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Acute Psychological Stress (acute + psychological_stress)

Distribution by Scientific Domains

Medical Sciences	66%

Selected Abstracts

The Effect of Acute Psychological Stress on QT Dispersion in Patients with Coronary Artery Disease

PACING AND CLINICAL ELECTROPHYSIOLOGY, Issue 9 2009
MUSTAFA HASSAN M.D.
Background: An acute psychological stress can precipitate ventricular arrhythmias and sudden cardiac death in patients with coronary artery disease (CAD). However, the physiologic mechanisms by which these effects occur are not entirely clear. Mental stress-induced myocardial ischemia occurs in a significant percentage of the CAD population. It is unknown if the proarrhythmic effects of psychological stress are mediated through the development of myocardial ischemia. Objectives: To examine the effects of psychological stress on QT dispersion (QTd) among CAD patients and whether these effects are mediated via the development of myocardial ischemia. Methods: Psychological stress was induced using a public speaking task. Twelve-lead electrocardiograms (ECG) were recorded at rest, during mental stress, and during recovery. QTd was calculated as the difference between the longest and the shortest QT interval in the 12-lead ECG. Rest-stress myocardial perfusion imaging was also performed to detect mental stress-induced myocardial ischemia. Results: Mental stress induced a significant increase in QTd compared to the resting condition (P < 0.001). This effect persisted beyond the first 10 minutes of recovery (P < 0.001). QTd was significantly associated with the development of mental stress ischemia with ischemic patients having significantly higher QTd during mental stress than nonischemic patients (P = 0.006). This finding remained significant after controlling for possible confounding factors (P = 0.01). Conclusion: An acute psychological stress induces a significant increase in QTd, which persists for more than 10 minutes after the cessation of the stressor. This effect seems to be, at least partially, mediated by the development of mental stress-induced myocardial ischemia. [source]

Maladaptation to mental stress mitigated by the adaptive immune system via depletion of naturally occurring regulatory CD4+CD25+ cells

DEVELOPMENTAL NEUROBIOLOGY, Issue 6 2006
Hagit Cohen
Abstract Peripheral cellular immunity was recently shown to play a critical role in brain plasticity and performance. The antigenic specificity of the participating T cells, however, was not investigated, and nor was their relevance to psychological stress. Here we show, using a mouse model, that adaptive immunity mitigates maladaptation to the acute psychological stress known to trigger abnormal behaviors reminiscent of human post-traumatic stress disorder. Assessment of behavioral adaptation (measured by the acoustic startle response and avoidance behavior) in mice after their exposure to predator odor revealed that maladaptation was several times more prevalent in T cell-deficient mice than in their wild-type counterparts. A single population of T cells reactive to central nervous system (CNS)-associated self-protein was sufficient to endow immune-deficient mice with the ability to withstand the psychological stress. Naturally occurring CD4+CD25+ regulatory T cells were found to suppress this endogenous anti-stress attribute. These findings suggest that T cells specific to abundantly expressed CNS antigens are responsible for brain tissue homeostasis and help the individual to cope with stressful life episodes. They might also point the way to development of immune-based therapies for mental disorders, based either on up-regulation of T cells that partially cross-react with self-antigens or on weakening of the activity of regulatory T cells. © 2006 Wiley Periodicals, Inc. J Neurobiol, 2006 [source]

Effects of psychological stress on the cerebral processing of visceral stimuli in healthy women

NEUROGASTROENTEROLOGY & MOTILITY, Issue 7 2009
C. Rosenberger
Abstract, The aim of the study was to analyse effects of psychological stress on the neural processing of visceral stimuli in healthy women. The brain functional magnetic resonance imaging blood oxygen level-dependent response to non-painful and painful rectal distensions was recorded from 14 healthy women during acute psychological stress and a control condition. Acute stress was induced with a modified public speaking stress paradigm. State anxiety was assessed with the State-Trait-Anxiety Inventory; chronic stress was measured with the Perceived Stress Questionnaire. During non-painful distensions, activation was observed in the right posterior insular cortex (IC) and right S1. Painful stimuli revealed activation of the bilateral anterior IC, right S1, and right pregenual anterior cingulate cortex. Chronic stress score was correlated with activation of the bilateral amygdala, right posterior IC (post-IC), left periaqueductal grey (PAG), and right dorsal posterior cingulate gyrus (dPCC) during non-painful stimulation, and with activation of the right post-IC, right PAG, left thalamus (THA), and right dPCC during painful distensions. During acute stress, state anxiety was significantly higher and the acute stress , control contrast revealed activation of the right dPCC, left THA and right S1 during painful stimulation. This is the first study to demonstrate effects of acute stress on cerebral activation patterns during visceral pain in healthy women. Together with our finding that chronic stress was correlated wit the neural response to visceral stimuli, these results provide a framework for further studies addressing the role of chronic stress and emotional disturbances in the pathophysiology of visceral hyperalgesia. [source]

The Effect of Acute Psychological Stress on QT Dispersion in Patients with Coronary Artery Disease

Self-reported health and cardiovascular reactions to psychological stress in a large community sample: Cross-sectional and prospective associations

PSYCHOPHYSIOLOGY, Issue 5 2009
Anna C. Phillips
Abstract Exaggerated cardiovascular reactions to acute psychological stress have been implicated in a number of adverse health outcomes. This study examined, in a large community sample, the cross-sectional and prospective associations between reactivity and self-reported health. Blood pressure and heart rate were measured at rest and in response to an arithmetic stress task. Self-reported health was assessed concurrently and 5 years later. In cross-sectional analyses, those with excellent/good self-reported health exhibited larger cardiovascular reactions than those with fair/poor subjective health. In prospective analyses, participants who had larger cardiovascular reactions to stress were more likely to report excellent/good health 5 years later, taking into account their reported health status at the earlier assessment. The findings suggest that greater cardiovascular reactivity may not always be associated with negative health outcomes. [source]

Stress activation of cellular markers of inflammation in rheumatoid arthritis: Protective effects of tumor necrosis factor , antagonists

ARTHRITIS & RHEUMATISM, Issue 2 2008
Sarosh J. Motivala
Objective Psychological stress is thought to aggravate disease activity in rheumatoid arthritis (RA), although the physiologic mechanisms are unclear. Tumor necrosis factor , (TNF,) is an inflammatory cytokine involved in the exacerbation of RA, and TNF, antagonists have emerged as efficacious treatments. The purpose of this study was to determine whether RA patients show increased monocyte production of TNF, following acute psychological stress and whether such responses are abrogated in RA patients taking TNF, antagonists. Methods A standardized stress task was administered to 3 groups of subjects: RA patients taking TNF, antagonists, RA patients not taking such medications, and healthy controls. Lipopolysaccharide-stimulated monocyte production of inflammatory cytokines was repeatedly measured using intracellular staining and flow cytometry. Subjective stress, cardiovascular responses, adrenocorticotropic hormone (ACTH) levels, and cortisol levels were also measured. Results The stress task induced increases in subjective stress, cardiovascular activity, and levels of ACTH and cortisol, with similar responses in the 3 groups. In addition, the stress task induced a significant increase (P < 0.001) in monocyte production of TNF, among RA patients who were not taking TNF, antagonists. However, monocyte production of TNF, did not change following psychological stress in RA patients taking TNF, antagonists or in healthy controls. Conclusion Brief psychological stress can trigger increased stimulated monocyte production of TNF, in RA patients. The use of TNF, antagonists protects against stress activation of cellular markers of inflammation in RA patients. [source]