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

This study examined the effects of psychological stress on hemoconcentration in women. Hematologic and hemodynamic variables were assessed in 17 women before and after a 3-min speech task. Significant changes in hematocrit, hemoglobin levels, red and white blood cell (WBC) count, and calculated plasma volume occurred during psychological stress (all ps < .05). Significant increases were also observed for total cholesterol, triglycerides, high density lipoprotein cholesterol, low density lipoprotein cholesterol, and free fatty acid (FFA; all ps < .05) during stress. After statistically correcting for the hemoconcentration effects of decreased plasma volume during stress, only WBC count and FFA concentration remained significantly elevated during the stress task (p < .006 and p < .05, respectively). In sum, acute stress alters hemoconcentration in women, which in turn can account for most stress-induced changes in lipids.
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PMID:Stress-induced hemoconcentration of blood cells and lipids in healthy women during acute psychological stress. 755 35

It is generally assumed that the stress response of different strains of rat will be identical following exposure to acute stress. In the present study we have examined the activation of the hypothalamo-pituitary-adrenal axis in the Wistar, Sprague-Dawley and CFY strains of rat following exposure to either the predominantly psychological stress of restraint or the physical stress of i.p. hypertonic saline injection. We have investigated the hypothalamic activation of corticotrophin-releasing factor (CRF) and proenkephalin A (PEA) mRNAs in the parvocellular cells of the paraventricular nucleus (PVN) and arginine vasopressin (AVP) in both the magnocellular and parvocellular regions in the PVN following acute stress. In addition we have measured corticosterone as an index of end-point activation. Circulating corticosterone and CRF mRNA were increased in all three strains following either stress. AVP and PEA mRNAs were increased following hypertonic saline but only in the CFY strain following restraint. Overall the relative increase in the parameters measured was greater in the CFY strain of rat than the other strains. These data demonstrate marked differences in response to acute stress in the three strains of rat examined. These varying responses must be taken into consideration when designing or interpreting any study investigating the stress response.
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PMID:The effects of restraint or hypertonic saline stress on corticotrophin-releasing factor, arginine vasopressin, and proenkephalin A mRNAs in the CFY, Sprague-Dawley and Wistar strains of rat. 789 84

Double staining in situ hybridization studies have shown that angiotensin II (AII) type 1 receptors (AT1) in the hypothalamic paraventricular nucleus (PVN) are located primarily in corticotropin releasing hormone (CRH) neurons of the parvicellular subdivision. The purpose of these studies was to investigate the role of AII regulating the hypothalamic-pituitary adrenal (HPA) axis, by correlating AT1 receptor expression levels in the PVN with the known changes in activity of the HPA axis under different stress paradigms, and manipulation of circulating glucocorticoids. AT1 receptor mRNA was measured by in situ hybridization using 35S-labelled cRNA probes and AII binding by autoradiography using 125I[Sar1,Ile8]AII in slide mounted hypothalamic sections. AT1 receptor mRNA levels and AII binding in the PVN were reduced by about 20% 18 h after adrenalectomy remaining at these levels up to 6 days after. This effect was prevented by corticosterone administration in the drinking water, or dexamethasone injection (100 mg, s.c., daily). Conversely, dexamethasone injection in intact rats caused a 20% increase in AT1 receptor mRNA in the PVN. AT1 receptor mRNA and binding in the PVN increased 4 h after exposure to stress paradigms associated with activation of the HPA axis (immobilization for 1 h, or i.p. injection of 1.5 M NaCl), and remained elevated after repeated daily stress for 14 days. Unexpectedly, two osmotic stress models associated with inhibition of the HPA axis (60 h water deprivation or 12 days of 2% saline intake) also resulted in increased AT1 receptor mRNA levels and AII binding in the parvicellular PVN. In intact rats, the stimulatory effect of acute stress on AT1 receptor mRNA in the PVN was significantly enhanced by dexamethasone administration (100 micrograms, s.c., 14 h and 1 h prior to stress), while in adrenalectomized rats, with or without glucocorticoid replacement, stress reduced rather than increased, AT1 receptor mRNA. Dexamethasone, 100 micrograms, injected sc within 1 min the beginning of immobilization in adrenalectomized rats, increased AT1 receptor mRNA in the PVN to levels significantly higher than those after dexamethasone alone, indicating that the stress induced glucocorticoid surge is required for the stimulatory effect of stress on AT1 receptor mRNA. The data suggest that AT1 receptor expression in the PVN is under dual control during stress: stress-activated inhibitory pathways and the stimulatory effect of glucocorticoids. The lack of specificity of the changes in AT1 receptor expression in the PVN following stressors with opposite effects on ACTH secretion (osmotic and physical-psychological stress) does not support a role for AII as a major determinant of the response of the HPA axis during stress.
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PMID:Increased expression of type 1 angiotensin II receptors in the hypothalamic paraventricular nucleus following stress and glucocorticoid administration. 856 20

In a previous study, we demonstrated that premenopausal women with visceral obesity have hyperactivity of the hypothalamic-pituitary-adrenal (HPA) axis, characterized by an exaggerated hormone response to corticotropin-releasing factor (CRF) and corticotropin (ACTH) stimulation. The hypothalamic peptide flow that stimulates the pituitary, particularly after a physiological stress challenge, involves not only CRF, but also arginine-vasopressin (AVP), which synergizes the CRF capacity to stimulate pituitary hormone secretion. Previous studies in humans have demonstrated that combining AVP with CRF permits maximal stimulation of the pituitary, providing a more appropriate method of assessing pituitary hormone reserve. We therefore investigated the response of the HPA axis to combined CRF and AVP stimuli in obese women with different obesity phenotypes. Moreover, we examined hormonal and cardiovascular responses to several mental stress tasks, according to previously standardized procedures. Two groups of age-matched premenopausal eumenorrheic obese women with visceral (V-BFD) or subcutaneous (S-BFD) body fat distribution and a group of normal-weight healthy controls were investigated. All women randomly underwent the following protocol: (1) a combined CRF/AVP test (100 micrograms plus 0.3 IU intravenously [IV], respectively); (2) a standardized stress test, which consisted of completing two puzzles and a mental arithmetic test; and (3) a control saline test. Blood samples for ACTH and cortisol determinations were obtained before and during each test, and measurements of arterial blood pressure and pulse rate were made at regular intervals during the stress test. After combined CRF/AVP administration, ACTH and cortisol were significantly higher in V-BFD than in the other two groups. In contrast, no significant hormonal variation was found in either group during stress tasks. During the stress test, pulse rate (but not arterial blood pressure) significantly increased after 8 and 15 minutes in the V-BFD group, whereas no significant variation was found in S-BFD and control women. A significant correlation was present between the pulse rate and change in cortisol level during the stress test at minutes 8 (r=.54, P<.05) and 15 (r=.57, p<.01) in all women considered together. Subjective emotional involvement during stressful tasks was measured by a two-dimensional short verbal scale, which revealed that the stress section had a more significant impact in obese V-BFD than in S-BFD and control women. These data therefore confirm that women with visceral obesity have hyperactivity of the HPA axis, and that the combined CRF/AVP stimulation may offer a good tool for investigating pituitary reserve in this obesity phenotype. Moreover, the results indicate that these women probably have a hyperreactive sympathetic response to acute stress that seems interrelated to that of the HPA axis.
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PMID:Hypothalamic-pituitary-adrenal axis activity and its relationship to the autonomic nervous system in women with visceral and subcutaneous obesity: effects of the corticotropin-releasing factor/arginine-vasopressin test and of stress. 860 43

Previous studies have demonstrated a potential relationship between psychological stress and platelet activation, which may serve as a link between stress and myocardial infarction (MI). However, the possibility that personality traits associated with coronary heart disease may affect platelet activation has not been adequately investigated. The effect of a laboratory stressor (Type A Structured Interview (SI) and speech task) on platelet activation was assessed in 14 stable post-MI patients and 15 age-matched healthy men, using a standardized method of measuring plasma beta-thromboglobulin (BTG) levels. BTG levels were increased after the stressor (average change = 2.0 ng/ml, p = .005). Increases in BTG with stress were related to higher SI ratings of Potential for Hostility (r = .53, p = .004) and Type A behavior (r = .43, p = .02) but not to Cook-Medley-rated hostility scores. Increases in norepinephrine levels and in diastolic blood pressure were nonsignificantly related to increases in BTG levels (ps < .10), whereas increases in epinephrine levels were unrelated. Despite ceasing aspirin and other platelet inhibitors for 10 days before testing, individuals taking platelet inhibitors before the study had less change in BTG with stress (p = .05). However, after statistical adjustment for this factor, SI ratings of Potential for Hostility were still strongly related to increases in BTG with stress (adjusted r = .56, p = .002). Contrary to expectations, healthy men tended to have greater change in BTG with stress than post-MI patients (p = .06). These results indicate that acute stress increases BTG levels and that hostility is related to greater platelet reactivity, independent of any long term effects of platelet inhibition.
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PMID:Effects of hostility on platelet reactivity to psychological stress in coronary heart disease patients and in healthy controls. 884 31

Acute stress elicits variable patterns of pituitary LH release in intact rats. While the pituitary-adrenal axis is capable of discrimination between stressors of graded intensity, the effects of variable glucocorticoid output on the direction and magnitude of LH release during stress remain unclear. The present studies compared the effects of a psychological stress and two different physical stressors on peripheral corticosterone (CORT) and LH concentrations. Plasma CORT levels were elevated during each stress, but this increase in hormone release was significantly greater in response to physical stress. This differential CORT sensitivity to psychological vs. physical stress was correlated with divergent patterns of pituitary LH release; novel environment (NE) stress resulted in a transient increase in plasma LH, whereas both physical stressors ultimately caused a reduction in circulating hormone levels. Pretreatment with the glucocorticoid receptor (GR) antagonist, RU 486, reversed physical stress-induced decreases in LH release, but did not further facilitate circulating LH during NE stress. Other studies showed that stimulation of GRs prior to stress with the potent ligand, dexamethasone (DEX), blunted the stimulatory effects of NE stress on circulating LH. Additional experiments investigated whether prolonged exposure to elevated glucocorticoid levels elicits adaptive responses from the hypothalamic-pituitary LH axis to acute stress. Chronic DEX administration resulted in a significant attenuation of the inhibitory LH response to acute immobilization, but had no impact upon the facilatory effects of NE stress on LH release. The current studies confirm previous reports of variation in the magnitude of CORT secretion elicited by stressors of different intensity, and provide new evidence that inhibitory patterns of pituitary LH release may be correlated with a high degree of activation of the pituitary-adrenal axis. Attenuation of the facilatory effects of novel environment stress on LH release by pretreatment with the GR agonist, DEX, suggests that GR-induced inhibition of LH requires occupation of GRs beyond that which occurs during this mild stressor. The present findings that stress-induced decreases in plasma LH are blunted by chronic glucocorticoid exposure support a role for glucocorticoid-dependent mechanisms in adaptation of GR-mediated inhibitory responses to stress.
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PMID:Stimulatory vs. inhibitory effects of acute stress on plasma LH: differential effects of pretreatment with dexamethasone or the steroid receptor antagonist, RU 486. 887 33

Psychological stress is extremely high in patients with oncological diseases. About 50% of all cancer patients show psychological signs and symptoms which are related to the multiple stress factors of their oncological illness. Although many psychological problems connected with cancer are well known, additional acute stress could result from new therapeutic strategies which require settings similar to intensive care, e.g. bone marrow transplantation. For 2 years the Department of Psychiatry in Innsbruck has provided a "liaison service" at the Department of Bone Marrow Transplantation. Within this observation period, 40 patients have received psychooncological care. The diagnostic distribution according to DSM III-R and specific psychooncological interventions are presented.
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PMID:[Psychiatric problems in bone marrow transplantation patients during isolation]. 899 80

Acute psychological stress is known to alter the distribution of circulating lymphocyte subsets and also to cause a reduction of plasma volume. Data were reanalyzed from 4 previously reported studies (E. A. Bachen et al., 1995; T. B. Herbert et al., 1994; A. L. Marsland, S. B. Manuck, T. V. Fazzari, C. J. Stewart, & B. S. Rabin, 1995; A. L. Marsland, S. B. Manuck, P. Wood, et al., 1995) to determine the extent to which changes in the concentration of lymphocyte subsets are attributable to such hemoconcentration. Meta-analytic procedures showed circulating concentrations of T-suppressor/cytotoxic (CD8) and natural killer (NK) cells to increase following acute laboratory challenge, whereas T-helper (CD4) and B- (CD19) cell populations did not change. Adjustments for concomitant hemoconcentration reduced the magnitude of stress-related increases in CD8 and NK cells significantly and revealed a decrease in CD4 and CD19 cell concentrations from baseline to stress measurements. These data provide evidence (a) that increases in circulating numbers of CD8 and NK cells following acute stress are partially attributable to hemoconcentration and (b) that CD4 and CD19 cell concentrations decrease during acute stress when hemoconcentration is taken into account.
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PMID:Lymphocyte subset redistribution during acute laboratory stress in young adults: mediating effects of hemoconcentration. 923 86

Adoptive immunotherapy represents a potentially effective approach by which to control the extent of viral infections in an immunocompromised host. However, the impact of psychological stress and its associated neuroendocrine components on the efficacy of such a treatment strategy has yet to be determined. In the studies described herein, we have developed and utilized a model of primary, local herpes simplex virus (HSV) infection in radiation-induced, immunosuppressed C57BL/6 mice to investigate the role of stress in altering the protective capacity of adoptively transferred lymphocytes that contribute to the resolution of primary HSV infection. The sublethal dose of irradiation chosen for this model was shown to abrogate the local, adaptive immune response to HSV infection as measured by the degree of in vivo lymphoproliferation, development of HSV-specific cytotoxic T lymphocytes (CTL), and production of gamma interferon (IFN-gamma). Both short- and long-term acute stress, applied in the form of physical restraint, diminished the effectiveness of adoptively transferred lymphocytes as was indicated by an enhancement of viral replication in the footpad tissue and an increased rate of mortality. A reduction in the levels of IFN-gamma at the site of primary HSV infection represented at least one mechanism underlying this suppression of anti-viral immunity. Furthermore, the time-dependent restoration of immune function following irradiation was shown to be compromised in mice subjected to the restraint stress procedure. Together, these findings emphasize the potential role of psychological stress in suppressing both the capability of adoptive immunotherapeutic procedures to combat viral infection and the reestablishment of immune function in individuals who have undergone immunosuppressive therapy.
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PMID:The impact of psychological stress on the efficacy of anti-viral adoptive immunotherapy in an immunocompromised host. 930 25

Acute mental and physical stress lead to a marked lymphocytosis, with circulating natural killer cell numbers showing the most prominent increase. Many studies have linked these acute stress effects on lymphocytes with an increase in catecholamine levels. However, the molecular mechanisms which mediate this redistribution of lymphocytes from lymphocyte reservoirs into the circulation remain unknown. We hypothesized that this form of lymphocytosis was in part due to shedding of cell adhesion molecules from the cell surface and a subsequent detachment of lymphocytes adhering to the vascular endothelium in lymphocyte reservoirs. In this study, healthy human volunteers (n = 12) were exercised on a treadmill until exhaustion. The circulating levels of the soluble cell adhesion molecules ICAM-1 and E-Selectin were determined by ELISA. The subjects were then randomly assigned to treatment with either propranolol or metoprolol and repeated the exercise protocol after 1 week of treatment. Prior to drug treatment, soluble ICAM-1 levels rose from 258 +/- 19 to 321 +/- 28 ng/ml following exercise and returned to approximate baseline levels of 263 +/- 22 ng/ml after 1 h of rest. This highly significant effect of exercise on circulating ICAM-1 levels (p < .005) was mitigated after treatment with the beta-adrenergic antagonists. Soluble E-Selectin levels were not significantly affected by exercise. These results suggest that dynamic exercise leads to shedding of the cell adhesion molecule ICAM-1 via adrenergic mechanisms. We believe that these findings will contribute to the understanding of how physical and mental stress modulate lymphocyte migration and adhesion.
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PMID:Dynamic exercise leads to an increase in circulating ICAM-1: further evidence for adrenergic modulation of cell adhesion. 951 20


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