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

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.
 ...
PMID:[Pain indicators in newborns]. 1879 72

In response to a pain-related acute stress, the expression of c-fos protein (Fos), a marker of acute neuronal excitation, was investigated in the hypothalamus of rats. Few Fos-immunopositive cells were seen 15 min after a single subcutaneous injection of 4% formalin in the hypothalamus, but only in the paraventricular nucleus (PVN). Fifteen minutes later, a high number of parvocellular neurons of the PVN showed Fos expression. By 60 min after injection, strong immunoreactivity appeared in the arcuate nucleus, but the Fos-positive neurons distributed almost exclusively in the ventromedial subdivision of the nucleus. Neurons in this part of the arcuate nucleus express mainly neuropeptide Y (NPY) that projects to the medial parvocellular subdivision of the PVN. It has been demonstrated by previous studies that this part of the arcuate nucleus receives blood partly from the anterior pituitary through the subependymal plexus of the median eminence, and that it establishes, together with the median eminence, a blood-brain barrier-free area in the medial basal hypothalamus. Since the PVN-projecting NPY neurons in the arcuate neurons are sensitive to alterations in circulating corticosterone levels, the existence of a possible short feedback route in the stress-activated hypothalamo-pituitary-adrenocortical system is discussed.
 ...
PMID:Stress-induced activation of neurons in the ventromedial arcuate nucleus: a blood-brain-CSF interface of the hypothalamus. 1912 91

Nociceptin/orphanin FQ (N/OFQ) and its NOP receptors are present in the central nervous system and in the periphery playing important roles in the modulation of gastrointestinal functions and pain. The aim of this study was to investigate the role of central and peripheral N/OFQ-NOP receptor system in the nociceptive response to colorectal distension (CRD) in basal condition and in two models of gut hypersensitivity triggered by both inflammation and stress. Male Wistar rats were tested in basal and in post-inflammatory conditions, i.e., 5 days after IC TNBS instillation (80 mg/Kg) and received N/OFQ (2 nmol/Kg IP), UFP-101 (a selective NOP receptor antagonist, 10 nmol/Kg IP), N/OFQ+UFP-101, N/OFQ (0.5 nmol/rat ICV) or vehicle. Female rats were tested in basal and after partial restraint stress receiving the same pharmacological treatment. CRD was performed using barostat and abdominal contractions were recorded by electromyography. In basal condition, N/OFQ, ICV and IP injected, did not modify basal visceral sensitivity. Both in TNBS and stress-induced hyperalgesia, IP but not ICV injection of N/OFQ significantly decreased the number of abdominal contractions. Peripheral injection of UFP-101 antagonized N/OFQ effect. Moreover, in post-inflammatory colitis, UFP-101, injected alone, exacerbated visceral hyperalgesia to CRD compared with vehicle. These findings indicate that in rats, N/OFQ, only peripherally injected, reduces visceral hypersensitivity triggered by inflammation or stress without affecting basal sensitivity. N/OFQ visceral anti-hyperalgesic effect involves peripheral NOP receptors. In a post-inflammatory, but not in an acute stress colitis model, N/OFQergic system is endogenously activated.
Pain 2009 Feb
PMID:Peripheral anti-nociceptive effect of nociceptin/orphanin FQ in inflammation and stress-induced colonic hyperalgesia in rats. 1914 91

Transient receptor ion channel 1 (TRPV1) is a nociceptor involved in visceral hypersensitivity. Aminoglycosides like neomycin are not only potent antibiotics but in vitro data suggest that neomycin also acts as a TRPV1-antagonist and alleviates somatic pain responses. To what extent neomycin reduces visceral hypersensitivity remains unknown. Therefore, we aimed to investigate whether neomycin can inhibit in vivo TRPV1-dependent hypersensitivity responses in two rat models of visceral pain. In the first model rats were pretreated with intraperitoneal (i.p.) capsazepine, the selective TRPV1 antagonist SB-705498, neomycin or vehicle alone and 30 min later instilled with intracolonic TRPV1-activating capsaicin. Likewise, rats were pretreated with 10 days oral neomycin and then subjected to intracolonic capsaicin. The visceromotor response (VMR) to distension was measured before and after capsaicin application. In addition, the VMR to distension was measured in adult maternal separated rats before and after acute stress. Before the 2nd distension protocol these rats were treated with i.p. neomycin, amoxycillin or vehicle alone. Our results showed that capsaicin administration induced an enhanced VMR to distension that was prevented by i.p. capsazepine, SB-705498 and neomycin. Oral neomycin treatment changed bacterial faecal content but could not inhibit capsaicin induced visceral hypersensitivity. In maternal separated rats acute stress induced an enhanced response to distension that was reversed by i.p. neomycin, but not amoxycillin. These data indicate that (i.p.) neomycin can inhibit visceral hypersensitivity to distension in a nonbactericidal manner and suggest that TRPV1-modulation may be involved.
 ...
PMID:Possible role for TRPV1 in neomycin-induced inhibition of visceral hypersensitivity in rat. 1929 29

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

Whereas acute stress often results in analgesia, chronic stress can trigger hyperalgesia/allodynia. This influence of long-term stress on nociception is relevant to numerous painful pathologies, such as fibromyalgia (FM), characterized by diffuse muscular pain (hyperalgesia) and/or tenderness (allodynia). Hence, there is a need for pre-clinical models integrating a chronic-stress dimension to the study of pain. Here, we assessed the effects of protracted/intermittent stress produced by daily, 1h restraint periods in cylinders, 4 days/week over 5 weeks, on eight models of hyperalgesia and allodynia in rats. This type of stress potentiated chemical hyperalgesia in the formalin model (160 and 76% increase of pain score above controls, during the early and late phases, respectively). It also produced thermal allodynia in response to cold (paw acetone test: 200% increase of allodynia score during week 3-5) and heat (42 degrees C tail immersion test: 15% decrease of withdrawal threshold, from week 2 onward). This stress also resulted in mechanical allodynia in the von Frey filaments model (60% decrease in threshold during week 2-5). However, such a stress regimen had no influence in the Randall-Selitto test of mechanical hyperalgesia, and in the tail immersion models of cold (4 degrees C) or hot (48 degrees C) thermal hyperalgesia, as well as cold (15 degrees C) allodynia. This model of prolonged/intermittent restraint stress may be useful in investigating the mechanisms linking stress and pain, and provide an assay to assess the potential therapeutic efficacy of drugs targeted against painful pathologies with a strong stress component, including but not restricted to FM.
 ...
PMID:Chronic restraint stress induces mechanical and cold allodynia, and enhances inflammatory pain in rat: Relevance to human stress-associated painful pathologies. 1961 33

The stress response is associated with a broad spectrum of physiological and behavioural effects including hypothalamo-pituitary-adrenal (HPA) axis activation, altered central nervous system activity, neuroimmune alterations, anxiety- and depressive-like behaviour and analgesia. While the acute stress response has essential survival value, chronic stress and dysfunction of the stress response can be maladaptive, contributing to the development and severity of psychiatric and pain disorders. The endogenous cannabinoid (endocannabinoid) system has emerged as an important lipid signalling system playing a key role in mediating and/or modulating behavioural, neurochemical, neuroendocrine, neuroimmune and molecular responses to stress. The weight of evidence, reviewed here, points largely to a system which serves to constrain HPA axis activity, facilitate adaptation or habituation of HPA axis and behavioural responses to stress, reduce anxiety- and depressive-like behaviour and mediate analgesic responses to unconditioned or conditioned stress. Possible involvement of the immune system and associated signalling molecules (e.g. cytokines) in endocannabinoid-mediated modulation of neuroendocrine and behavioural responses to stress is considered. The goal now should be to exploit our understanding of the role of the endocannabinoid system in fundamental stress physiology and pathophysiological processes to better understand and treat a range of stress-related disorders including anxiety, depression and pain.
 ...
PMID:Endocannabinoid-mediated modulation of stress responses: physiological and pathophysiological significance. 1961 42

The immobility response is an innate antipredatory behavior in a broad variety of species. The immobility response varies in its postural components but in general is characterized by an absence of movement and a relative unresponsiveness to stimuli. Experimentally in rats, clamping the neck followed by body inversion and manual restrain elicits a response called "immobility by clamping the neck". Stress reactions protect animals against predators and are characterized by activation of the sympathetic and hypothalamic-pituitary-adrenal systems. However, in mammals, the role of acute stress as a modulator of immobility response has been less studied. The aim of our study was to assess the effects of acute stress and the injection of corticosterone (5mg/kg, ip) on immobility by clamping the neck in rats. We observed that either previous acute stress caused by forced exposure to elevated open platform or application of a heat-pain stimulus to the rat's tail during the immobility increased the duration of the immobility response caused by clamping the neck. Also, the corticosterone produced a rapid increase (15 min after injection) in the duration of this immobility response. Our results show that the acute stress, in rats, is a facilitator of the immobility response and suggest a possible nongenomic rapid action of corticosterone over brain structures that control this behavior.
 ...
PMID:The effects of acute stress and acute corticosterone administration on the immobility response in rats. 1977 3

The relationship between acute stress disorder (ASD), posttraumatic stress disorder symptoms (PTSD), and chronic pain was investigated in a longitudinal study of injured accident victims (N = 323, 64.7% men). Assessments took place 5 days (T1), 6 (T2) months, and 12 (T3) months postaccident. Relations between pain and posttraumatic stress symptoms were tested by structural equation modeling. Subjects diagnosed with full or subsyndromal PTSD at T2 and at T3 (14 and 19%) reported significantly higher pain intensity. Cross-lagged panel analysis yielded a mutual maintenance of pain intensity and ASD or PTSD symptoms across T2. Across the second half year, PTSD symptoms impacted significantly on pain but not vice versa. Clinicians need to pay careful attention to PTSD symptoms in accident survivors suffering from chronic pain.
 ...
PMID:Mutual influence of posttraumatic stress disorder symptoms and chronic pain among injured accident survivors: a longitudinal study. 1992 22

Among individuals with rheumatoid arthritis (RA), stress-associated disease flare can severely impact well-being. Psychological factors such as personal mastery may buffer an individual from the negative effects of those flares. We tested the hypothesis that a high sense of personal mastery would prospectively predict stress reactivity. Measures of pain,perceived stress, fatigue, and mean arterial pressure (MAP) were collected before, during, and after two interpersonal stressors conducted on 73 individuals with RA. Factor analysis of the personal mastery scale yielded two independent factors: a 5-item "fatalism" component and a 2-item "control" component. Individuals with high fatalism scores reported overall greater joint pain at baseline and those scoring high on control exhibited lower MAP, and reported less stress and fatigue at baseline. After controlling for baseline differences, those high in control exhibited greater MAP increase during stress, and less drop in pain when compared to those low in control. These results suggest that individuals high in control may be more susceptible to the effects of acute stress; however, the overall beneficial aspects of high control outweigh the acute negative effects. Personal mastery may play a role in the experience of pain, stress, and fatigue for people with RA.
 ...
PMID:Personal mastery predicts pain, stress, fatigue, and blood pressure in adults with rheumatoid arthritis. 2113 65


<< Previous 1 2 3 4 5 6 7 8 9 10 Next >>