuating the maternal stress response to surgery for cesarean delivery.

HYPERTHERMIA IN CAPTURED IMPALA (AEPYCEROS MELAMPUS): A FRIGHT NOT FLIGHT RESPONSE

To investigate the patterns and mechanisms of capture-induced hyperthermia, we surgically implanted 26 impala (Aepyceros melampus) with miniature thermometric data loggers, which measured body temperatures continuously throughout capture procedures. Four groups of impala, which were habituated to varying levels of handling and boma-housing, were captured by net restraint or by chemical immobilization. The study took place between July 1999 and December 2005. Irrespective of whether impala were chemically captured, net-captured, or disturbed by exposure to a stressor, they developed a precipitous increase in body temperature. This increase in body temperature was not related to activity levels; animals that had low activity levels before immobilization had larger increases in body temperature compared to those that had high activity levels but were not immobilized (t = 3.6, P = 0.001, n = 5). Similarly this increase in body temperature was not related to environmental heat load at the time of darting and immobilization (r = -0.05, P = 0.85). Body temperature increase also did not depend on whether the animals were captured using drugs or not. However, we found that those animals that were habituated more to handling and boma-housing had smaller increases in body temperatures (F = 37, P<0.001) and smaller stress responses, indicated by lower plasma cortisol concentrations (F = 5.5, P<0.05), and less fractious behavior, compared to those animals that were habituated less or not at all. Therefore we believe that capture-induced hyperthermia in impala is caused predominantly by stress, which induces a rapid rise in body temperature.

RETRACTED: A randomized study of the effects of preoperative ketorolac on general anaesthesia for caesarean section

Ketorolac may attenuate the maternal stress response to tracheal intubation, while avoiding opioid-induced neonatal depression. We aimed to evaluate the haemodynamic and hormonal effects of prophylactic ketorolac on surgical stress and analgesia after caesarean delivery. After ethical approval, 90 patients scheduled for elective caesarean delivery were randomly allocated receive either ketorolac 15 mg i.v. bolus 20 min before induction, followed by an infusion of 7.5 mg/h (n=45), or saline placebo (n=45). Anaesthesia was maintained with 50% nitrous oxide in oxygen with 0.5% isoflurane. Haemodynamic variables, plasma cortisol concentrations, uterine relaxation, need for supplementary doses of oxytocin, peri-operative blood loss, haematocrit, Apgar scores at 1 and 5 min, postoperative pain scores at rest and movement, and tramadol consumption were recorded. After induction, patients receiving ketorolac had a smaller increase in heart rate, systolic and mean arterial blood pressure (P<0.001) and lower plasma cortisol concentrations, (32.2+/-7.61 vs. 45+/-15.1 microg/dL, P<0.05), lower pain scores at rest and movement for the first two postoperative hours (P<0.001) and a longer time to first request for analgesia. Fewer patients in the ketorolac group received tramadol in the four hours after surgery (7 (15.6%) vs. 14 (31.1%), P=0.004). There were no differences between groups in peri-operative blood loss, vomiting or Apgar scores. There was no echocardiographic evidence of premature closure of the ductus arteriosus in the newborns. Prophylactic ketorolac is safe and effective in attenuating the maternal stress response to intubation and improves the quality of analgesia after caesarean delivery.

Assessment of adrenocortical function in the critically ill

To review current concepts in the diagnosis of adrenocortical disease in the critically ill patient.A review of articles reported on adrenocortical insufficiency in the acutely ill patient.The contribution of adrenal insufficiency to the morbidity of critically ill patients is currently under renewed scrutiny. The debate continues about the role of steroids in sepsis and essentially the question remains unanswered. Central to this debate is the issue of whether adrenal insufficiency is common in the critically ill patient. What is incontrovertible is that adrenocortical function is essential for host survival during critical illness, but what constitutes adrenocortical insufficiency in critically ill patients is not clear. Absolute adrenocortical insufficiency (diagnosed by very low plasma cortisol concentrations) is uncommon in the intensive care population. The diagnosis of relative adrenocortical insufficiency (elevated basal plasma cortisol with a subnormal increase in plasma concentrations following an ACTH stimulus) continues to generate debate. The controversy surrounding the role of steroids in sepsis and the confusion over the criteria for diagnosing adrenal insufficiency in the critically ill are reviewed.We suggest that the following caveats be borne in mind when diagnosing adrenal insufficiency in the critically ill patient. Firstly, the gold standard for the diagnosis has not been established. Secondly, caution must be exercised when interpreting a single plasma cortisol value. In the event of a single result indicating adrenal hypofunction, we suggest repeating the measurements after a 6 to 12 hour interval. The clinician must also be aware of variations in cortisol concentrations induced by the assay. Thirdly, the clinician must be aware of the potential limitations of the conventional high dose corticotrophin test. We also suggest that plasma free cortisol is more relevant than total plasma cortisol in the assessment of adrenal function in critical illness and that the low dose corticotrophin test is more sensitive than the conventional high dose test. These areas should be the subject of further investigations.

Adrenocortical responsiveness is blunted in twin relative to singleton ovine fetuses.

Twin fetuses experience much higher rates of perinatal mortality/morbidity than age- and weight-matched singletons. Across species, the prepartum increase in fetal plasma cortisol is responsible for maturing a number of systems in preparation for birth and the immediate postnatal period. In sheep, it is known that basal adrenocortical function is delayed in twins relative to singletons. Thus, it could be argued that relative immaturity in twins may explain their increased susceptibility to stress in the perinatal period and their relatively poor perinatal outcome. However, whether adrenocortical responsiveness to stress is also diminished in the twin fetus and whether the fetal cardiovascular, metabolic and endocrine defences to acute stress are comparatively weak in the twin fetus is unknown. This study investigated the effect of twinning on adrenocortical responsiveness to either the physiological stress of acute hypoxaemia or to an exogenous ACTH test, and on the fetal cardiovascular, metabolic and endocrine responses to acute hypoxaemic stress. Twenty Welsh Mountain sheep fetuses were chronically instrumented (1-2% halothane) at 121 +/- 3 days of gestation (term is ca 145 days) with amniotic and vascular catheters and with a transit-time flow probe around a femoral artery. The animals were divided into two groups based upon fetal number (singletons, n= 10; twins, n= 10), as determined at surgery. At 130 +/- 2 days, a 1 h episode of acute, isocapnic hypoxaemia (to reduce carotid P(O(2)) to 12 +/- 1 mmHg) was induced in all fetuses by reducing the maternal inspired O(2) fraction (F(IO(2)); 9% O(2) in N(2)). Fetal cardiovascular variables were recorded at 1 s intervals throughout the experimental protocol and arterial blood samples taken at appropriate intervals for biophysical (blood gases, glucose, lactate) and endocrine (catecholamines, vasopressin, cortisol, ACTH) measures. At 133 +/- 2 days a 2.5 microg bolus dose of synthetic ACTH (Synacthen; Ciba Pharmaceuticals, UK) was injected i.v. into eight of the singleton and six of the twin fetuses to determine adrenocortical steroidogenic sensitivity to exogenous ACTH. Under basal conditions, twins had lower plasma cortisol concentration, arterial blood pressure and femoral blood flow relative to singleton fetuses. Twins responded to acute hypoxaemia with similar pressor and vasopressor responses compared to singleton fetuses. However, the rate pressure product, an index of myocardial work, tended to decrease during hypoxaemia in twins, in contrast to the increase observed in singletons. Similar increases in the fetal plasma concentrations of ACTH, AVP, noradrenaline and adrenaline were observed during hypoxaemia in both groups; however, both the increments in fetal plasma concentration of cortisol in response to acute hypoxaemia and to exogenous ACTH were blunted in twins relative to singletons. This study shows that basal adrenocortical function as well as adrenocortical responsiveness is blunted in the twin relative to the singleton fetus. Further, the mechanism for adrenocortical blunting resides at the level of the adrenal cortex rather than higher up the axis. Relative adrenocortical immaturity in the twin fetus may reflect a specific endocrine adaptation to prolong gestation in multiple ovine pregnancies; however, such an adaptation does not affect the cardiovascular, metabolic or endocrine defence responses to acute hypoxaemia in the twin fetus.

Endocrine and Cardiovascular Responses to Corticotropin-Releasing Hormone in Patients with Posttraumatic Stress Disorder: A Role for Atrial Natriuretic Peptide?

Hypothalamic-pituitary-adrenocortical (HPA) axis data, such as low plasma cortisol concentrations in spite of increased corticotropin-releasing hormone (CRH) levels in patients with posttraumatic stress disorder (PTSD), are difficult to interpret. Atrial natriuretic peptide (ANP) may be an explanatory link in the neuroendocrine pathophysiology of the disorder, since it is a neuromodulator with antianxiety effects that inhibits HPA activity at multiple levels. Seventeen patients with chronic PTSD and 17 healthy control subjects were given 100 µg of human CRH at 3 p.m. ANP, adrenocorticotropic hormone (ACTH), and cortisol levels in plasma as well as blood pressure and heart rate were measured during basal conditions and after CRH stimulation. Basal ANP levels were significantly lower in PTSD patients in comparison with normal controls, but the response to CRH was undistinguishable. In contrast to our expectation, no significant differences in basal or CRH-stimulated ACTH or cortisol parameters could be observed. Systolic and diastolic blood pressures at baseline and after CRH were significantly elevated in PTSD patients. All group differences remained significant after controlling for basal blood pressure and/or body mass index. Our data do not support a role of ANP in abnormal HPA axis regulation in PTSD. However, the persistently low ANP plasma levels in PTSD patients despite elevated blood pressure may serve to facilitate anxiety behavior and have adverse long-term cardiovascular consequences. Further studies to assess ANP secretion in PTSD patients and to clarify its pathophysiological impact are needed.

Effects of vehicle movements during transport on the stress responses and meat quality of sheep

Two groups of 26 lambs were transported for 15 hours either on smooth highways or on rougher secondary roads. Nine of the animals in each group were monitored for heart...

Independent effects of obesity and cortisol in predicting cardiovascular risk factors in men and women.

Recent data suggest that higher plasma cortisol may be associated with hypertension and insulin resistance in otherwise healthy men, as it is in Cushing's syndrome. However, obesity in women is associated with lower plasma cortisol concentrations. This study sought to establish whether plasma cortisol is associated with cardiovascular risk factors in women as it is in men, and whether these relationships in either sex are confounded by obesity. A population-based cross-sectional study. The MONICA study in northern Sweden. From a target cohort of 2500, 1921 subjects took part and 226 were randomly selected because they attended between 07.00 and 09.00 h after an overnight fast. A 75 g oral glucose tolerance test was performed and blood sampled at baseline and 2 h after glucose. Plasma cortisol was lower in relatively obese subjects: in men, this was observed only in the 2 h sample (r = -0.23, P = 0.02) and in women only in the fasting sample (r = -0.26, P < 0.01). Simple regression analysis did not identify relationships between plasma cortisol and blood pressure, serum lipids, fasting insulin or glucose tolerance. However, after adjusting for the effect of obesity by multiple regression, higher plasma cortisol was independently associated with higher diastolic blood pressure in men (r = 0.21, P = 0.04) but not in women, and higher fasting serum triglyceride levels in women (r = 0.28, P < 0. 001) but not in men. Increasing obesity and plasma cortisol concentrations make independent and sex-specific contributions to variations in blood pressure and aspects of the insulin resistance syndrome. Adverse cardiovascular risk is greatest in those with the combination of obesity and failure to downregulate plasma cortisol levels.

Influence of Exercise Mode and Carbohydrate on the Immune Response to Prolonged Exercise

The influence of exercise mode and 6% carbohydrate (C) versus placebo (P) beverage ingestion on lymphocyte proliferation, natural killer cell cytotoxicity (NKCA), Interleukin (IL)-1beta production, and hormonal responses to 2.5 hr of intense running and cycling (approximately 75% VO2max) was measured in 10 triathletes serving as their own controls. The C versus P condition (but not exercise mode) resulted in higher plasma glucose concentrations, lower plasma cortisol concentrations, reduced postexercise lymphocytosis and NKCA, and a lessened T-cell reduction during recovery, No condition or mode effects were observed for concanavalin A and phytohemagglutinin-induced lymphocyte proliferation. Significant mode (but not condition) effects were observed for lipopolysaccharide-induced IL-1beta production over time. However, when expressed per monocyte, the mode effect was abolished and a sustained suppression in IL-1beta/monocyte was observed in all sessions throughout recovery. These data indicate that carbohydrate ingestion significantly affects plasma glucose and cortisol concentrations, blood lymphocyte counts, and NKCA, whereas exercise mode has no effect on these parameters.

Temperature-dependent cortisol distribution among the blood compartments in man.

This study was conducted to investigate the effect of temperature on the amount of cortisol bound to the erythrocytes and the distribution of cortisol in whole blood at various temperatures. The amount of cortisol bound to the erythrocytes was determined in a way that did not disturb the equilibrium distribution of cortisol between plasma and erythrocytes. Total and free cortisol concentrations in plasma and the amount of cortisol bound to the erythrocytes were determined at 20, 30, 37, and 40 C in the blood of six healthy persons. The amount of cortisol bound to the erythrocytes showed a perfect linear relation with the free cortisol concentration and was independent from the temperature. The average ratio of the erythrocyte-associated and free cortisol was 2.38 +/- 0.06. Computer simulations of the distribution of cortisol among the blood compartments showed that the free and loosely bound fraction (albumin and erythrocytes) was highly temperature dependent: at 30 C, this fraction was 3-5 times lower than at 37 C. It was demonstrated by computer simulation that changes in the concentration of cortisol-binding globulin had an effect on the fractional distribution of cortisol among the blood components. These shifts in the cortisol distribution, between the erythrocyte and the plasma compartment, can also be the cause of apparently high or low free and total plasma cortisol concentrations. Differences up to 25% in the free cortisol concentration can be observed. We conclude that the erythrocyte-associated cortisol fraction is relatively undervalued but can serve as an important transport vehiculum and storage compartment for cortisol. This fraction can have a considerable effect on the total plasma and free cortisol concentration when strict temperature control during sample handling is not considered.

Stress enhanced reduction in peripheral blood lymphocyte numbers in dairy cows during endotoxin-induced mastitis

Two groups of Holstein dairy cows, which showed either high- (HC; n = 8) or low (LC; n = 10) plasma cortisol concentrations in response to a psychological stressor (novel–environment test) in their first lactation, were used 1 year later for studying the effects of psychological stress on various aspects of the host defence during endotoxin-induced mastitis. Social isolation was used as a stressor; endotoxin was used to activate the host defence. HC-cows appeared to be more stressed by the experimental procedure than LC-cows. One hour after having been isolated, rectal temperature increased (+ 0.59°C) in HC- but not in LC-cows. Handling, related to the intra-mammary administration of endotoxin, induced a higher increase in cortisol concentration in HC- than in LC-cows 1 h after injection. In addition, HC-cows vocalised significantly more frequently (595 ± 222) than LC-cows (81 ± 24) between 1.5 and 9.5 h after isolation. Between 3 and 5.5 h after endotoxin-treatment, cortisol concentrations increased profoundly in both LC- and HC-cows and peaked at 24.6 ± 3.8 and 22.8 ± 3.1 ng ml −1, respectively. The rise in plasma cortisol concentration was associated with a decrease in the number of circulating lymphocytes between 0 and 8 h post injection (PI). Between 8 and 10 h PI, the number of circulating lymphocytes in HC-cows further decreased (40%) to 1.58×10 6 cells ml −1 and remained so until 21 h PI. This was not the case with the LC-cows. The results show that a differing sensitivity of dairy cows to environmental stressors is associated with a significant difference in the number of circulating leukocytes following intra-mammary administration of endotoxin during a period of social isolation. The results further suggest that, apart from adrenocortical hormones, other factors related to general stress-responsiveness modulate the number of peripheral lymphocytes in dairy cows during endotoxin-induced mastitis. During environmental stress, these factors may enhance endotoxin-induced reduction in circulating lymphocyte numbers, particularly in cows that are sensitive to environmental stressors. As to the clinical relevance of these differences in stress responsiveness, no differences between LC- and HC-cows were found in disease incidence nor in duration of a disease episode during both the 1st and 2nd lactation. In the 2nd lactation, HC-cows tended to produce less milk than LC-cows.