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

The metabolic adaptation of the hindlimb in the fetus to a reversible period of adverse intrauterine conditions and, subsequently, to a further episode of acute hypoxemia has been examined. Sixteen sheep fetuses were chronically instrumented with vascular catheters and transit-time flow probes. In nine of these fetuses, umbilical blood flow was reversibly reduced by 30% from baseline for 3 days (umbilical cord compression), while the remaining fetuses acted as sham-operated, age-matched controls. Acute hypoxemia was subsequently induced in all fetuses by reducing maternal fractional inspired oxygen concentration for 1 h. Paired hindlimb arteriovenous blood samples were taken at appropriate intervals during cord compression and acute hypoxemia, and by using femoral blood flow and the Fick principle, substrate delivery, uptake, and output were calculated. Umbilical cord compression reduced blood oxygen content and delivery to the hindlimb and increased hindlimb oxygen extraction and blood glucose and lactate concentration in the fetus. However, hindlimb glucose and oxygen consumption were unaltered during umbilical cord compression. In contrast, hindlimb oxygen delivery and uptake were significantly reduced in all fetuses during subsequent acute hypoxemia, but glucose extraction, oxygen extraction, and hindlimb lactate output significantly increased in sham-operated control fetuses only. Preexposure of the fetus to a temporary period of adverse intrauterine conditions alters the metabolic response of the fetal hindlimb to subsequent acute stress. Additional data suggest that circulating blood lactate may be derived from sources other than the fetal hindlimb under these circumstances. The lack of hindlimb lactate output during acute hypoxemia in umbilical cord-compressed fetuses, despite a significant fall in oxygen delivery to and uptake by the hindlimb, suggests that the fetal hindlimb may not respire anaerobically after exposure to adverse intrauterine conditions. hypoxia
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PMID:Hindlimb glucose and lactate metabolism during umbilical cord compression and acute hypoxemia in the late-gestation ovine fetus. 1266 62

Exposure of Chinese hamster V79 fibroblasts to mild and repetitive H2O2 doses in culture for 15 weeks produced no change in lipid peroxidation status, GSH/GSSG ratio and glutathione peroxidase activity of these cells (VST cells). In contrast, in VST cells catalase levels underwent a prominent increase which could be significantly inhibited and brought down to control levels after treatment with the catalase inhibitor 3-aminotriazole (3-AT). When control (VC) cells were exposed to UV radiation (UVC 5 J/m2) or H2O2 (7.5mM, 15 min), intracellular reactive oxygen species (ROS) levels rose prominently with significant activation of caspase-3. Marked nuclear fragmentation and lower cell viability were also noted in these cells. In contrast, VST cells demonstrated a significantly lower ROS level, an absence of nuclear fragmentation and an unchanged caspase-3 activity after exposure to UVC or H2O2. Cell viability was also significantly better preserved in VST cells than VC cells after UV or H2O2 exposures. Following 3-AT treatment of VST cells, UVC radiation or H2O2 brought about significantly higher elevations in intracellular ROS, increases in caspase-3 activity, significantly lowered cell viability and marked nuclear fragmentation, indicating the involvement of high catalase levels in the cytoprotective effects of repetitive stress. Therefore, upregulation of the antioxidant defense after repetitive oxidative stress imparted a superior ability to cope with subsequent acute stress and escape apoptotic death and loss of viability.
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PMID:Enhancement of catalase activity by repetitive low-grade H2O2 exposures protects fibroblasts from subsequent stress-induced apoptosis. 1294 22

Recent research suggests that high-altitude hypoxia may serve as a model for prolonged oxidative stress in healthy humans. In this study, we investigated the consequences of prolonged high-altitude hypoxia on the basal level of oxidative damage to nuclear DNA in muscle cells, a major oxygen-consuming tissue. Muscle biopsies from seven healthy humans were obtained at sea level and after 2 and 8 weeks of hypoxia at 4100 m.a.s.l. We found increased levels of strand breaks and endonuclease III-sensitive sites after 2 weeks of hypoxia, whereas oxidative DNA damage detected by formamidopyrimidine DNA glycosylase (FPG) protein was unaltered. The expression of 8-oxoguanine DNA glycosylase 1 (OGG1), determined by quantitative RT-PCR of mRNA levels did not significantly change during high-altitude hypoxia, although the data could not exclude a minor upregulation. The expression of heme oxygenase-1 (HO-1) was unaltered by prolonged hypoxia, in accordance with the notion that HO-1 is an acute stress response protein. In conclusion, our data indicate high-altitude hypoxia may serve as a good model for oxidative stress and that antioxidant genes are not upregulated in muscle tissue by prolonged hypoxia despite increased generation of oxidative DNA damage.
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PMID:Oxidative DNA damage and repair in skeletal muscle of humans exposed to high-altitude hypoxia. 1458 Jul 89

In case new diagnostic procedures for Alzheimer's dementia (AD) appear, Nuclear Medicine (NM) would like to be aware of them in order to evaluate its own contribution to diagnose AD by SPET and PET brain studies. Recently, sleep disturbances were studied in AD and tend to be diagnostic for early AD. In AD the actual time of night sleep was found to be 5.7 h, while awakeness time for the same night sleep increased to 2.7 h. Also in AD, the REM and the slow wave stage (SWS) during sleep are shorter and hypopnea and apnea phases are abundant. Internal body temperature during night sleep is only slightly increased in AD, while in temporofrontal dementia and in normal individuals this increase is significant. The circadian rhythm of melatonin is disturbed in AD. The normal duration of inspiration and expiration during daytime which is reversed during normal night sleep, has not been studied in patients with AD. However, this reverse condition favoring inspiration is expected to provide more oxygen to the brain. Chronic but not acute stress causes memory loss and is currently being studied by us as a possible causative factor for memory loss in AD. Tomographic SPET and PET brain studies can locate the site of brain damage in AD. This is important since memory has recently been classified into four categories, namely episodic, semantic, procedural and working memory. In early AD only procedural memory remains intact. This means that these patients may drive a car, do computer word processing and play some games at home or/and in the field. This memory is located in specific nuclei in the cerebellum and the occipital frontal area which do not relate to sites of other kinds of memory. This difference could be well identified by tomographic SPET or PET studies. Thus NM may also diagnose the early stage of AD. Another issue refers to the indications that the unified Medicare and Medicaid system in the USA has issued on September 15, 2004 for performing a PET (18)F-FDG study for AD. These indications are fully described in this editorial.
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PMID:[Alzheimer's dementia, sleep disorders and nuclear medicine]. 1588 44

This study tested the hypothesis that calcitonin gene-related peptide (CGRP) has a role in mediating the in vivo fetal adrenal glucocorticoid response to acute stress. The hypothesis was tested by investigating the effects of fetal treatment with a selective CGRP antagonist on plasma ACTH and cortisol responses to acute hypoxemia in the late-gestation sheep fetus. Under anesthesia, six fetuses at 0.8 of gestation were surgically instrumented with vascular catheters. Five days later, fetuses were subjected to 0.5-h hypoxemia during treatment with either iv saline or a CGRP antagonist, in randomized order, on different days. Treatment started 30 min before hypoxemia and ran continuously until the end of the challenge. Arterial blood samples were collected for plasma ACTH and cortisol measurements (RIA) and blood gas monitoring. CGRP antagonism did not alter basal arterial blood gas or endocrine status. During hypoxemia, similar falls in arterial partial pressure of oxygen occurred in all fetuses. During saline infusion, acute hypoxemia induced significant increases in fetal ACTH and cortisol concentrations. During CGRP antagonism, the pituitary-adrenal responses were markedly attenuated. Correlation of paired plasma ACTH and cortisol values from all individual fetuses during normoxia and hypoxemia showed positive linear relationships; however, neither the slope nor the intercept of the peptide-steroid relationship was affected by CGRP antagonism. These data support the hypothesis that CGRP is involved in the in vivo regulation of fetal adrenocortical steroidogenesis during acute hypoxemia. In addition, the data reveal that CGRP may have a role in the control of other components of the hypothalamo-pituitary-adrenal axis during stimulated conditions in fetal life.
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PMID:The role of calcitonin gene-related Peptide in the in vivo pituitary-adrenocortical response to acute hypoxemia in the late-gestation sheep fetus. 1605 28

The mechanisms controlling ATP generation in the transition from normal resting conditions to either high work states or ischemia are poorly understood. ATP generation depends upon compartmentation between the mitochondria and cytosol of metabolic pathways and key energy transfer species that cannot be easily assessed experimentally. We developed a multicompartment mathematical model of cardiac metabolism to simulate the metabolic responses to ischemia and increased workload. The model is based on mass balances, transport, and metabolic processes in cardiac tissue, and has three distinct compartments (blood, cytosol, and mitochondria). In addition to distinguishing between cytosol and mitochondria, the model includes a cytosolic subcompartment for glycolytic metabolic channeling. The model simulations predict the rapid activation of glycogenolysis and lactate production at the onset of ischemia, and support the concept of localization of glycolysis to a cytosolic subcompartment. In addition, simulations show that mitochondrial NADH/NAD(+) is primarily determined by oxygen consumption during ischemia, while cytosolic NADH/NAD(+) and lactate production are largely a function of glycolytic flux during the initial phase, and is controlled by mitochondrial NADH/NAD(+) and the malate-aspartate shuttle during the steady state. Finally, the model predicts that metabolic activation with an abrupt increase in workload requires parallel activation of ATP hydrolysis, glycolysis, mitochondrial dehydrogenases, the electron transport chain, and ADP phosphorylation. Taken together, these studies demonstrate the importance of metabolic compartmentation in the regulation of cardiac energetics in response to acute stress, and they highlight the usefulness of computational models in this line of investigation.
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PMID:Role of cellular compartmentation in the metabolic response to stress: mechanistic insights from computational models. 1713 80

Angiotensin II (Ang II) induces reactive oxygen species (ROS) production by human vascular smooth muscle cells (hVSMCs). ROS have been implicated in the development of both acute stress-induced premature senescence (SIPS) and chronic replicative senescence. Global oxidative DNA damage triggers SIPS and telomere DNA damage accelerates replicative senescence, both mediated via p53. This study tests the hypothesis that DNA is an important target for Ang II-induced ROS leading to senescence via telomere-dependent and independent pathways. DNA damage was quantified using the Comet assay, telomere DNA length by Southern blotting and hVSMC senescence by senescence-associated beta-galactosidase staining. Exposure to Ang II increased DNA damage in hVSMCs within 4 hours. Inhibition by an AT1 receptor antagonist (losartan metabolite: E3174) or catalase, confirmed that Ang II-induced DNA damage was AT1 receptor-mediated, via the induction of ROS. Acute exposure to Ang II resulted in SIPS within 24 hours that was prevented by coincubation with E3174 or catalase. SIPS was associated with increased p53 expression but was not dependent on telomere attrition because overexpression of human telomerase did not prevent Ang II-induced SIPS. Exposure to Ang II over several population doublings accelerated the rate of telomere attrition (by >2-fold) and induced premature replicative senescence of hVSMCs--an effect that was also attenuated by E3174 or catalase. These data demonstrate that Ang II-induced ROS-mediated DNA damage results in accelerated biological aging of hVSMCs via 2 mechanisms: (1) Acute SIPS, which is telomere independent, and (2) accelerated replicative senescence which is associated with accelerated telomere attrition.
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PMID:Angiotensin II-mediated oxidative DNA damage accelerates cellular senescence in cultured human vascular smooth muscle cells via telomere-dependent and independent pathways. 1799 83

DEFINITION OF PAIN: The International Association for the Study of Pain has defined pain as "an unpleasant sensory and emotional experience associated with actual or potential tissue damage or described in terms of such damage." The interpretation of pain is subjective. Each person forms an internal construct of pain through encountered injury. PAIN AND NEWBORN: The issue of pain perception in newborns, its management and prevention has been neglected for decades. The inability of "self-report" of painful experience has contributed significantly to misunderstanding of the importance of this problem and inadequate treatment. The main characteristic of this 'critical window of brain development' period is rapid enlargement of brain volume and its great plasticity. Harmful short-term and long-term consequences can arise as a consequence of disturbance of the sophisticated balance between newborn and its surrounding. NEONATAL PAIN INDICATORS: As a response to a present painful stimulus, the newborn adapts to this acute stress with changes in endocrine, vegetative, immune and behavioral area. An ideal pain indicator in neonatal period does not exist. There are several different groups of them, namely contextual and developmental indicators (gestational age, contributed illness, medication, for example), physiological (heart rate, vagal tone, breathing rate, blood pressure, oxygen saturation, transcutaneous partial pressures of oxygen and carbon-dioxide, intracranial pressure, palm sweating) and behavioral ones (face expression, movements of limbs, cry), several neonatal pain scales were constructed on the basis of these indicators.
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PMID:[Pain indicators in newborns]. 1879 72

Neuroendocrine stress (NES) causes increase of glucocorticoids and alters physiological levels of reactive oxygen species production in cells, which might involve modifications in the antioxidant defense system. We investigated the hypothesis that acute, chronic, or combined stress alters copper-zinc superoxide dismutase (CuZnSOD) expression pattern at both, mRNA and subcellular protein level in the cerebral cortex and hippocampus of rats and that there may be a relationship between stress-induced corticosterone and CuZnSOD expression. The most effective stress model which led to the most pronounced changes in CuZnSOD expression patterns was also investigated. Our results demonstrated that acute stress immobilization up-regulates mRNA expression of hippocampal CuZnSOD, while cytosolic protein expression of this enzyme was increased in both brain structures. Chronic stress isolation had no effect on either mRNA and protein expression level and caused a lack of significant up-regulation to a novel acute stressors. The presence of this protein in nuclear fractions of both brain structures was also confirmed. The elevated cytosolic CuZnSOD protein levels following acute immobilization might reflect on the defense system against oxidative stress. Chronic isolation compromises CuZnSOD protein expression, which may lead to the inefficient defense against reactive oxygen species (ROS). The stress-triggered CuZnSOD protein expression was not correlated by the corresponding mRNA. The results suggest that different stress models exert a different degree of influence on mRNA and protein level of CuZnSOD in both brain structures as well as serum corticosterone.
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PMID:Differential regulation of CuZnSOD expression in rat brain by acute and/or chronic stress. 1928 69

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.
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PMID:Effects of psychological stress on the cerebral processing of visceral stimuli in healthy women. 1936 54


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