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

Previous reports indicate that the central nucleus of the amygdala (CeA) stimulates adrenocorticotropin and corticosterone secretion, suggesting a role for this region in central hypothalamo-pituitary-adrenocortical (HPA) stress regulation. To evaluate this hypothesis, this study assessed the impact of CeA lesion on the response of hypophysiotrophic paraventricular nucleus (PVN) neurons to acute restraint and chronic unpredictable stress exposure. In contrast to previous reports, CeA lesions did not affect corticosterone or ACTH secretion induced by acute stress. Acute restraint increased PVN corticotropin releasing hormone (CRH) mRNA expression, increased the number of parvocellular PVN neurons expressing the co-secretagogue arginine vasopressin (AVP), and induced cFOS mRNA expression in the parvocellular PVN. However, there was no additional effect of CeA lesion on any measure of PVN activation. Chronic unpredictable stress exposure induced long-term activation of the HPA axis, noted by thymic involution, adrenal hypertrophy and increased PVN CRH mRNA expression. Stress-induced changes in thymus and adrenal weights were not affected by CeA lesion. Further, CeA lesion rats did not differ from controls in post-stress CRH mRNA expression. However, basal CRH mRNA expression was increased in the PVN of CeA rats, suggesting that the CeA plays a role in long-term inhibition of the PVN. The results of these studies are not consistent with the hypothesis that the CeA is necessary for stress-induced pituitary-adrenocortical activation. Rather, this region may play a stressor-specific modulatory role in regulation of HPA function.
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PMID:Hypothalamo-Pituitary-Adrenocortical Regulation Following Lesions of the Central Nucleus of the Amygdala. 978 50

The hippocampus plays an important role in central stress integration. The present study tests the hypothesis that the ventral subiculum, as a principal source of hippocampal efferents, is involved in co-ordination of hypothalamo-pituitary-adrenocortical and behavioural responses to cognitively-processed information. Basal hypothalamo-pituitary-adrenocortical activation appears to be normal in ventral subiculum lesion rats, as basal corticosterone and adrenocorticotropic hormone secretion, anterior pituitary pro-opiomelanocortin and type 1 corticotropin-releasing hormone receptor messenger RNA expression, adrenal and thymus weight, and splenic mitogen activity are not affected by lesion. Lesions of the ventral subiculum induce glucocorticoid hypersecretion following restraint stress or open field exposure, whereas responses to ether inhalation are unaffected. Interestingly, ventral subiculum lesion does not affect fast glucocorticoid negative feedback inhibition of restraint-induced adrenocorticotropic hormone release. Corticotropin-releasing hormone immunoreactivity is increased in the hypothalamic paraventricular nucleus of ventral subiculum lesion rats, and is differentially depleted by acute stress exposure (relative to sham-lesion rats). However, ventral subiculum lesion does not affect basal and stress-induced corticotropin-releasing hormone, arginine vasopressin and cFOS messenger RNA expression in paraventricular nucleus neurons. Behavioural analysis reveals that ventral subiculum lesion rats are hyper-responsive to open field exposure, showing decreased total ambulation and reduced incidence of central square entry. The results suggest that the ventral subiculum plays a specific role in integrating cognitively-processed stimuli (e.g., restraint and open field exposure) into appropriate neuroendocrine and behavioural responses to stress. Enhanced stress-induced glucocorticoid secretion and increased corticotropin-releasing hormone biosynthesis are likely due to removal of oligosynaptic inhibitory input to the paraventricular nucleus subsequent to ventral subiculum lesion.
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PMID:Ventral subiculum regulates hypothalamo-pituitary-adrenocortical and behavioural responses to cognitive stressors. 988 60

OBJECTIVE: Since perinatal stress events are well known to exert long-term influences on the function of hypothalamic-pituitary-adrenal (HPA) axis in rats, to investigate the consequences of exposure to IL-1, a potent stimulator of this axis, during early postnatal life. METHODS: Wistar rats were treated twice a day with 0.02 ug human recombinant IL-1 from day 1-4 of age, while controls received the vehicle only. RESULTS: IL-1 -treatment had no significant influence on the mortality and body weight. However, at the end of treatment period on the 4th day of life, the thymus weight was decreased in the IL-1 -treated group (P<0.01), while the adrenals were clearly enlarged (P<0.0002). These responses were associated with a nearly 4-fold elevation of the plasma corticosterone (CS) level as compared to vehicle-treated controls (P<0.001). At the age of seven months the stimulated CS levels induced by an acute stress (novel environment) were lower in rats treated neonatally with IL-1 than in controls (P<0.01). This functional disturbance was associated with morphological alterations in the parvicellular part of the paraventricular nucleus (PVN) which is the main hypothalamic regulation centre of the HPA axis. A strong reduction of the numerical density of neurons was found in the neonatally IL-1 -treated rats (P<0.005) while the neuronal nuclei were clearly enlarged (P<0.0005). CONCLUSION: As a part of an infection-induced stress response during critical periods of development, IL-1 might be capable of inducing a permanent structural malorganization of the PVN and, consequently, functional malprogramming of the HPA axis in rats.
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PMID:Long-term Effects of Early Postnatally Administered Interleukin-1-beta on the Hypothalamic-Pituitary-Adrenal (HPA) Axis in Rats. 1033 May 21

Chorioamnionitis represents the leading cause of preterm birth and related pathologic conditions as well as of fetal death and frequently occurs in symptom-free mothers. Recent radiologic findings have indicated that thymus size is significantly reduced in preterm infants born to mothers with subclinical, histologically proven chorioamnionitis. However, an accurate morphologic description of the thymus gland in fetuses and neonates with chorioamnionitis is lacking, although it is known that infection and other stress processes may cause lymphocyte depletion in the thymuses of infants and older babies (acute stress involution). We describe morphologic modifications in the thymus of fetuses with histologically proven chorioamnionitis and newborn infants with chorioamnionitis and proven sepsis. The main findings included (1) decreased organ volume (ANOVA, P < .0024); (2) reduced corticomedullary ratio (P < 10(-6)); (3) significant changes in the relationship between thymic parenchyma and thymic interstitial tissue with resulting increased organ complexity (P = .03); (4) severe reduction of thymocytes; and (5) other degenerative processes such as monocyte/macrophage infiltration of Hassall's bodies. These results indicate that chorioamnionitis, with or without sepsis, is associated with significant morphologic modifications in the thymus. We wish to note that the described thymic pathology is only one aspect of the fetal systemic inflammatory response syndrome with which chorioamnionitis is associated.
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PMID:Acute thymic involution in fetuses and neonates with chorioamnionitis. 1101 81

The process of lipid peroxidation (LPO), the activity of antioxidant enzymes, and the effects of piracetam (300 mg/kg) and cerebrolysin (0.1 ml/kg) were studied in the brain, liver, thymus, spleen, and blood serum of white male rats under acute stress (immobilization) conditions. The results of analyses confirmed that the stress syndrome development involves the LPO acceleration and retardation stages not coinciding in various tissues. The antioxidant effect of the nootropic agents in CNS has a permanent character, being independent of the initial status of the animal organism. The effect of both drugs upon the LPO level in peripheral tissues has a modulative character and can be considered as a sum of the central antistressor action and the direct influence upon the functional activity of effectors.
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PMID:[Characteristics of lipid peroxidation in various tissues during acute stress and its correction by pyracetam and cerebrolysin]. 1102 5

In various stressful conditions, the thymus is subjected to incidental involution, mostly due to the thymocytolytic effect of secreted glucocorticosteroids. The aim of this study was to examine acute thymic involution in sick neonates and to compare the morphological grade with some clinical and laboratory parameters. The influence of the illness on thymus tissue was investigated in 100 neonates who were treated and died in a neonatology intensive care unit. The preterm infants (n = 73) were born before the 37th week of gestation. Analysis of 57 placentas showed inflammation in 32% and circulatory disturbances in 23% of the cases. The causes of death were confirmed by autopsy: 35 were preterm infants with respiratory distress syndrome without infection, 22 were malformed, and 10 had birth trauma or asphyxia. In contrast, 29 of the preterm infants had an infection, mostly pneumonia or sepsis, and 4 of the term infants had such infections. Acute thymus involution was histologically graded (0-4) according to the method of van Baarlen (see text). Resting state (grade 0) was found in 25 of 38 neonates who lived <12 h. In 13 of 38 neonates who lived <12 h, thymus involution suggested prenatal stress. The grade of thymus involution related to the duration of illness (p < 0.001). Placental inflammation was associated with features of thymus involution (p < 0.048). Infection as a cause of death was connected to advanced thymus involution (p < 0.001). In preterm newborns, infection was more often connected with acute thymus involution than was respiratory distress syndrome (p < 0.003). Among the parameters measured in all available peripheral blood samples taken 24 h before death, only the lymphocyte count related to the grade of acute thymus involution (p < 0.05), with an increase in percentage of lymphocytes in peripheral blood smears from grade 0 to 2 and a decrease from grade 2 to 4. Although the white blood cell count is highly variable, a low percentage of lymphocytes might be a sign of advanced accidental thymus involution following acute stress.
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PMID:The grade of acute thymus involution in neonates correlates with the duration of acute illness and with the percentage of lymphocytes in peripheral blood smear. Pathological study. 1274 50

In vivo effects of acute stress induced by corticosterone 21-acetate in male Gallus domesticus thymus are studied and the steroid actions are evaluated in terms of cell proliferation, apoptosis and cytokine response in 10- and 21-day-old chickens. Steroid treatment induced thymocyte apoptosis and cell death decreased in the cortical-medullar direction and was more evident in younger animals. 24 h after treatment, the observed effect was reversed. The mitotic activity and thymic cells containing cytokine-like molecules were also affected. Indeed, the acute stress stimulated cytokine immunoreactivity to anti-IL-1alpha, IL-6 and TNF-alpha antibodies both in epithelial cells and interdigitating cells located in medullar and cortical-medullar regions. The increased cytokine expression observed after 12 h was maintained after 24 h. The comparison between 10- and 21-day-old chickens showed a lower number of cells containing cytokine-like molecules in younger specimens. The present findings suggest that cytokines activated by acute stress in vivo could contribute to restoring immunological homeostasis and influence thymic glucocorticoid-mediated functions.
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PMID:Corticosterone 21-acetate in vivo induces acute stress in chicken thymus: cell proliferation, apoptosis and cytokine responses. 1516 29

The hypothalamo-pituitary-adrenal (HPA) axis is a key component of the stress reaction. Most contemporary reviews mention the corticotropin-releasing hormone and arginine vasopressin (AVP)-containing parvocellular neurons of the hypothalamic paraventricular nucleus as the endocrinomotor component of the system. Although there are many studies about the role of AVP in the stress activation, there is evidence consistent and inconsistent with the general view on the importance of AVP. We propose a list of experiments that may provide critical evidence for or against the widely held opinion. The naturally AVP-deficient Brattleboro rat seems to be a good tool for studying the role of AVP. Our experiments on Brattleboro rats with restraint and ip hypertonic saline injection did not support the prominent role of AVP in acute stress, although in forced swim the lack of AVP influenced the HPA axis activation. Among different chronic stress situations (14 days' restraint, chronic morphine or ip hypertonic saline treatment, streptozotocin-induced diabetes mellitus), the role of AVP was not confirmed by changes in somatic parameter (i.e., body, thymus, and adrenal weight changes).
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PMID:The role of vasopressin in hypothalamo-pituitary-adrenal axis activation during stress: an assessment of the evidence. 1524 Mar 64

The influence of physical activity stress (swimming until exhaustion) and age on the antibody-dependent cellular cytotoxicity (ADCC) of lymphocytes from spleen, thymus and axillary lymph nodes in BALB/c mice was studied. The results indicate that the ADCC activity decreases after the acute stress both in young and in old mice. However, when swimming until exhaustion is performed after 1 month training, the ADCC activity increases except in the case of spleen lymphocytes from old mice. The basal ADCC capacity of spleen lymphocytes from old controls is higher (P<0.05) than from young controls, but there are no statistically significant differences in this respect between young and old animals in lymphocytes from thymus and axillary lymph nodes. No correlations between the increase in serum corticosterone levels and ADCC response are found.
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PMID:Influence of physical activity stress and age on the ADCC of lymphocytes from mice. 1537 58

In this study, hematopoietic cells from mice pretreated with CVE and exposed to acute cold/restraint stress were stimulated in the presence of growth factors to form colonies, thus providing accurate information about the modulation of the green algae of the stress-induced changes in the hematopoietic response. Our results demonstrated that exposure to acute stress affected hematopoiesis. Mice exposed for a 2.5-hour time period of cold and restraint presented diminished clonal capacity for CFU-GM content per femur, which was decreased by as much as 50% compared with that in control mice, in spite of the significant increase in serum colony-stimulating activity (CSA). Treatment with 50 mg/kg CVE for 5 days, previously to the stress regimen, attenuates the effects of the stress, since comparable levels of myeloid progenitors were found in the bone marrow of both CVE/stress and control mice. Moreover, the sera from stressed mice pretreated with CVE further increased the CFU-GM formation. On the contrary, the spleen seemed to be less sensitive to acute stress in our experimental conditions. These findings are in line with our previous reports showing that the stress-induced reduction in bone marrow CFU-GM of rats exposed to electric shocks is mediated by activation of the HPA axis and by secretion of opioid agonists. No changes were observed in bone marrow, spleen and thymus total cell counts, and in relative organ weights. However, a 50% reduction in the body weight loss produced by the stress was observed in mice given the extract.
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PMID:Myelopoietic response in mice exposed to acute cold/restraint stress: modulation by Chlorella vulgaris prophylactic treatment. 1551 78


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