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Query: UMLS:C0848237 (acute stress)
 4,619 document(s) hit in 31,850,051 MEDLINE articles (0.00 seconds)

Successful adaptation to stress is a prerequisite for the survival of all organisms living in an environment in which noxious stimuli are constantly present. Higher organisms, including human beings, have developed complex mechanisms to tolerate the myriad of insults that occur to cellular constituents and organ systems after trauma with its resultant blood loss and tissue injury. Surgical stress can be conceptualized in this context, and it is therefore not surprising that human beings have developed an array of integrated stress-response axes that work in concert to return the host to a sustainable homeostatic plateau. The most important aspects of these axes are depicted in Figure 24. Surgical stress activates the higher cortical center of the brain and the spinal and baroreceptor reflexes that stimulate the hypothalamus to secrete CRH. CRH stimulates the release of ACTH from the pituitary gland, which causes the release of glucocorticoids from the adrenal cortex. Simultaneously, in a parallel fashion, surgical stress activates the sympathetic system to release catecholamines. Glucocorticoids and catecholamines are the major effectors of stress adaptation and interact at multiple levels in a synergistic fashion. They bind to specific receptors that are present in virtually every organ, although the number and affinity of a given tissue's receptor vary dramatically for individual ligands. Receptor occupancy results in short-term and long-term effects that ultimately improve the host's prospects of tolerating the stressful event. The short-term effects result in rapid actions, such as cardiovascular and metabolic responses that benefit the host in a "fight or flight" reaction. The long-term effects generally occur through alterations in gene transcription that prepare the host for, or adapt the host to, repetitive or chronic stress. Changes in the phosphorylation state of intracellular proteins are a common mode of action for both the short-term and long-term responses. These stress-responsive proteins have an enormous functional capacity: they alter enzymatic pathways, modulate hormone levels, and act as transcription factors to modify the expression of stress-responsive genes. During the last decade considerable progress has been made in explaining the complex signal transduction pathways mediating these responses. The importance of the HSPs in the host response to acute stress and their intimate association with activation of the HPA axis and sympathetic nervous system have recently been appreciated. The HSPs are likely to be induced early during organ rejection or ischemia and thus serve as diagnostic indicators.(ABSTRACT TRUNCATED AT 400 WORDS)
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PMID:Endocrine and molecular responses to surgical stress. 804 59

The effect of single and chronic ACTH administration on serum levels of the corticosteroid-binding globulin (CBG) and pituitary-adrenal (PA) responsiveness to acute immobilization (IMO) stress was studied in adult Sprague-Dawley rats. Single ACTH administration significantly reduced CBG levels but did not alter PA response to acute IMO. Chronic ACTH administration caused a greater fall in CBG than single ACTH administration and blunted PA response to IMO. The effect of chronic ACTH administration on CGB levels recovered 2 days after the last administration, but the ACTH response to IMO was normal only by day 7 after the last ACTH injection. The present data indicate that ACTH administration to rats reduced CBG levels and impaired PA response to acute stress, but impaired PA responsiveness cannot be solely attributed to changes in CBG.
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PMID:The effect of acute and chronic ACTH administration on pituitary-adrenal response to acute immobilization stress. Relationship to changes in corticosteroid-binding globulin. 805 31

We have investigated the effects of monosodium glutamate (MSG) lesioning of the arcuate nucleus on both central and peripheral components of the hypothalamo-pituitary-adrenocortical (HPA) axis under basal conditions and under acute and chronic stress. Plasma ACTH levels were lower in MSG-lesioned rats (27 +/- 7 pg/ml) compared with controls (71 +/- 18 pg/ml) while corticosterone levels were elevated (523 +/- 84 ng/ml compared with 176 +/- 34 ng/ml). Quantitative in situ hybridization histochemistry revealed that corticotrophin-releasing factor mRNA levels in the medial parvocellular part of the hypothalamic paraventricular nucleus were significantly lower in MSG-treated rats. MSG lesioning resulted in an enhanced response of corticosterone to restraint stress (1309 +/- 92 ng/ml compared with 628 +/- 125 ng/ml in sham-lesioned animals), while ACTH responses to restraint stress in MSG-lesioned and sham-MSG groups were not significantly different (160 +/- 24 pg/ml and 167 +/- 24 pg/ml respectively). These data suggest that MSG-lesioned rats have an increased adrenocortical sensitivity. In rats subjected to the chronic osmotic stimulus of drinking 2% saline for 12 days, plasma ACTH levels were significantly reduced (15 +/- 5 pg/ml) and the ACTH and corticosterone responses to restraint stress were eliminated. ACTH levels were also reduced in MSG-treated animals given 2% saline and the ACTH response to acute stress remained absent in these animals. However, a robust corticosterone response to restraint stress was observed in saline-treated MSG-lesioned rats.(ABSTRACT TRUNCATED AT 250 WORDS)
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PMID:Neonatal monosodium glutamate treatment alters both the activity and the sensitivity of the rat hypothalamo-pituitary-adrenocortical axis. 807 49

Effect on the acute stress response of dietary inclusion of 3 ppm salbutamol (beta-2-adrenergic agonist) at two levels of protein were investigated in growing pigs (from 25 kg live weight). The trial comprised six litters (blocks) of four females allocated randomly to four treatment groups in accordance with a 2 x 2 factorial arrangement. The response to an open-field test and to an intruder were measured at 50 kg live weight. Salbutamol increased immobility and looking, reduced total exploration, and increased plasma ACTH after test. At high dietary levels of protein, salbutamol also increased the latency to attack. High dietary levels of protein reduced standing still, latency to contact a novel object and an intruder, and level of plasma cortisol before test. Moreover, high protein without salbutamol seemed to reduce the latency to attack an intruder. In conclusion, chronic treatment with salbutamol shifted the acute stress response in pigs toward a passive response, whereas high dietary level of protein provoked an active response, which may have consequences in pig production.
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PMID:Dietary salbutamol and level of protein: effects on the acute stress response in pigs. 815 81

A variety of chronic stress paradigms have been shown to increase basal activity in the hypothalamic-pituitary-adrenocortical axis, resulting in hypercorticoidism. Despite this, chronically stressed rats typically exhibit facilitated ACTH responses to acute novel stress, suggesting that the activity of some central neural component(s) in the axis is facilitated by chronic stress. We have used the chronic stress of streptozotocin (STZ)-induced diabetes in rats to determine diurnal sensitivity of basal and stimulated ACTH secretion to exogenous corticosterone (B) feedback in vivo. Control and STZ-diabetic rats were adrenalectomized or adrenalectomized and implanted with a 30% or 50% B pellet at the time of vehicle/STZ injection. Rats were killed 5 days later, under basal conditions or after 6 min of restraint, in the morning or evening. We show that basal ACTH secretion in both the morning and evening was similarly suppressed by B in STZ-diabetic and control rats. However, stress-induced ACTH secretion was significantly greater in STZ-diabetic compared to control rats throughout the range 3-7 micrograms/dl B, when tested in the morning. Suppression of evening stress-induced ACTH secretion by B was also significantly different in STZ-diabetic rats; however, the IC50 values for the inhibition of ACTH by B did not differ. This result shows that in the evening after stress and under basal conditions in both the morning and evening, sensitivity to B feedback is normal in chronically stressed, STZ-diabetic rats. Despite the observed facilitation of morning stress-induced ACTH secretion in STZ-diabetic rats, there were no differences in hypothalamic CRF content between control and STZ-diabetic tissue. We conclude that 1) the facilitatory input to the paraventricular nucleus functions primarily at the time of the circadian trough to maintain or enhance acute stress responsiveness in chronically stressed, hypercorticoid rats; and 2) the sensitivity of ACTH to inhibition by B is normal in rats chronically stressed by STZ-induced diabetes.
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PMID:Streptozotocin-diabetic rats exhibit facilitated adrenocorticotropin responses to acute stress, but normal sensitivity to feedback by corticosteroids. 824 90

In conclusion, we have demonstrated that in the primate increased activity of the immune system and the consequent IL-1 release result in the activation of neuropeptides of the adrenal axis, mainly CRF and AVP. These neuropeptides, through a direct effect on the GnRH pulse generator or indirectly through the hypothalamic endogenous opioid peptides, inhibit the GnRH pulse generator. Some of the POMC derivatives, such as alpha-MSH, may antagonize these effects. The consequential decrease in GnRH pulse frequency results in an acute decrease in LH and FSH secretion. This decrease in gonadotropin release may explain the deleterious effects of stress on the menstrual cycle. However, an acute decrease in gonadotropins following activation of the adrenal axis is not observed in the presence of estradiol. Thus, during the menstrual cycle, a relative protection against the deleterious effects of acute stress may exist. How potent this protective mechanism is against repetitive stress is not known.
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PMID:Neuropeptides, the stress response, and the hypothalamo-pituitary-gonadal axis in the female rhesus monkey. 825 5

Stress induces an imbalance of neuroimmunomodulation, a phenomenon involving the immune, central nervous and endocrine systems. Receptors to substances involved in stress reactions and anxiety, like adrenaline, acetylcholine, histamine, endomorphines, ACTH and several neuropeptides, are present on lymphocytes and lymphocytes can secrete various hormones and neuropeptides. Peripheral and central, cortical and subcortical nervous structures influence immune response. Steroids play a dose dependent inhibitory role perhaps via GIF (Glucocorticoid Increasing Factor) and cytokines (IL 1). In rats, stress induces an increase of corticosterone levels and a lymphopenia depending on the presence of adrenals and pituitary, whereas functional responses to mitogens appear decreased in animals even after surgical removal of adrenals and/or pituitary. Immune response vary according to the degree of control over stressors, to the type of stressor and the animal species. Chronic or repeated stress tends to stimulate immune reaction, contrary to acute stress. In man grief reactions, terminal illness of a spouse, divorce, examinations, caregiving to Alzheimer patients have been used as models of stress, with immune consequences. Pathological anxiety has been less studied, with only few anomalies reported in DSM III-R panic disorder. The immune system participation in the adaptive response to stress is reviewed.
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PMID:[Stress and panic. Immunologic aspects]. 828 94

The contribution of the magnocellular vasopressinergic system to the regulation of ACTH secretion was studied by analysis of hypothalamic-adrenal axis function in rats subjected to water deprivation for 48 h. Water deprivation resulted in marked increases in plasma osmolarity and vasopressin (VP) levels and hypothalamic VP mRNA and immunoreactive (ir) VP in magnocellular neurons. While CRH mRNA levels in the paraventricular nucleus were decreased, irCRH accumulation in paraventricular nucleus neurons after colchicine treatment was normal or increased. Similarly, the irCRH content in the median eminence and its release under stress were similar in control and water-deprived rats. While basal plasma ACTH levels were similar in both groups (34.5 +/- 3.8 and 39.8 +/- 3.3 pg/ml), levels stimulated by CRH injection (10 micrograms, i.v.) or 15-min immobilization stress were reduced by 47% (P < 0.01) and 43% (P < 0.05), respectively, in water-restricted rats. The decreased ACTH responses were not prevented by injection of CRH (7.5 micrograms/day, sc) during the period of water deprivation. In contrast to the ACTH responses, basal and CRH-stimulated plasma corticosterone levels were significantly elevated (P < 0.001), and the responses to acute stress were normal. The inhibition of ACTH secretion was not due to increased glucocorticoid feedback, since similar blunted ACTH responses to acute immobilization stress were observed in adrenalectomized rats receiving corticosterone replacement. Despite similar levels of pituitary POMC mRNA, pituitary ACTH content was reduced in water-deprived rats, suggesting a posttranscriptional inhibition of POMC synthesis or processing. The data demonstrate that osmotic activation of the magnocellular VP system is accompanied by reduced responsiveness of the corticotrophs, an effect that is not due to increased glucocorticoid feedback or hypothalamic CRH deficiency. These findings suggest that the magnocellular vasopressinergic system does not play an important role in the regulation of ACTH secretion during chronic osmotic stimulation.
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PMID:Regulation of the hypothalamic-pituitary-adrenal axis during water deprivation. 838 Mar 75

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.
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PMID:Immobilization stress rapidly decreases hypothalamic corticotropin-releasing hormone secretion in vitro in the male 344/N Fischer rat. 839 19

To explore the interactions between the hypothalamic-pituitary-adrenocortical axis and the immune system under stress conditions, we used an experimental rat model for chronic tail-restraint devised earlier for ground studies in space physiology. The system was used in two positions: (1) the orthostatic restraint position (OR) and (2) the antiorthostatic position (AOR) after the rat hind limbs had been raised by a head-down tilt. After 7 days of either restraint, sequential blood samples were taken via an indwelling aortic cannula, before and at various time intervals between 15 and 300 min after an intravascular infusion of 25 micrograms/kg lipopolysaccharide (LPS). The plasma titers of adrenocorticotropin (ACTH), corticosterone (CORT) and interleukin-1 beta (IL-1 beta) were assayed. Under basal conditions, both OR and AOR restraints induced a 5-fold increase in IL-1 beta with no significant changes in ACTH and CORT levels. A robust increase in all three variables was observed after LPS injection. However, the IL-1 beta response to LPS was significantly higher in both restrained groups than in controls. Both the amplitude and the percentage of individually restrained rats displaying elevated IL-1 beta levels were increased up to 5 h. In contrast, the ACTH and CORT post-LPS responses were normal in the OR group. They were unusually dissociated in the AOR rats, which displayed depressed ACTH levels associated with slightly increased CORT levels. Our results suggest that immune-neuroendocrine responses to chronic restraint stress may differ from those generally observed in acute stress.
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PMID:Chronic restraint enhances interleukin-1-beta release in the basal state and after an endotoxin challenge, independently of adrenocorticotropin and corticosterone release. 852 95


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