Search PubMed⌕ Search

SEARCH · Search PubMed

Results for “STRESS”

Search indexed PubMed citations on genomics, clinical trials, systematic reviews and public health. Explore titles, authors and supplied subject terms, then open the PubMed record.

Quote a phrase for an exact phrase match. Source license links do not imply unrestricted reuse.

At least 1,225 records · Page 68Linked to original sources

[Stress echocardiography versus scintigraphy in evaluating coronary heart disease: stress echocardiography is superior].

Stress echocardiography has evolved as a routinely employed non-invasive method for the evaluation of patients with coronary artery disease. The diagnostic accuracy of stress echocardiography for the detection of myocardial ischemia is comparable to scintigraphic myocardial perfusion imaging, and may even have a higher specificity for the evaluation of myocardial viability. User-friendliness including patient and investigator safety, availability and mobility of the method, and environmental compatibility, is superior to that of scintigraphy. The potential for future developments, especially in the field of digital imaging and telecommunication, is great. Last but not least, echocardiography is the method most familiar to cardiologists. The sum of these arguments renders stress echocardiography the superior method to scintigraphy in the evaluation of patients with coronary artery disease.

Coronary Circulation↗

The relationship between acute stress disorder and posttraumatic stress disorder in severely injured trauma survivors.

This prospective longitudinal study was designed to investigate the relationship between acute stress disorder (ASD) and the subsequent development of posttraumatic stress disorder (PTSD) in a population of severely injured hospitalised trauma survivors. Symptoms of ASD were assessed just prior to discharge in 307 consecutive admissions to a Level 1 Trauma Centre, with PTSD assessments completed at 3 and 12 months post-injury. A well-established structured clinical interview was adopted for both assessments. Only 1% of the sample met criteria for an ASD diagnosis (at a mean of 8 days post-injury), while the incidence of PTSD was 9% at 3 months and 10% at 12 months. Although all ASD symptom clusters contributed to the prediction of subsequent PTSD severity, logistic regression indicated that only re-experiencing and arousal predicted a categorical PTSD diagnosis. The dissociative symptoms that form the core of ASD were rarely endorsed and showed high specificity but low sensitivity, resulting in a high proportion of false negative diagnoses. Reducing the number of dissociative symptoms required for a diagnosis ameliorated, but did not resolve, the problem. In this particular population, the low sensitivity of the ASD diagnosis renders it a poor screening test for use in identifying high risk individuals for early intervention and prevention strategies.

Adolescent↗

Stress-induced analgesia: prediction of posttraumatic stress symptoms in battered versus nonbattered women.

BACKGROUND: Chronic and inescapable trauma is implicated in the stress-induced analgesia (SIA) response. METHODS: A sample of 27 chronically battered women was compared with 28 trauma-exposed nonbattered women on their SIA response at 1 month postindex assault. RESULTS: For the battered women sample, the SIA response at 1 month postindex assault was found to significantly predict an increase in posttraumatic stress disorder-related hyperarousal at 3 months postindex assault. Furthermore, the battered women showed a significant increase in depression symptoms from 1 to 3 months postindex assault compared with the nonbattered women, who showed a significant decrease. CONCLUSIONS: The findings suggest that the chronic and inescapable nature of trauma exposure in the battered women might account for an SIA response that is qualitatively different from that seen in the nonbattered women. It is suggested that the mechanism underlying the SIA response in battered women might be opioid mediated and that it might be responsible for the significant prediction of physiologic hyperarousal. Furthermore, this hyperarousal might moderate the relationship between the SIA response and depression.

Analgesia↗

Psychological stress, but not physical stress, causes increase in diazepam binding inhibitor (DBI) mRNA expression in mouse brains.

Effects of conditioned emotional stimuli (CES), which induce psychological stress, on the expression of cerebral diazepam binding inhibitor (DBI) mRNA in mouse were examined using a communication box. Cerebral DBI mRNA expression significantly increased in a time-dependent manner after the application of CES. The maximal enhancement of DBI mRNA expression was observed 2 days after the application of CES, and this increase faded out over 7 days after the treatment. Flunitrazepam (1 mg/kg), an agonist for central benzodiazepine (BZD) receptors, completely abolished the CES-induced elevation of cerebral DBI contents and its mRNA expressions. These results indicate that cerebral DBI is enhanced by psychological stress, which is regulated by central BZD receptors.

Animals↗

Oxidative stress, antioxidants and stress tolerance.

Traditionally, reactive oxygen intermediates (ROIs) were considered to be toxic by-products of aerobic metabolism, which were disposed of using antioxidants. However, in recent years, it has become apparent that plants actively produce ROIs as signaling molecules to control processes such as programmed cell death, abiotic stress responses, pathogen defense and systemic signaling. Recent advances including microarray studies and the development of mutants with altered ROI-scavenging mechanisms provide new insights into how the steady-state level of ROIs are controlled in cells. In addition, key steps of the signal transduction pathway that senses ROIs in plants have been identified. These raise several intriguing questions about the relationships between ROI signaling, ROI stress and the production and scavenging of ROIs in the different cellular compartments.

Adaptation, Physiological↗

Acute stress reactions: can biological responses predict posttraumatic stress disorder?

What biological responses characterize those acute trauma reactions that develop into chronic psychiatric disorder? The need to understand the genesis of posttraumatic psychological disorders has resulted in much attention on biological reactions in the initial aftermath of trauma exposure. This review outlines the prevailing biological models of acute stress reaction and critiques the available evidence concerning biological responses to trauma that are associated with subsequent psychological disorder. The roles of peritraumatic dissociation and vulnerability factors for acute stress reaction are also reviewed. The major challenges for research on psychobiological responses to trauma are highlighted.

Acute Disease↗

Early childhood trauma and disorders of extreme stress as predictors of treatment outcome with chronic posttraumatic stress disorder.

History of early childhood trauma was prevalent and highly correlated with Disorders of Extreme Stress Not Otherwise Specified (DESNOS) in a sample of veterans in inpatient treatment for chronic posttraumatic stress disorder (PTSD). DESNOS predicted reliable change on a variety of measures of psychiatric symptomatology (including PTSD) and psychosocial functioning independently of the effects of PTSD diagnosis and early childhood trauma history. DESNOS also predicted treatment outcome on PTSD and quality of life measures after controlling for the effects of ethnicity, war zone trauma exposure severity, initial level of symptomatic severity or quality of life, Axis I (PTSD and major depression) and Axis II (personality disorder) diagnostic status, and early childhood trauma history. Early childhood trauma was not predictive of outcome. DESNOS appears to play an important role in assessment and treatment planning for psychotherapeutic rehabilitation of chronic PTSD.

Adult↗

Disorders of extreme stress following war-zone military trauma: associated features of posttraumatic stress disorder or comorbid but distinct syndromes?

Disorders of extreme stress not otherwise specified (DESNOS) and posttraumatic stress disorder (PTSD) were found to be comorbid but distinct among military veterans seeking inpatient PTSD treatment: 31% qualified for both conditions, 29% were diagnosed PTSD only, 26% were classified DESNOS only, and 13% met criteria for neither. PTSD diagnosis was associated with elevated levels of war-zone trauma exposure and witnessing atrocities and with impairment on the Mississippi Scale for Combat-Related PTSD and the Penn Inventory. DESNOS classification (but not PTSD) was associated with (a) early childhood trauma and participation in war-zone atrocities, (b) extreme levels of intrusive trauma reexperiencing, (c) impaired characterological functioning (object relations), and (d) use of intensive psychiatric services. PTSD and DESNOS may be comorbid but distinct posttraumatic syndromes and, as such, warrant careful clinical and scientific investigation.

Adult↗

The relationship between acute stress disorder and posttraumatic stress disorder: a 2-year prospective evaluation.

Previous research established that 78% of a sample of motor vehicle accident survivors initially diagnosed with acute stress disorder (ASD) were subsequently diagnosed with posttraumatic stress disorder (PTSD) at 6 months posttrauma. Although the previous study provided initial evidence for the utility of the ASD diagnosis, the relationship between ASD and PTSD was assessed over a relatively short period. The present study reassessed that original sample 2 years following the trauma to establish the longer term relationship between ASD and PTSD. ASD was diagnosed in 13% of participants, and 21% were diagnosed with subsyndromal ASD. In terms of participants who participated in all 3 assessments, 63% who met the criteria for ASD, 70% who met the criteria for subsyndromal ASD, and 13% who did not meet the criteria for ASD were diagnosed with PTSD at 2 years posttrauma. These findings indicate the importance of considering multiple pathways to the development of PTSD.

Acute Disease↗

The relationship between acute stress disorder and posttraumatic stress disorder following cancer.

In this study, the authors investigated the relationship between acute stress disorder (ASD) and posttraumatic stress disorder (PTSD) following cancer diagnosis. Patients who were recently diagnosed with 1st onset head and neck or lung malignancy (N=82) were assessed for ASD within the initial month following their diagnosis and reassessed (n=63) for PTSD 6 months following their cancer diagnosis. At the initial assessment, 28% of patients had ASD, and 32% displayed subsyndromal ASD. At follow-up, PTSD was diagnosed in 53% of patients who had been diagnosed with ASD and in 11% of those who had not met criteria for ASD; 36% of patients with PTSD did not initially display ASD. In this study, the authors question the use of the ASD diagnosis to identify recently diagnosed patients at risk of PTSD.

Aged↗

The stress response, psychoneuroimmunology, and stress among ICU patients.

Multiple stressors, physical and psychological, may beset intensive care unit patients. This article opens with a description of the stress cascade and its connection with immunity. Examples of intensive care unit stressors follow, along with various proposed interventions to reduce psychological stress among intensive care unit patients. Although researchers have yet to establish that such interventions will positively impact immune function, they are an essential component of compassionate and holistic care.

Critical Illness↗

Job loss, unemployment, work stress, job satisfaction, and the persistence of posttraumatic stress disorder one year after the September 11 attacks.

The influence of unemployment and adverse work conditions on the course of psychopathology after a mass disaster is unclear. We recruited a representative sample of adults living in the New York City metropolitan area six months after the September 11 attacks and completed follow-up interviews on 71% of the baseline sample six months later (N = 1939). At follow-up, posttraumatic stress disorder (PTSD) persisted in 42.7% of the 149 cases with PTSD at baseline. In multivariable models, unemployment at any time since baseline predicted PTSD persistence in the entire cohort (P = 0.02) and among persons employed at follow-up (P = 0.02). High levels of perceived work stress predicted PTSD persistence among persons employed at follow-up (P = 0.02). Persons unemployed in the aftermath of a disaster may be at risk for poor mental health in the long-term.

Adaptation, Psychological↗

Effects of chronic food restriction stress and chronic psychological stress on the development of adjuvant arthritis in male long evans rats.

The aim of the present experiments was to study the effect of stress of chronic food restriction (FR) and of repeated psychological challenge (PS) on the development of adjuvant arthritis in the Long Evans male rats. In the FR series, four groups of animals were compared: non-treated control (C) and arthritic (AA) rats, both with free access to food and water, and two analogous groups with a 40% food restriction-FR and AA-FR. All animals were killed 22 days after injection of cFA. In the PS series, stress was induced by random daily exposures of the rats to isolation, over-crowding, food/water deprivation, foot shock, tilting, fear for 14 days before cFA injection and 12 days thereafter (groups: C, AA, PS, and AA-PS). Arthritis causes swelling of the hindpaw, which was prevented in the AA-FR group. PS causes more severe disease symptoms: AA-PS rats had more severe hindpaw swelling than AA rats. Forty percent food restriction associated with elevated CORT levels mitigated inflammatory parameters activated during AA. PS worsened the disease. These results suggested that activated CORT is not the only cause of disease suppression, but some metabolic changes during FR play a role.

Animals↗

Urethral closure mechanisms under sneeze-induced stress condition in rats: a new animal model for evaluation of stress urinary incontinence.

The urethral closure mechanism under a stress condition induced by sneezing was investigated in urethane-anesthetized female rats. During sneezing, while the responses measured by microtip transducer catheters in the proximal and middle parts of the urethra increased, the response in the proximal urethra was almost negligible when the bladder response was subtracted from the urethral response or when the abdomen was opened. In contrast, the response in the middle urethra during sneezing was still observed after subtracting the bladder response or after opening the abdomen. These responses in the middle urethra during sneezing were significantly reduced approximately 80% by bilateral transection of the pudendal nerves and the nerves to the iliococcygeous and pubococcygeous muscles but not by transection of the visceral branches of the pelvic nerves and hypogastric nerves. The sneeze leak point pressure was also measured to investigate the role of active urethral closure mechanisms in maintaining total urethral resistance against sneeze-induced urinary incontinence. In sham-operated rats, no urinary leakage was observed during sneeze, which produced an increase of intravesical pressure up to 37 +/- 2.2 cmH2O. However, in nerve-transected rats urinary leakage was observed when the intravesical pressure during sneezing exceeded 16.3 +/- 2.1 cmH2O. These results indicate that during sneezing, pressure increases elicited by reflex contractions of external urethral sphincter and pelvic floor muscles occur in the middle portion of the urethra. These reflexes in addition to passive transmission of increased abdominal pressure significantly contribute to urinary continence mechanisms under a sneeze-induced stress condition.

Animals↗

Acute stress response and posttraumatic stress disorder in traffic accident victims: a one-year prospective, follow-up study.

OBJECTIVE: This study was designed to assess the natural course of posttraumatic symptoms formation, as well as the degree to which acute stress reactions predict later posttraumatic stress disorder (PTSD) in injured traffic accident victims. METHOD: A prospective, 1-year follow-up study was carried out on 74 injured traffic accident victims and a comparison group of 19 patients who were hospitalized for elective orthopedic surgery. Participants were interviewed within the first week following the accident, and follow-up interviews were performed 1, 3, 6, and 12 months after the accident. At 12 months, a structured clinical interview was administered to determine a formal DSM-III-R diagnosis of PTSD. RESULTS: Twenty-four (32%) of the 74 traffic accident victims, but none of the 19 comparison subjects, met DSM-III-R criteria for PTSD at 1 year. Traffic accident victims who developed PTSD had higher levels of premorbid and comorbid psychopathology. Levels of posttraumatic symptoms were significantly higher from the outset in the subjects who developed PTSD and worsened progressively over the first 3 months, in contrast to subjects without PTSD, who manifested gradual amelioration of symptoms during this time. Existence of posttraumatic symptoms immediately after the accident was a better predictor of later PTSD than was accident or injury severity. CONCLUSIONS: In this study, a significant portion of injured traffic accident victims manifested PTSD 1 year after the event. The development of PTSD at 1 year can be predicted as early as 1 week after the accident on the basis of the existence and severity of early PTSD-related symptoms. However, the first 3 months following the accident appear to be the critical period for the development of PTSD.

Accidents, Traffic↗

Paraventricular nucleus mediates prolactin secretory responses to restraint stress, ether stress, and 5-hydroxy-L-tryptophan injection in the rat.

The role of the paraventricular nucleus (PVN) in mediating acute stimulatory PRL responses was investigated in conscious male rats. Electrolytic lesions, verified histologically at autopsy, were stereotaxically made in the PVN region, and sham lesions were made in control rats. Blood was obtained through a chronically indwelling catheter in the right atrium. PVN-lesioned (PVL) rats showed significantly lower T3 levels 1 week after surgery (less than 34.4 ng/dl) compared with sham (mean +/- SEM, 91.2 +/- 5.0 ng/dl) and intact (86.8 +/- 2.0 ng/dl) animals, verifying a lesion in the PVN. T3 was restored to normal (95.6 +/- 1.8 ng/dl) by daily sc administration of T4 (10 micrograms/kg BW) for at least 4 days before the day of the experiments. Basal PRL levels in PVL rats did not differ significantly from those in control or sham-lesioned animals. In response to restraint stress, plasma PRL levels of PVL rats did not rise, in contrast to marked elevation in PRL in sham and intact rats [PRL levels (mean +/- SEM; nanograms per ml), basal to peak: PVL, 4.3 +/- 0.3 to 4.5 +/- 0.4; sham, 4.5 +/- 0.5 to 47.0 +/- 4.1; intact, 4.0 +/- 0.3 to 46.3 +/- 4.9]. PVL also resulted in the complete inhibition of PRL secretion induced by 30-min inhalation of ether (basal to peak: PVL, 3.3 +/- 0.3 to 4.5 +/- 0.2; sham, 5.7 +/- 0.8 to 19.9 +/- 0.9; intact, 3.3 +/- 0.4 to 27.9 +/- 4.0). The stimulatory effect on plasma PRL in sham and intact rats by one iv bolus injection of the serotonin precursor 5-hydroxy-L-tryptophan (5-HTP; 10 mg/kg BW) was completely abolished in PVL animals (basal to peak: PVL, 3.7 +/- 0.6 to 5.2 +/- 1.4; sham, 6.7 +/- 0.6 to 36.0 +/- 0.5; intact, 4.1 +/- 1.2 to 33.3 +/- 3.2). In contrast to the marked alteration in PRL regulation, PVL rats exhibited a typical ultradian rhythm of plasma GH secretion during a 6-h observation period and increased release of GH induced by iv injection of 5-HTP [GH (nanograms per ml), basal to peak; PVL, 4.5 +/- 0.6 to 21.0 +/- 4.9; sham, 3.7 +/- 0.3 to 18.4 +/- 4.4; intact, 2.9 +/- 0.1 to 17.8 +/- 3.5]. These findings indicate that PRL responses to stress and to serotonin act through the PVN, the site of origin of several putative PRL-releasing factors.(ABSTRACT TRUNCATED AT 400 WORDS)

5-Hydroxytryptophan↗

Approach to novel functional foods for stress control 3. Establishment of stress-resistant rat model and its mechanism.

A stress-resistant rat model was introduced. SPORTS (Spontaneously-Running-Tokushima-Shikoku) rats showed significantly shorter time of immobility in the forced swim test compared to control Wister rats. Increase norepinephrine concentration secondary to decreased activity of monoamine oxidase A (MAOA) in hippocampus was observed in this model rats. This model rats are considered to be useful for studying the mechanism of psychological stress.

Animals↗

A prospective study of psychophysiological arousal, acute stress disorder, and posttraumatic stress disorder.

This study investigated the role of acute arousal in the development of posttraumatic stress disorder (PTSD). Hospitalized motor-vehicle-accident survivors (n = 146) were assessed for acute stress disorder (ASD) within 1 month of the trauma and were reassessed (n = 113) for PTSD 6 months posttrauma. Heart rate (HR) and blood pressure (BP) were assessed on the day of hospital discharge. Participants with subclinical ASD had higher HR than those with ASD and no ASD. Participants who developed PTSD had higher HR in the acute posttrauma phase than those without PTSD. Diagnosis of ASD and resting HR accounted for 36% of the variance of the number of PTSD symptoms. A formula composed of a diagnosis of ASD or a resting HR of > 90 beats per minute possessed strong sensitivity (88%) and specificity (85%) in predicting PTSD. These findings are discussed in terms of acute arousal and longer term adaptation to trauma.

Accidents, Traffic↗