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

Neuroendocrine correlates of chronic stress in human infants have not been established. The goal of the present study was to create an animal model of continuous chronic stress using the immature rat to measure basal plasma corticosterone, and secretion of plasma corticosterone in response to an acute stress. This was achieved by modulation of the cage environment for rat pups and their mothers. During postnatal days 2-9, pups were maintained in three groups: (1) handled, (2) not handled and with ample bedding; and (3) not handled with limited bedding. On postnatal day 9, some pups from each group were subjected to acute cold-separation stress and were killed 90, 240, or 360 min later along with unstressed controls. The group not handled and with limited bedding manifested increased plasma corticosterone output even without cold exposure and a sustained increase of plasma corticosterone after cold-separation stress. Plasma corticosterone interanimal variability was increased and body weight was decreased in these pups, typical of a state of chronic stress. The first model of continuous stress in infant rats in which upregulation of hypothalamic-pituitary-adrenal axis is achieved without maternal separation is presented. This paradigm may more closely approximate the human situation of chronically stressed, neglected infants.
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PMID:Abnormal corticosterone regulation in an immature rat model of continuous chronic stress. 888 44

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

Lipid peroxidation (LPO) is one of the main events induced by oxidative stress. The aim of our study was to investigate the influence of 30 min cold-immobilization (model of acute stress used in this experiment) on LPO in the brain, heart, liver and stomach homogenates of the rats. LPO was determined by measuring of the contents of thiobarbituric acid reactive substances (TBARS), conjugated dienes (CD) and sulfhydryl groups (SH). Experimental stress induced enhancement of TBARS formation in the liver and increased level of the CD in the heart, stomach and liver, while in the brain both parameters were found to be decreased. The levels of TBARS were not changed in the heart and in the stomach, too. The concentrations of SH-groups were decreased in the heart, brain and stomach, while in the liver the parameter was found to be not changed. The results of this study showed the increase of LPO in the heart, stomach and liver under stress conditions. It could be supposed that LPO may be involved in mechanisms of stress injury in different tissues.
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PMID:Lipid peroxidation during acute stress. 899 36

Chronic cold stress (4 degrees C) produced a sustained increase in mean arterial pressure in both normotensive and borderline hypertensive rats (BHR). The high blood pressure in BHRs was significantly reversed by a neuropeptide Y (NPY) Y1 receptor antagonist suggesting that NPY is involved in mediating stress-induced hypertension. Corresponding increases in adrenal NPY messenger RNA and NPY immunoreactivity were found during the stress; furthermore, chronic cold stress also potentiated the pressor response of rats to a subsequent acute stress test in which NPY has been shown to play a role. These results suggest that chronic cold stress-induced hypertension is mediated by elevated NPY release and vascular tone as a result of increased NPY gene expression and storage.
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PMID:Role of neuropeptide Y in cold stress-induced hypertension. 949 68

Weanling pigs (n = 132) were used to investigate the effects of three common stressors (and a control) and differing social status on behavior, immunity, plasma cortisol, blood chemical, and performance measures. Eleven blocks of 12 pigs each were evaluated. Each pen contained three pigs of dominant (DOM), intermediate (INT), or submissive (SUB) social status. Two weeks later, random pens of pigs experienced either a control treatment (CON) or they were stressed for 4 h by shipping (SHIP), heat-stressed (HEAT) with overhead heat lamps in their home pens, or cold-stressed (COLD) by direct application of water and an air current. Treatments did not influence body weights; however, percentage weight loss during SHIP was greater than for other treatments. Body weights were heavier for DOM pigs than for INT and SUB pigs. Social status had large effects on plasma cortisol, globulin, acute-phase proteins, body weight, and weight changes. Only acute shipping stress resulted in weight loss. Many immune and blood measures were not changed among acutely stressed pigs; however, the relationship between social status and mitogen-induced lymphocyte proliferation and natural killer cell cytotoxicity was disrupted during acute stress. Pig behavior was significantly changed by each stress treatment in a unique manner. During acute stress, behavioral changes seem to be the most consistent and reliable indicators.
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PMID:Behavioral, endocrine, immune, and performance measures for pigs exposed to acute stress. 949 55

The development of neuroendocrine functions depends not only on genetically determined mechanisms but also on phenotypic signals. Some of these signals may derive from the immune system. For example, interleukin-1 beta (IL-1 beta) stimulates glucocorticoid output during the early postnatal period, and administration of this cytokine at birth induces permanent alterations in the HPA axis in adulthood. We have extended these studies and found that the glucocorticoid response elicited in 5-day-old mice by a low dose of IL-1 beta is not desensitized by previous exposure to the cytokine. We have also compared the magnitude of the increase in corticosterone levels induced by IL-1 in 3-day-old and adult mice to that caused by acute stress. IL-1 beta and acute stress caused a comparable increase in corticosterone levels in adult mice. In newborn mice, however, IL-1 beta, but not restraint or cold stress, stimulated corticosterone output. Thus, IL-1 beta can elicit a corticosterone response during the postnatal stress-hyporesponsive period. Furthermore, when the corticosterone levels attained following IL-1 beta administration were compared to the basal levels of the hormone at a given age, the increase in plasma corticosterone levels was several fold higher in newborn than in adult animals. These data, together with the long-lasting endocrine effects of cytokine exposure at birth, suggest an important role of immune cytokines in the programming of neuroendocrine functions during ontogeny.
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PMID:Interleukin-1, but not stress, stimulates glucocorticoid output during early postnatal life in mice. 962 43

Exposure to acute stressors activates both the hypothalamic-pituitary-adrenal (HPA) and cardiovascular systems. Prior chronic stress enhances HPA responses to novel, acute stressors, but whether it alters cardiovascular responsivity to novel, acute stress is unknown. In the present study, we examined mean arterial blood pressure (MAP) and heart rate (HR) to two distinct stimuli, restraint and formalin, following prior exposure to 7 days of intermittent cold. In two sets of control and chronically stressed animals, we measured MAP and HR for 60 min following onset of 30 min restraint and MAP, HR and behavioral responses to intraplantar injection of formalin. Chronic stress raised MAP and HR under resting conditions and elevated HR during, but not following termination of, restraint. These increases in HR during restraint were due to the differences in resting levels of HR, since both control and chronically stressed animals exhibited similar increases from resting levels in HR during restraint. Conversely, chronically stressed animals exhibited lower changes in MAP and HR from resting levels following termination of restraint. Formalin produced the characteristic biphasic pattern of cardiovascular and behavioral responses. Prior chronic stress did not alter behavior, but increased MAP and HR in Interphase and only MAP in Phase 2. The increases in MAP during Interphase and Phase 2 were a result of the elevations in resting levels of MAP, but even when differences in resting levels were taken into account, HR remained elevated in the Interphase in chronically stressed animals. Together, these data demonstrate that prior chronic intermittent cold stress modifies cardiovascular function both under resting conditions and, in very specific ways, under stimulated conditions produced by restraint and formalin. We propose that these modifications are produced by brain regions that are known to regulate cardiovascular function and which are activated by chronic stress.
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PMID:The effects of prior chronic stress on cardiovascular responses to acute restraint and formalin injection. 966 56

Age-appropriate acute stress, such as cold exposure, provokes the secretion of corticotropin releasing factor (CRF) from the hypothalamus, leading to a robust increase of plasma corticosterone in the immature rat. This activation of the hypothalamic-pituitary-adrenal system is accompanied by a stress-induced increase of steady-state CRF-mRNA expression in the hypothalamic paraventricular nucleus (PVN). In the current study, we analysed changes in CRF-mRNA expression in the PVN and the central nucleus of the amygdala (ACe) in the immature rat in response to a single episode of cold stress and three repeated exposures to this same stressor. CRF-mRNA expression in the PVN increased after a single, but not repeated exposures to cold stress, while repeated acute stress increased the content of the CRF peptide in the anterior hypothalamus. In the ACe, repeated episodes of cold stress resulted in increased expression of CRF-mRNA. These findings indicate a differential regulation of CRF gene expression in the PVN and ACe of the immature rat by single and repeated acute stress.
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PMID:Corticotropin releasing factor mRNA expression in the hypothalamic paraventricular nucleus and the central nucleus of the amygdala is modulated by repeated acute stress in the immature rat. 974 83

Metabolic differences between cardiomyopathic hamsters (CMHs), as they progress through various physiologic phases before reaching end-stage heart failure (HF), and healthy hamsters (HHs) are often difficult to demonstrate. We suggest that metabolic differences, magnified by application of chronic stress (S: cold immobilization 2 hr/day for 5 days) followed by acute stress (AS: 55 min global ischemia /30 min reperfusion), can be used to characterize different stages in this cardiomyopathic process. High performance liquid chromatography (HPLC) and 31P NMR methods were used to monitor the effects of acute stress applied to nonstressed (NS) and previously stressed CMHs (NS-2.5-month NS-5-month; S-2.5-month, S-5-month) and HHs (NS-HH, S-HH). Cardiac tissue extracts from nonstressed and stressed hamsters were analyzed for ATP and PCr at baseline and after completion of ischemia/reperfusion (AS) using HPLC. In nonstressed hamsters, ATP and PCr were 12% lower in CMHs (both NS-2.5- and NS-5-month) than in NS-HHs. After exposure to stress, ATP was 26% lower in CMHs (S-2.5- and S-5-month) compared to S-HHs, whereas there were minimal differences in PCr between the groups. 31P NMR monitoring of metabolism in the perfused beating heart during application of acute stress produced similar changes (%) in ATP and PCr in all groups (NS and S), whereas Pi increase was less in NS-5-month (118%) compared to NS-2.5-month (179%) and NS-HHs (306.8%), P < 0.05; and in S-5-month (148%) compared to S-2.5-month (216%) and S-HHs (222%). The changes in myocardial pH were inversely related to changes in Pi: NS-5-month (-13.5%); NS-2.5-month (-9.7%); NS-HH (-17.7%). pH changes in stressed cardiomyopathic hamsters were similar to those of S-HHs. The postischemic recovery of ATP and Pi return closer to baseline values in cardiomyopathic hamsters (both NS and S) compared to healthy hamsters. The data suggest that cardiomyopathic hamsters have baseline metabolic abnormalities, and their responses to chronic cold immobilization stress, acute ischemia, and chronic cold immobilization stress plus acute ischemia are different from those in HHs. These responses may help to characterize specific stages of disease.
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PMID:Metabolic abnormalities and differential responses to stress associated with hamster cardiomyopathy. 975 Dec 22

Animals prenatally exposed to ethanol typically exhibit hypothalamic-pituitary-adrenal (HPA) hyperresponsiveness to stressors. In contrast to previous studies that have investigated effects of prenatal ethanol exposure on HPA responses to acute or intermittent stressors, our study investigated HPA responses to a chronic continuous stressor, cold stress (4 degrees C for 0, 1, or 3 days). We tested the hypothesis that prenatal ethanol exposure would result in increased plasma corticosterone (CORT) and adrenocorticotropin (ACTH) responses and increased peptide [corticotropin-releasing factor and vasopressin] mRNA levels in the paraventricular nucleus (PVN) of the hypothalamus compared to that in control animals. In addition, CORT and ACTH responses were measured after exposure to an acute stressor (i.p. isotonic saline injection), superimposed during chronic cold exposure, to examine possible sensitization of the HPA response to the acute stress. Thus, blood samples were collected at the end of each of the three periods of cold exposure, either before (0 min) or 15 min after acute stress. The subjects were adult male and female Sprague-Dawley rat offspring from prenatal ethanol (E), pair-fed (PF), and ad libitum-fed control (C) treatment groups. Exposure to cold stress resulted in significant body weight loss in E males at 1 day and in both males and females of all prenatal treatment groups by 3 days of cold stress. Males in all prenatal groups also exhibited significant increases in adrenal weight:body weight ratios. Cold stress alone (0 min condition) increased CORT levels in E males and overall ACTH levels in E males and females compared to controls. ACTH levels were also higher overall in E compared to control males after acute stress (15 min condition). Sensitization of the CORT response to acute stress was observed in males but not females across all prenatal treatment groups. Corticotropin-releasing factor and vasopressin mRNA levels in the PVN were not significantly affected by prenatal treatment or chronic cold stress in either males or females. In contrast, both males and females displayed increases in PVN thyrotropin-releasing hormone (TRH) mRNA levels after cold stress. These data support and extend previous work demonstrating differential effects of prenatal ethanol exposure on HPA responsiveness of male and female offspring, and suggest that E males may be more vulnerable to the effects of chronic cold stress than E females.
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PMID:Effects of prenatal ethanol exposure on hypothalamic-pituitary-adrenal responses to chronic cold stress in rats. 1006 60


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