Gene/Protein Disease Symptom Drug Enzyme Compound
Pivot Concepts:   Target Concepts:
Query: UMLS:C0848237 (acute stress)
 4,619 document(s) hit in 31,850,051 MEDLINE articles (0.00 seconds)

Acute exposure of male rats to cold (5C)leads to a rapid increase of plasma levels of thyrotropin (TSH), prolactin (PRL), corticosterone, and L-thyroxine. Exposure to ether is similarly followed by a rapid increase of plasma levels of PRL and corticosterone, while TSH release is inhibited. Acute treatment with dexamethasone (500 mug) inhibits almost completely the PRL response to both exposure to cold and ether stress, while the plasma TSH response to cold is only delayed and the decrease of plasma TSH observed after ether stress is unchanged. Basal plasma levels of both TSH and PRL are lowered after treatment with the steroid. Thyroxine treatment lowers the plasma TSH concentration to undetectable levels without affecting the plasma PRL response to cold or ether exposure. The present data suggest that the rise of plasma PRL observed after cold exposure is not related to TRH and may suggest that common mechanisms control ACTH and PRL secretion during acute stress exposure.
 ...
PMID:Effect of pharmacological blockade of ACTH and TSH secretion on the acute stimulation of prolactin release by exposure to cold and ether stress. 18 Dec 37

The effects of acute stress during a parachute jump on hormonal responses were studied in 12 experienced and 11 inexperienced military parachutists. Each subject performed two jumps. Prior to and immediately after each jump blood samples were drawn and analysed for plasma levels of cortisol, prolactin, thyrotropin (TSH), somatotropin (STH), and luteinizing hormone (LH). While there was a significant increase in cortisol, prolactin and TSH levels after both jumps, no alterations could be observed in STH and LH levels. Stress-induced hormonal responses were not affected by jump experience. There was also no association between the endocrine variables and anxiety scores.
 ...
PMID:Acute psychological stress increases plasma levels of cortisol, prolactin and TSH. 156 28

The effect of chronic stress on basal and stress-induced alterations of TSH and GH was studied in adult male rats. Chronically stressed rats were subjected 6 days per week for 4 weeks to several acute stressors including saline injections, noise, ether and forced swimming. Each day, one stressor was chosen randomly. Twenty hr after the last stress session, basal levels of TSH were normal or increased, with no altered pituitary response to TRH. In contrast, the TSH rise induced by acute stress was blunted in chronically stressed rats. Chronic stress resulted in lower basal and acute stress levels of GH. These modifications were probably due to changes in the release of hypothalamic regulatory hormones, because no evidence for altered TSH response to TRH, and GH response either to GHRH or to somatostatin, was found. Some abnormal responses of GH to TRH and of TSH to GHRH were observed in chronically stressed rats. These data indicate that this type of chronic stress induced significant changes in basal and acute stress levels of GH and TSH in the rat.
 ...
PMID:The effects of chronic intermittent stress on basal and acute stress levels of TSH and GH, and their response to hypothalamic regulatory factors in the rat. 289 9

The effect of chronic noise stress on the response of anterior pituitary hormones to the same or to another stressor (forced swimming) was studied in adult male Wistar rats. Both acute stressors increased corticosterone, prolactin, LH and TSH secretion and inhibited GH secretion. Previous chronic exposure to noise reduced corticosterone response to the same stimulus without modifying corticosterone response to a novel acute stress. Neither prolactin nor TSH responses to acute noise were reduced by previous chronic exposure to noise. Since chronic noise increased basal levels of LH and decreased those of GH, the response of these hormones to acute stress was expressed as percent changes of their respective basal values. It was found that chronically stressed rats showed diminished LH response to noise but not to forced swimming. GH showed the same pattern without reaching statistical significance. These data indicate that the response of some anterior pituitary hormones can adapt after repeated exposure to the same stressor. When adaptation occurred, this was specific for the stressor which the animals were repeatedly exposed to. The pituitary-adrenal axis appears to be the most reliable index of adaptation to chronic stress among all the anterior pituitary endocrine axes.
 ...
PMID:Response of anterior pituitary hormones to chronic stress. The specificity of adaptation. 377 44

The levels of beta-endorphin, insulin, cortisol, GH, glucagon, prolactin and TSH were measured in serum samples of 9 hyperglycaemic patients (3 female, 6 male) with a mean age of 4.1 years admitted to the pediatric emergency unit. All patients were in acute stress due to severe diseases (acute gastroenteritis, bronchopneumonia, septicaemia, etc.). Initial and repeat blood samples for hormone determination were taken at admission and in the recovery phase (after 4-6 weeks of treatment). OGTT was also performed in the recovery phase. The hyperglycaemia, monitored hourly following the initial determination, returned to normal in all patients in 1-5 h without specific treatment. Mean serum glucose values at admission and in the recovery phase were 287.0 and 84.1 mg/dl. Concomitant to the hyperglycaemia encountered in these patients in the acute phase of stress, an increase was noted in all hormone levels excluding glucagon and cortisol. All elevated hormone levels fell to normal in 4-6 weeks with significant differences from initial levels for beta-endorphin (P < 0.05) and insulin (P < 0.01). OGTT gave a normal curve. These results indicate that stress hyperglycaemia, despite high insulin levels, is associated with an increase in beta-endorphin levels. The results also show that hyperglycaemia in acute disease does not alter OGTT in short-term follow up.
 ...
PMID:beta-Endorphin and some hormonal levels in children with acute stress hyperglycaemia. 795 15

Corticotropin-Releasing-Hormone (CRH) is the principal secretagogue for plasma ACTH and corticosterone secretion and plays an important role in coordinating a variety of physiological and behavioral responses to stress. To explore whether there is a rapid change in the secretory response of the hypothalamic CRH neuron during acute stress, we report here a study of the effects of KCl and norepinephrine (NE) on CRH release in vitro from rat hypothalami explanted after 5, 30, 60, and 120 minutes of immobilization. We also measured the plasma levels of ACTH, beta-endorphin, corticosterone, prolactin, GH, and TSH at these intervals. As the duration of immobilization increased, KCl and NE-induced CRH release in vitro progressively fell. After reaching a maximal rise after 30 minutes of immobilization, plasma ACTH, beta-endorphin, and prolactin progressively fell in plasma, whereas corticosterone remained elevated up to 120 minutes; TSH and GH secretion rapidly declined and remained suppressed. Taken together, these data suggest that during immobilization stress, the responsiveness of the hypothalamic CRH neuron rapidly falls, owing either to CRH depletion and/or desensitization to NE, and this is paralleled by a concomitant decrease in pituitary-adrenal responsiveness.
 ...
PMID:Immobilization stress rapidly decreases hypothalamic corticotropin-releasing hormone secretion in vitro in the male 344/N Fischer rat. 839 19

An unexplained hallmark of prolonged critical illness is the fact that food does not prevent or reverse protein wasting, while fat is paradoxically accrued. This 'wasting syndrome' often persists after the underlying disease has been resolved and thus perpetuates intensive care dependency. Although the crucial role of an intact hypothalamus-pituitary axis for homeostasis during stress is well recognized, the differences between the neuroendocrine changes observed in acute and prolonged critical illness were only recently described. Novel insights in this area are reviewed here. The initial endocrine stress response consists primarily of a peripheral inactivation of anabolic pathways while pituitary activity is essentially amplified or maintained. These responses presumably provide the metabolic substrates and host defense required for survival and to delay anabolism, and thus should be considered as adaptive and beneficial. Persistence of this acute stress response throughout the course of critical illness was hitherto assumed. This assumption has now been invalidated, since a uniformly reduced pulsatile secretion of ACTH, TSH, LH, prolactin (PRL) and GH has been observed in protracted critical illness, causing diminished stimulation of several target organs. Impaired pulsatile secretion of anterior pituitary hormones in the chronic phase of critical illness seems to have a hypothalamic rather than a pituitary origin, as administration of relevant releasing factors evoked immediate and pronounced pituitary hormone release. A reduced availability of TRH, one of the endogenous ligands of the GH-releasing peptide (GHRP) receptor (such as the recently discovered ghrelin) and, in very long-stay critically ill men, also of GHRH, appear to be involved. This hypothesis was further explored by investigating the effects of continuous i.v. infusion of GHRH, GHRP, TRH and their combinations for several days. Pulsatile secretion of GH, TSH and PRL was re-amplified by relevant combinations of releasing factors which also substantially increased circulating levels of IGF-I, GH-dependent binding proteins, thyroxine and tri-iodothyronine (T3) while avoiding a rise in reverse T3. Active feedback-inhibition loops prevented overstimulation of target organs and metabolic improvement was noted with the combined infusion of GHRP and TRH. Whether this novel endocrine strategy will also enhance clinical recovery from critical illness remains to be explored.
 ...
PMID:Novel insights into the neuroendocrinology of critical illness. 1087 25

Chronic stress, understood as a disturbance of the body homeostasis, is partially driven by many hormonal pathways. Prolactine, TSH (Thyrotropin), vasopresin, FSH (Follicle-Stimulating Hormone), LH (Luteinizing Hormone), and GH (Growth Hormone) have been involved in many stress reactions. In acute stress, there are many evidences for the increased both cathecolaminergic and hypothalamic-pituitary-adrenal axis. In chronic conditions, these hyperactivations are controversial and some cases may present a true hypoadrenalism. There is no evidence that treating such androgen/glucocorticoids deficiency may relief chronic pain processes such as fibromyalgia. However, treating somatotroph axis dysfunctions (somatostatin, GH/IGF1 [growth hormone/ insulin-like growth factor-1]) with recombinant GH in carefully seleccioned subgroups of fibromyalgic syndrome, offers us an in-vivo model of the capacity of some hormones to modulate pain.
 ...
PMID:[Stress and chronic pain: An endocrine perspective]. 2179 52

Stress is generally a natural phenomenon that affects behaviour, physiological processes, and neuroendocrine, neurochemical, neurological and immune responses. Many somatic and mental disorders are thought to result from chronic stress. Stress-induced gonadal dysfunction is not restricted to humans, but is observed in all higher animals. Stress-induced gonadal dysfunction comprises disturbances of the hypothalamic-pituitary-gonadal axis and of spermatogenesis. Various stressors induce changes in the secretion of neurotransmitters and hormones, such as CRH, ADH, beta-endorphins, somatostatin, VIP, PRL, GH, TSH, dopamine, serotonin, neuropeptide Y, melatonin, ACTH, glucocorticosteroids, catecholamines and androgens. In acute stress, testicular function is principally modified by cytokines and fluctuating concentrations of gonadotropins, while in chronic stress, hypogonadotropic hypogonadism and disruption of spermatogenesis of varying severity, including spermatogenetic arrest, are observed. In spite of the decades-long interest in the relationships between psychological stress and the function of male gonads, many questions in this area remain unanswered.
 ...
PMID:Psychological stress and the function of male gonads. 2237 97

Thyroid hormones play an important role in cell growth and differentiation and regulation of oxygen consumption and thermogenesis. The effect of altitude and vitamin supplementation on thyroid hormone levels in animals or humans performing acute exhaustive exercise have not been investigated before. Therefore, we thought to test whether exhaustive exercise-induced stress with antioxidant supplementation was capable of modulating the level of thyroid hormones at different altitudes. Serum levels of T4 (Thyroxin), T3 (Triiodothyronine), and TSH (Thyroid Stimulating Hormone) were measured in rats (N=36) born and bred in low altitude (600 m above sea level) and high altitude (2200 m above sea level) following forced swimming with or without vitamins C and E (25 mg/kg) pre-treatments. Thyroid levels were significantly decreased in resting rats at high altitude compared to low altitude, and swimming exercise moderately increased T3 and TSH at both high and low altitudes, whereas T4 was markedly increased (62 %) at low altitude compared to a moderate high altitude increase (28 %). Co-administration of vitamins C and E augmented the observed forced swimming-induced thyroid release. However, the conversion of T4 to T3 was reduced in both altitude areas following swimming exercise and vitamin pre-treatment had no effect. We conclude that acute stress induced thyroidal hormones in rats, which was augmented by antioxidant drugs in both high and low altitude areas. These findings may play an important role in the human pathophysiology of thyroid gland at different altitudes.
...
PMID:Exhaustive exercise and vitamins C and E modulate thyroid hormone levels at low and high altitudes. 2754 Mar 43


1