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

Given the bidirectional nature of the communication between the immune and hypothalamic-pituitary-adrenal (HPA) systems, we examined whether animals that exhibit differences in HPA responses to stress would also exhibit differences in their plaque-forming cell (PFC) responses to sheep red blood cells (SRBC). Neonatally handled (H) animals exhibit lower HPA responses to a number of acute stressors in adulthood compared to nonhandled (NH) animals. Furthermore, these differences also emerge as a function of chronic, intermittent cold stress. We hypothesized that H and NH animals may exhibit differences in the PFC response to SRBC under conditions of acute and/or chronic stress (H CHR and NH CHR). Exposure to acute (4 hr) cold decreased PFC responses in both H and NH animals compared to nonstressed H and NH animals. The decrease in PFC response produced by chronic, intermittent cold stress was similar in H and NH animals and was not different from that found in acutely stressed animals. In H CHR animals reexposed to cold stress, the PFC response was not different from acutely stressed or chronically stressed H and NH animals. In contrast, the PFC response in NH CHR animals reexposed to cold stress was lower than all other groups studied. Thus, neonatal handling prevented prior chronic stress-induced suppression of the PFC response to a subsequent stress. These data suggest that there may be subpopulations of individuals in whom prior chronic stress does not exacerbate the immune suppression produced by acute stress. However, those chronically stressed individuals in whom immune suppression does occur may be more vulnerable to infection and disease.
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PMID:Plaque-forming cell responses and antibody titers following injection of sheep red blood cells in nonstressed, acute, and/or chronically stressed handled and nonhandled animals. 891 94

This review article integrates empirical findings from various scientific disciplines into a proposed psychoneuroimmunological (PNI) model of the acute coronary syndrome (ACS). Our starting point is an existing, mild, atherosclerotic plaque and a dysfunctional endothelium. The ACS is triggered by three stages. (1) Plaque instability: Pro-inflammatory cytokines (IL-1, IL-6, TNF-alpha) and chemoattractants (MCP-1, IL-8) induce leukocyte chemoattraction to the endothelium, and together with other triggers such as the CD40L-CD40 co-stimulation system activate plaque monocytes (macrophages). The macrophages then produce matrix metalloproteinases that disintegrate extra-cellular plaque matrix, causing coronary plaque instability. Acute stress, hostility, depression and vital exhaustion (VE) have been associated with elevated pro-inflammatory cytokines and leukocyte levels and their recruitment. (2) Extra-plaque factors promoting rupture: Neuro-endocrinological factors (norepinephrine) and cytokines induce vasoconstriction and elevated blood pressure (BP), both provoking a vulnerable plaque to rupture. Hostility/anger and acute stress can lead to vasoconstriction and elevated BP via catecholamines. (3) Superimposed thrombosis at a ruptured site: Increases in coagulation factors and reductions in anticoagulation factors (e.g. protein C) induced by inflammatory factors enhance platelet aggregation, a key stage in thrombosis. Hostility, depression and VE have been positively correlated with platelet aggregation. Thrombosis can lead to severe coronary occlusion, clinically manifested as an ACS. Thus, PNI processes might, at least in part, contribute to the pathogenesis of the ACS. This chain of events may endure due to lack of neuroendocrine-to-immune negative feedback stemming from cortisol resistance. This model has implications for the use of psychological interventions in ACS patients.
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PMID:Molecular and cellular interface between behavior and acute coronary syndromes. 1223 62

T lymphocytes and monocytes/macrophages are the most abundant cells found in the atherosclerotic plaque. These cells can migrate towards the activated endothelium through the local release of chemotactic cytokines, or chemokines. Given the important role of leukocyte migration in atherosclerosis and the role of stress in mediating leukocyte trafficking, the present study examined the effects of an acute stressor on the redistribution of T cells (CD3+) and monocytes that express the chemokine receptors CCR5, CCR6, CXCR1, CXCR2, CXCR3, and CXCR4. Forty-four undergraduate students underwent a public speaking task. The acute stressor induced sympathetic cardiac activation, parasympathetic cardiac withdrawal, lymphocytosis, and monocytosis (all p<.001). Although the total number of T lymphocytes did not change, there was a selective increase in the number of circulating T cells expressing CXCR2, CXCR3, and CCR5. The ligands of these receptors are chemokines known to be secreted by activated endothelial cells. Analyses of individual differences in stress-induced responses demonstrated a positive relationship between sympathetic cardiac reactivity and mobilization of the various T cell subsets (.35<r<.56;p<.05). For the monocytes, all sub-populations increased in parallel with total monocyte numbers, with no relation to changes in sympathetic cardiac drive. These results indicate that acute stress induces a mobilization of T cells that are primed to respond to inflamed endothelium. Acute stressors may thus promote the recruitment of circulating immune cells into the sub-endothelia, and therefore accelerate atherosclerotic plaque formation and potentially contribute to the complications that follow acute stressful events. This mechanism may help explain the link between stress, reactivity, and cardiovascular disease.
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PMID:Acute stress evokes selective mobilization of T cells that differ in chemokine receptor expression: a potential pathway linking immunologic reactivity to cardiovascular disease. 1283 27

The combined effects of stress and antigen on interleukin-1beta (Il-1beta) have rarely been studied locally at the site of microbial challenges in vivo, so far. We here propose a model for the analysis of such effects in humans and examine its utility for acute stress trials. Twelve students (6 male, 6 female) refrained from oral hygiene in two antagonistic quadrants for 28 days to allow for increasing bacterial stimulation of the respective gingival sites due to accumulation of microbial plaque. Good oral hygiene was maintained in the remaining quadrants. At day 27 and 28 students were subjected to either stress ('public speech') or a control condition, in a cross-over design. Samples of gingival crevicular fluid (GCF) which emerges between the tooth surface and the gingival epithelium as transudate of healthy and exudate of inflamed gingival tissue, were taken immediately after stress and 60 min later for Il-1beta analysis. Salivary cortisol was assessed to prove the validity of the stress protocol. Stress induced a profound increase of salivary cortisol (p=.001). Repeated measures (stress x time x hygiene) ANOVA with gender as between factor revealed significant stress (p=.014) and hygiene (p=.038) effects on GCF-Il-1beta concentrations and tentatively significant hygiene x time (p = .097) and stress x time x hygiene x gender (p=.107) interactions. Stress induced an increase of Il-1beta as did plaque accumulation. The merits of the proposed model are discussed. It is concluded that it is well suited for the assessment of the effects of stress on inflammatory responses in vivo in humans.
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PMID:Acute stress effects on local Il-1beta responses to pathogens in a human in vivo model. 1526 39

The brains of Alzheimer's disease (AD) patients are morphologically characterized by neurofibrillar abnormalities and by parenchymal and cerebrovascular deposits of beta-amyloid peptides. The generation of beta-amyloid peptides by proteolytical processing of the amyloid precursor protein (APP) requires the enzymatic activity of the beta-site APP cleaving enzyme 1 (BACE1). The expression of this enzyme has been localized to the brain, in particular to neurons, indicating that neurons are the major source of beta-amyloid peptides in brain. Astrocytes, on the contrary, are known to be important for beta-amyloid clearance and degradation, for providing trophic support to neurons, and for forming a protective barrier between beta-amyloid deposits and neurons. However, under certain conditions related to chronic stress, the role of astrocytes may not be beneficial. Here we present evidence demonstrating that astrocytes are an alternative source of BACE1 and therefore may contribute to beta-amyloid plaque formation. While resting astroyctes in brain do not express BACE1 at detectable levels, cultured astrocytes display BACE1 promoter activity and express BACE1 mRNA and enzymatically active BACE1 protein. Additionally, in animal models of chronic gliosis and in brains of AD patients, there is BACE1 expression in reactive astrocytes. This would suggest that the mechanism for astrocyte activation plays a role in the development of AD and that therapeutic strategies that target astrocyte activation in brain may be beneficial for the treatment of AD. Also, there are differences in responses to chronic versus acute stress, suggesting that one consequence of chronic stress is an incremental shift to different phenotypic cellular states.
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PMID:Alzheimer's disease beta-secretase BACE1 is not a neuron-specific enzyme. 1566 71

Acute mental stress is a potent trigger of acute coronary syndromes. Catecholamine-induced hypercoagulability with acute stress contributes to thrombus growth after coronary plaque rupture. Melatonin may diminish catecholamine activity. We hypothesized that melatonin mitigates the acute procoagulant stress response and that this effect is accompanied by a decrease in the stress-induced catecholamine surge. Forty-five healthy young men received a single oral dose of either 3 mg melatonin (n = 24) or placebo medication (n = 21). One hour thereafter, they underwent a standardized short-term psychosocial stressor. Plasma levels of clotting factor VII activity (FVII:C), FVIII:C, fibrinogen, D-dimer, and catecholamines were measured at rest, immediately after stress, and 20 min and 60 min post-stress. The integrated change in D-dimer levels from rest to 60 min post-stress differed between medication groups controlling for demographic and metabolic factors (P = 0.047, eta(p)(2) = 0.195). Compared with the melatonin group, the placebo group showed a greater increase in absolute D-dimer levels from rest to immediately post-stress (P = 0.13; eta(p)(2) = 0.060) and significant recovery of D-dimer levels from immediately post-stress to 60 min thereafter (P = 0.007; eta(p)(2) = 0.174). Stress-induced changes in FVII:C, FVIII:C, fibrinogen, and catecholamines did not significantly differ between groups. Oral melatonin attenuated the stress-induced elevation in the sensitive coagulation activation marker D-dimer without affecting catecholamine activity. The finding provides preliminary support for a protective effect of melatonin in reducing the atherothrombotic risk with acute mental stress.
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PMID:Effect of oral melatonin on the procoagulant response to acute psychosocial stress in healthy men: a randomized placebo-controlled study. 1841 May 84

Psychosocial stress is suggested to play a significant role in development of cardiovascular disease. To evaluate the effects of repeated exposure to stress on atherosclerosis in atherosclerosis-prone ApoE(-/-) mice we used five different stressors. We further sought to determine whether stress combined with high salt diet induces dysfunctional neurohormonal regulation and impaired salt excretion, thus amplifying the atherogenic potential of salt. The five stressors were evaluated in male C57BL/6 mice and ApoE(-/-) mice (studies I and II) and then used in female ApoE(-/-) mice to study their effect on atherosclerosis (study III). The mice in study III received standard or high salt diet (8%) alone or in combination with stress for 12 weeks. Urine and plasma were collected for corticosterone and lipid analysis, respectively. Acute blood pressure (BP) and heart rate (HR) responses to stress were measured using telemetry. Plaque burden was assessed in the thoracic aorta and aortic root. Plaque morphology was investigated regarding macrophages and collagen content. Urinary corticosterone chronically increased in stressed mice (P<0.05 control vs. stress, P<0.05 control salt vs. stress salt). BP and HR increased acutely during all stressors (P<0.05). Body weight gain decreased significantly in the stress group (P<0.05 vs. control). However, stress did not alter plasma lipid levels, plaque area or plaque morphology. Increased BP and HR suggest an acute stress-related response in ApoE(-/-) mice. Furthermore, stress chronically decreased body weight gain and increased urinary corticosterone levels. Notably, despite an apparent stress effect, stress affected neither atherogenesis nor plaque morphology.
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PMID:Repeated exposure to stressors do not accelerate atherosclerosis in ApoE-/- mice. 1883 87

Takotsubo cardiomyopathy is a syndrome characterized by acute regional systolic dysfunction of the left ventricle, frequently related to psycho-physical acute stress, and usually reversible. This rare syndrome involves more often the female sex with the highest frequency of occurrence between the seventh and eighth decade of life. Etiology has not been clarified yet and several hypotheses have been postulated: multiple epicardial coronary artery damage, abnormal coronary microcirculation, catecholamine-mediated cardiac toxicity, and neurogenic stunning. Clinical presentation is not easy to distinguish from an acute coronary syndrome: chest pain at rest or dyspnea, new-onset electrocardiographic changes, characterized by ST-segment elevation or T-wave inversion. Coronary angiography, which should be performed within 48 h of symptom onset in order to be diagnostic, excludes the presence of significant atherosclerotic stenosis or plaque rupture. Ventricular angiography shows the typical regional wall motion abnormalities (apical akinesia and hyperkinesia of the mid-basal segments) that give to the syndrome its name (takotsubo is a traditional Japanese octopus trap or pot). Echocardiography performed in the acute phase also evidences wall motion abnormalities that characteristically regress in the following days. There is no specific treatment for this syndrome, but supportive and symptomatic therapy is usually administered.
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PMID:[Takotsubo cardiomyopathy: a consensus document]. 2010 3

Numerous naturalistic, experimental, and mechanistic studies strongly support the notion that-as part of fight-or-flight response-hemostatic responses to acute psychosocial stress result in net hypercoagulability, which would protect a healthy organism from bleeding in case of injury. Sociodemographic factors, mental states, and comorbidities are important modulators of the acute prothrombotic stress response. In patients with atherosclerosis, exaggerated and prolonged stress-hypercoagulability might accelerate coronary thrombus growth following plaque rupture. Against a background risk from acquired prothrombotic conditions and inherited thrombophilia, acute stress also might trigger venous thromboembolic events. Chronic stressors such as job strain, dementia caregiving, and posttraumatic stress disorder as well as psychological distress from depressive and anxiety symptoms elicit a chronic low-grade hypercoagulable state that is no longer viewed as physiological but might impair vascular health. Through activation of the sympathetic nervous system, higher order cognitive processes and corticolimbic brain areas shape the acute prothrombotic stress response. Hypothalamic-pituitary-adrenal axis and autonomic dysfunction, including vagal withdrawal, are important regulators of hemostatic activity with longer lasting stress. Randomized placebo-controlled trials suggest that several cardiovascular drugs attenuate the acute prothrombotic stress response. Behavioral interventions and psychotropic medications might mitigate chronic low-grade hypercoagulability in stressed individuals, but further studies are clearly needed. Restoring normal hemostatic function with biobehavioral interventions bears the potential to ultimately decrease the risk of thrombotic diseases.
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PMID:Stress and hemostasis: an update. 2411 7

Mast cells accumulate in the perivascular tissue during atherosclerotic plaque progression and contribute to plaque destabilization. However, the specific triggers for mast cell activation in atherosclerosis remain unresolved. We hypothesized that psychological stress-induced activation of mast cells may contribute to plaque destabilization. To investigate this, apoE-/- mice on Western-type diet were exposed to 120' restraint stress. A single episode of restraint caused a significant increase in mast cell activation in the heart. In addition to a rise in serum corticosterone and changes in circulating leukocyte populations, we observed an increase in the circulating pro-inflammatory cytokine interleukin (IL)-6 in the stressed mice. Subsequent characterization of the atherosclerotic plaques revealed a high incidence and larger size of intraplaque hemorrhages in stressed mice. In mast cell-deficient apoE-/- mice, restraint stress affected circulating leukocyte levels, but did not increase plasma IL-6 levels. Furthermore, we did not observe any intraplaque hemorrhages in these mice upon stress, strongly indicating the involvement of a mast cell-dependent response to stress in atherosclerotic plaque destabilization. In conclusion, we demonstrate that acute stress activates mast cells, which induces the incidence of intraplaque hemorrhage in vivo, identifying acute stress as a risk factor for atherosclerotic plaque destabilization.
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PMID:Stress-induced mast cell activation contributes to atherosclerotic plaque destabilization. 3076 59


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