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PubMed2001

Psychological stress perturbs epidermal permeability barrier homeostasis: implications for the pathogenesis of stress-associated skin disorders.

BACKGROUND: A large number of skin diseases, including atopic dermatitis and psoriasis, appear to be precipitated or exacerbated by psychological stress. Nevertheless, the specific pathogenic role of psychological stress remains unknown. In 3 different murine models of psychological stress, it was recently shown that psychological stress negatively impacts cutaneous permeability barrier function and that coadministration of tranquilizers blocks this stress-induced deterioration in barrier function. OBJECTIVES AND METHODS: The relationship between psychological stress and epidermal permeability barrier function was investigated in 27 medical, dental, and pharmacy students without coexistent skin disease. Their psychological state was assessed with 2 well-validated measures: the Perceived Stress Scale and the Profile of Mood States. Barrier function was assessed simultaneously with the stress measures at periods of presumed higher stress (during final examinations) and at 2 assumed, lower stress occasions (after return from winter vacation [approximately 4 weeks before final examinations] and during spring vacation [approximately 4 weeks after final examinations]). RESULTS: The subjects as a group demonstrated a decline in permeability barrier recovery kinetics after barrier disruption by cellophane tape stripping, in parallel with an increase in perceived psychological stress during the higher vs the initial lower stress occasions. During the follow-up, presumed lower stress period, the subjects again displayed lower perceived psychological stress scores and improved permeability barrier recovery kinetics, comparable to those during the initial lower stress period. Moreover, the greatest deterioration in barrier function occurred in those subjects who demonstrated the largest increases in perceived psychological stress. CONCLUSION: These studies provide the first link between psychological status and cutaneous function in humans and suggest a new pathophysiological paradigm, ie, stress-induced derangements in epidermal function as precipitators of inflammatory dermatoses.

Adult↗

PubMed1995

Biochemical and behaviour changes induced by acute stress in a chronic variate stress model of depression: the effect of amitriptyline.

This paper examines the biochemical and behaviour changes induced by an acute stress (five 10-s, 1-mA foot-shocks) in three groups of rats: (1) never stressed, (2) subjected to chronic variate stress for 20 days, (3) subjected to the same chronic stress and treated with 5 mg/kg per day amitriptyline. After 15 min, acute stress led to a marked reduction in cortical beta-adrenoceptor and 5-HT2 receptor density, whereas the density of the 5-HT1A receptors was unchanged. Chronic stress also increased beta-adrenoceptor and 5-HT2 receptor density and had no effect on 5-HT1A. Acute stress diminished the density of beta-adrenoceptors in chronically stressed animals, but did not alter that of the two 5-HT populations. Amitriptyline alone reduced beta-adrenoceptor and 5-HT2 receptor densities only. Acute stress applied to animals treated with amitriptyline reduced 5-HT1A receptors, and caused a further beta-adrenoceptor decrease, but had no further effect on the 5-HT2 receptors. On behaviour, chronic stress diminished reactivity to the acute stress. This reduction was fully abolished by amitriptyline. An open-field study showed that acute stress reduced motor activity, increased latency times and diminished rearing in the controls, whereas chronic stress reduced motor activity only. No significant changes in behaviour were induced by the acute stress in animals subjected to chronic stress. The combination of chronic stress with amitriptyline was accompanied by a diminution of exploratory activity that persisted after the acute stress.(ABSTRACT TRUNCATED AT 250 WORDS)

Amitriptyline↗

PubMed2003

Stress and transtheoretical model indicators of stress management behaviors in HIV-positive women.

OBJECTIVE: Women are particularly prone to stress with respect to living with HIV. Stress management behaviors can mediate the stress response and improve health outcomes in HIV-positive individuals. The purpose of this descriptive cross-sectional study was to examine stress and Transtheoretical Model (TTM) indicators of stress management behaviors in HIV-positive women. METHODS: 126 HIV-positive women recruited from diverse HIV-care clinics in northeast Ohio completed standardized self-report research instruments to measure stress, stress management behaviors, stage of change, self-efficacy, and decisional balance (pros and cons). RESULTS: Women reported higher levels of stress in the later phase of HIV infection (P<.05). Highly stressed women in this study reported infrequently using stress management behaviors and a low level of perceived efficacy to manage stress although they perceived the pros of managing stress to be high (P<.01). Stress management behaviors were significantly related to stage of change (P<.01), self-efficacy (P<.01), and the cons of managing stress (P<.05). Graphed patterns of decisional balance examined by stage of change and stress management behavior were atypical in this sample. CONCLUSIONS: Clinicians and researchers can use the TTM to describe behavioral indicators of stress management in HIV+ women. However, further research is needed to more fully understand behavioral processes HIV+ women can use to adopt and maintain stress management behaviors.

Adaptation, Psychological↗

PubMed1990

Effects of stress, non-stress cyclicity on hypothalamic noradrenaline release in rats.

The effects of continuous stress and intermittent stress at short intervals on rat hypothalamic noradrenaline (NA) release were assessed by measuring the levels of a principal metabolite of NA, 3-methoxy-4-hydroxy-phenylethyleneglycol sulfate (MHPG-SO4) in male Wistar rats. The rats were exposed to one of five restraint stress conditions, unstressed (control), six 15 min intermittent stress periods (interspersed with 18 min non-stress periods), three 30 min intermittent stress periods (interspersed with 45 min non-stress periods), 90 min continuous stress period or 180 min continuous stress period. The 15 min intermittently stressed rats had significantly larger increases in hypothalamic MHPG-SO4 than the single 90 min and 180 min continuously stressed rats, while the 30 min intermittently stressed rats were significantly different from only the 180 min continuously stressed rats. In a comparison of the 15 min and 30 min intermittently stressed rats, which had the same total duration of stress exposure; the 15 min group had larger increases in MHPG-SO4 levels than the 30 min group. This study provides supporting evidence for the role of stress cyclicity in determining the extent of stress-induced NA release from the hypothalamus.

Animals↗

PubMed2003

Region specific increases in oxidative stress and superoxide dismutase in the hippocampus of diabetic rats subjected to stress.

Oxidative stress and modulation of anti-oxidant enzymes may contribute to the deleterious consequences of diabetes mellitus and to the effects of chronic (i.e. 21 day) stress in the CNS. We therefore compared the effects of short- and long-term exposure to diabetes-induced hyperglycemia, restraint stress and the combined effects of restraint stress and diabetes upon parameters of oxidative stress in the rat hippocampus. Whereas 7 days of restraint stress or hyperglycemia, or the combination, produced similar increases in oxidative stress markers 4-hydroxy-2-nonenal (HNE) and malondialdehyde (MDA) throughout the hippocampus, 21 days of stress or hyperglycemia did not increase these markers in the dentate gyrus. In contrast, Ammon's horn still showed elevated levels of these lipid peroxidation products, especially in diabetic rats subjected to 21 days of restraint stress. The expression of two anti-oxidant enzymes, copper/zinc superoxide dismutase (Cu/Zn-SOD) and manganese SOD, was also differentially regulated by stress and hyperglycemia in a time- and region-specific manner in the rat hippocampus. Although long-term stress decreased both SOD isoforms, diabetes increased Cu/Zn-SOD expression in DG with or without 21 days of repeated stress. These increases may account for the finding that protein-conjugated HNE and MDA levels returned to control levels between 7 days and 21 days of hyperglycemia or the combination of diabetes and stress. These results suggest that while other anti-oxidant pathways may account for decreases in oxidative stress in the long-term stress paradigm, increases in Cu/Zn-SOD expression may contribute to the region-specific attenuation of oxidative stress in the diabetic rat hippocampus.

Animals↗

PubMed2002

Effect of prenatal stress on the hormonal response to acute and chronic stress and on immune parameters in the offspring.

The effect of prenatal stress on the time course of the corticosterone response to acute and chronic stress and on hematological and immunological parameters in the offspring were analized in the present study. Pregnant Sprague-Dawley rats were stressed daily for 2 hours during the last week of gestation, and female and male off-spring were studied during adulthood. Corticosterone response to acute immobilization stress was not significantly different in either control or prenatally stressed rats. However, after 10 days of immobilization stress the corticosterone response completely disappeared in the control animals but not in the prenatally stressed group: high levels of corticosterone were found during the first hour of stress, although they were lower than those found in acutely stressed rats. Adrenal hypertrophy in response to prenatal stress was observed in females but not in male offspring, and chronic stress only increased adrenal weights in the male control group. Prenatal stress decreased the total peripheral leukocyte count, altered its diferential count decreasing lymphocytes and increasing neutrophil and eosinhophil counts, and significantly reduced the percentage of peripheral lymphocyte T CD8+ subset in male offspring. Chronic stress also reduced the percentage of the peripheral T CD8+ lymphocyte subset in the control group but not in the prenatally stressed group. These results suggest that the exposure to stress during pregnancy alters the adaptative response of the hypothalamus-pituitary-adrenocortical axis to chronic stress and presumably the immune competence in the offspring.

Acute Disease↗

PubMed1985

Differential effects of morphine on core temperature in stressed and non-stressed rats.

The effects of morphine on body temperature were studied in rats in two different states - stressed and non-stressed. Morphine injected subcutaneously (s.c.) produced a dual action on body temperature in non-stressed rats. Hyperthermia occurred at lower doses (2.5-10 mg/kg) while hypothermia was produced with a higher dose (20 mg/kg). Both of these effects of morphine were reversed by naloxone (0.1-5.0 mg/kg). Stressing the rats (immobilization with wire mesh) produced slight hypothermia which was markedly potentiated by morphine (5-20 mg/kg) in a dose-dependent manner. Enhancement of hypothermia by morphine in the stressed animals was antagonized by pretreatment with naloxone (0.1-5.0 mg/kg). When rats were treated with morphine (10 mg/kg) 1 h before stress, and were then exposed to immobilization stress, the hyperthermia exhibited in the non-stressed state changed to hypothermia in the stressed state. When the rats which were treated with morphine and then stressed for 1 h were released from stress, the hypothermia observed in the stressed state progressively changed to hyperthermia. Furthermore, these morphine effects, i.e. hyper- and hypothermia in the non-stressed and stressed states, respectively, were reversed but not eliminated by naloxone. These results suggest that the effects of morphine on core temperature in rats are altered depending upon the state of the animals. That is, morphine appears to have a dual action, hyperthermia in the non-stressed state and hypothermia in the stressed state. It also appears that these actions are mediated via opiate receptors.

Animals↗

PubMed2003

Phosphorylated cyclic AMP response element binding protein expression induced in the periaqueductal gray by predator stress: its relationship to the stress experience, behavior and limbic neural plasticity.

Electrophysiological studies in cats and recently in rats implicate neuroplasticity in the periaqueductal gray (PAG) and its afferents in stressor-induced increases in fearful behavior and anxiety-like behavior (ALB). Such increases may model aspects of affective changes following traumatic stress in humans. The present study explored the role of neuroplasticity in PAG and its connection with the central nucleus of the amygdala (ACE) in male rodent anxiety-like response to predator stress. In the first of two studies, the effects of predator stress on the induction of phosphorylated cyclic AMP response element binding protein (pCREB) were investigated. pCREB expression in the PAG and ventromedial hypothalamus (VMH) was examined immunohistochemically. Predator stress increased the degree of pCREB expression in PAG cells (measured densitometrically) but did not increase the number of cells expressing pCREB (measured stereologically). Moreover, predator stress-specific increase in pCREB-like immunoreactivity (lir) was restricted to the right lateral column of the PAG. In addition, pCREB lir in the right lateral column likely reflects aspects of the stress experience because the stressor (cat behavior) and the response to the stressor (rat defensive behavior) are highly predictive of degree of pCREB expression. There was no effect of predator stress on pCREB lir in the VMH. Because pCREB expression has been associated with long-lasting potentiation (LLP) of neural transmission, we examined the effects of predator stress on transmission in the ACE-PAG pathway in a second study. Predator stress elevated evoked potential measures of ACE-PAG transmission in the right hemisphere but not in the left hemisphere 11-12 days after predator stress. This finding is consistent with the longer-lived effects of pharmacological stress on amygdalo-PAG transmission in the right hemisphere but not in the left hemisphere in cats. Of interest is the fact that the same aspects of the stressor experience and reaction to it, which are predictive of the degree of pCREB expression, are also highly predictive of the degree of potentiation of measures of ACE-PAG transmission. Behavioral analyses revealed that the most consistent effects of predator stress are on behavior in the plus maze (open arm exploration and risk assessment) and on startle. In addition, covariance analysis suggests that ACE-PAG potentiation mediates some but not all of the changes in ALB produced by predator stress. Because pCREB expression may be a precursor to neuroplastic changes in certain forms of memory and LLP, the present findings complement studies in the cat, showing that neuroplastic changes in the PAG underlie changes in affect following stress. Furthermore, these findings suggest that neuroplastic changes in PAG may be important mediators of predator stress-induced changes in affective behavior in rodents. Finally, consistent with cat and human studies, the right hemisphere appears particularly important in long-term response to stress.

Animals↗

PubMed2001

Role of stress in functional gastrointestinal disorders. Evidence for stress-induced alterations in gastrointestinal motility and sensitivity.

Psychological stress is widely believed to play a major role in functional gastrointestinal (GI) disorders, especially irritable bowel syndrome (IBS), by precipitating exacerbation of symptoms. The available data clearly demonstrate that inhibition of gastric emptying and stimulation of colonic transit is the most consistent pattern in the motility response of the GI tract to acute or short-term stress. Thus, one might propose that these alterations might play a pathophysiological role in dyspeptic symptoms and alterations in stool frequency and consistency in patients with stress-related functional GI disorders. Taken together, the above-mentioned studies suggest that the colonic motor response to stress is exaggerated in IBS. There is evidence that an increased emotional response is associated with this difference in colonic, and perhaps also gastric motor responses to certain stressors. However, almost no valid data are available so far from human studies addressing the question if differences in motility responses to stress between patients with functional GI disorders and healthy subjects are due to an altered stress response associated with an imbalance of the autonomic nervous system or increased stress susceptibility. We can summarize that in experimental animals the most consistent pattern of GI motor alterations induced by various psychological and physical stressors is that of delaying gastric emptying and accelerating colonic transit. Endogenous corticotropin-releasing factor (CRF) in the brain plays a significant role in the central nervous system mediation of stress-induced inhibition of upper GI and stimulation of lower GI motor function through activation of brain CRF receptors. The inhibition of gastric emptying by CRF may be mediated by interaction with the CRF-2 receptor, while CRF-1 receptors are involved in the colonic and anxiogenic responses to stress. Endogenous serotonin, peripherally released in response to stress, seems to be involved in stress- and central CRF-induced stimulation of colonic motility by acting on 5HT-3 receptors. Taken together, the limited data available from investigations in healthy subjects and patients with functional GI disorders provide some evidence that stress affects visceral sensitivity in humans. Acute psychological stress seems to facilitate increased sensitivity to experimental visceral stimuli, if the stressor induces a significant emotional change. In summary, studies in experimental animals suggest that stress-induced visceral hypersensitivity is centrally mediated by endogenous CRF and involvement of structures of the emotional motor system, e.g. the amygdala. Stress-induced activation or sensitization of mucosal mast cells in the GI tract seem to be involved in stress-associated alterations of visceral sensitivity.

Colon↗

PubMed1993

Neonatal facilitation of stress-induced adrenocorticotropin secretion by prior stress: evidence for increased central drive to the pituitary.

The adrenocortical system of the neonatal rat exhibits both normal pituitary (ACTH) and blunted adrenal corticosterone (B) responses to a variety of different stressors. It is established that although circulating levels of B are low during the first 2 weeks of life, efficient inhibition of ACTH secretion by B is observed in neonatal rats. We investigated the ability of the hypothalamo-pituitary unit to respond to two consecutive, 1 h apart, exposures to 3 min ether vapor (stress 1 and stress 2) and whether an exogenously provided B signal that mimicked the amount of B secreted after the first stress could impair stress-induced ACTH secretion. We also determined in vivo and in vitro whether previous stress could alter pituitary responses to CRF, arginine vasopressin (AVP), or a combination of both peptides. After stress 2, 10-day-old neonates showed similar or increased peak (5 min = control) ACTH secretion compared to stress 1, although the area under the curve over 60 min after stress was comparable between stresses 1 and 2. Stress-induced B secretion was significantly elevated (P < 0.05) 60 min after stress 1, and the mean area (n = 5 experiments) was 39.3 +/- 14 micrograms/dl.60 min. Exogenously injected B (0.1 mg/kg BW) instead of stress 1 was able to mimic the magnitude of the B signal observed after stress 1 (area = 56.4 micrograms/dl.60 min) and significantly reduced (56.4 +/- 18% of ether peak) the peak ACTH secretion seen after stress 2. Doses of 1 and 0.01 mg B/kg BW also reduced peak ACTH amplitude to 20.6 +/- 6.6% and 73.7 +/- 30% of the ether peak value, respectively. Previous exposure to ether stress did not affect the in vivo ACTH response to CRF (10 micrograms/kg) or AVP (5 micrograms/kg) measured 30 min after ip injection, but increased (P < 0.05) the response to CRF plus AVP treatment. When pituitaries from previously stressed 13-day-old pups were incubated in vitro, basal ACTH release was increased, and the ACTH response to CRF (1 and 10 nM), expressed as a percentage of the control value, was reduced. A similar observation was made when intact pituitaries were treated with CRF (0.1 nM) during the preincubation period.(ABSTRACT TRUNCATED AT 400 WORDS)

Adrenocorticotropic Hormone↗

PubMed2000

Oxidative stress and HNE conjugation of GLUT3 are increased in the hippocampus of diabetic rats subjected to stress.

Recent studies demonstrate that cellular, molecular and morphological changes induced by stress in rats are accelerated when there is a pre-existing strain upon their already compromised adaptive responses to internal or external stimuli, such as may occur with uncontrolled diabetes mellitus. The deleterious actions of diabetes and stress may increase oxidative stress in the brain, leading to increases in neuronal vulnerability. In an attempt to determine if stress, diabetes or stress+diabetes increases oxidative stress in the hippocampus, radioimmunocytochemistry was performed using polyclonal antisera that recognize proteins conjugated by the lipid peroxidation product 4-hydroxy-2-nonenal (HNE). Radioimmunocytochemistry revealed that HNE protein conjugation is increased in all subregions of the hippocampus of streptozotocin (STZ) diabetic rats, rats subjected to restraint stress and STZ diabetic rats subjected to stress. Such increases were not significant in the cortex. Because increases in oxidative stress may contribute to stress- and diabetes-mediated decreases in hippocampal neuronal glucose utilization, we examined the stress/diabetes mediated HNE protein conjugation of the neuron specific glucose transporter, GLUT3. GLUT3 immunoprecipitated from hippocampal membranes of diabetic rats subjected to stress exhibited significant increases in HNE immunolabeling compared to control rats, suggesting that HNE protein conjugation of GLUT3 contributes to decreases in neuronal glucose utilization observed during diabetes and exposure to stress. Collectively, these results demonstrate that the hippocampus is vulnerable to increases in oxidative stress produced by diabetes and stress. In addition, increases in HNE protein conjugation of GLUT3 provide a potential mechanism for stress- and diabetes-mediated decreases in hippocampal neuronal glucose utilization.

Aldehydes↗

PubMed2002

pH, abscisic acid and the integration of metabolism in plants under stressed and non-stressed conditions. II. Modifications in modes of metabolism induced by variation in the tension on the water column and by stress.

The hydrolysis of ATP(4-) by the plasmalemma and tonoplast H(+)/ATPases and by the tonoplast pyrophosphatase results in the export of a proton to the apoplast or vacuole with remaining in the cytoplasm. As the enzymes that synthesize ATP(4-) require as a substrate it is proposed that protons are an essential substrate for ATP(4-) synthesis. Thus, the entry of protons to the cytoplasm by sym- and antiports will control the rate of ATP(4-) synthesis. Evidence is adduced that plants control the tension on the water column by removing water to or from the 'cellular reservoir' and guard cells by generating osmotic gradients. Schemes are presented that propose a series of metabolic changes that result in a seamless transition through the following states: (1) the import of K(+), Cl(-) and water from the apoplast to the vacuole, the K(+) being admitted to the cytoplasm via a Ca(2+)-activated K(+)-H(+) symport and the water via a Ca(2+)-activated aquaporin; (2) the continued import of K(+) and water from the apoplast to the vacuole with the concomitant export of protons and the synthesis of malate from glucose in the cytoplasm for importation into the vacuole; (3) when the tension on the water column is optimal, respiration and photosynthesis is maximal resulting in biosynthetic reactions and growth; (4) when tension on the water column increases, K(+), Cl(-) and water are exported from the vacuole to the apoplast; (5) the continued export of K(+) and water from the vacuole to the apoplast with malate for export being synthesized in the cytoplasm; the export of K(+) resulting in the acidification of the vacuole; and (6) a further increase in tension results in the deactivation of the plasmalemma H(+)/ATPase by a further increase in cytoplasmic Ca(2+) which also indirectly activates the alternative oxidase. It is suggested that mitochondrial pyruvate is partly oxidized by the TCA cycle and is partly exported to the cytoplasm where it is carboxylated to form malate(1-) for continued export to the apoplast. K(+) is transferred from the vacuole to the apoplast, the K(+) being replaced by protons from the export of mitochondrial pyruvate. The maintenance of the tonoplast electrochemical gradient is thought to result in an increase in the pH of the apoplast which may cause the hydrolysis of abscisic acid precursors with the resulting abscisic acid opening Ca(2+) channels so that the above events are reinforced. (7) This mode is proposed to continue by the metabolism of glucose to four phosphoenolpyruvate, three of which are carboxylated to malate(1-) for continued export to the apoplast with K(+) from the vacuole, the 'stress-tolerant quiescent state'.

Abscisic Acid↗

PubMed1993

Immobilization stress-induced oral opioid self-administration and withdrawal in rats: role of conditioning factors and the effect of stress on "relapse" to opioid drugs.

The effect of 15 min/day of immobilization (IM) stress on oral self-administration (SA) of morphine (0.5 mg/ml) or fentanyl (25 micrograms/ml) and withdrawal was examined in rats. In addition, the role of conditioning factors in these effects was assessed. For each drug, four groups of subjects were exposed for 50 days to IM stress prior to the drug SA period [Paired-Stress (P-S) groups], to IM stress prior to the drug SA period on half of the days and after the drug SA period on the rest of the days [Partial Paired-Stress (PP-S) groups], to IM stress several hours after the drug SA period [Unpaired-Stress (UP-S) groups], or to no IM stress [Control (C) groups]. The P-S and PP-S groups increased their drug SA during choice days in which both the opioid solution and water were available, and tended to manifest a more severe withdrawal syndrome after a naloxone challenge compared with the UP-S and C groups. Reinstatement of the opioid SA under conditions of paired-stress or no stress was further examined after 3 weeks without exposure to either stress or drugs. The paired stress animals had higher levels of drug SA and manifested a more severe withdrawal syndrome than those tested without stress. These results indicate that the learned association between exposure to stress and the drug availability may mediate, in part, the stress-induced enhancement of opioid SA and withdrawal effects.

Animals↗

PubMedDate not supplied

[Inherent efficiency of stress-limiting systems as a factor of the resistance to stress-induced disorders].

A hypothesis is substantiated in accordance to which a resistance of an organism to stress damages depends upon genetically determined peculiarities of its regulatory stress-limiting systems that restrict stress reaction and its detrimental effects. A comparison of differences between the stress resistance and the activity of the stress-limiting systems (dopaminergic, serotoninergic, nitric oxide and heat shock proteins systems) in rats of two strains August and Wistar indicates that the higher hereditary activity of mentioned systems is associated with the higher resistance to acute emotional stress; and the lower hereditary activity of these systems associated with the lower resistance to this stress. At the same time the adaptation to repeated non-damaging exposures to stressor aimed to rise the stress resistance leads to opposite results in rats of the mentioned strains. In the animals with the higher hereditary resistance to acute stress (August rats) the adaptation reduces this resistance. In the animals with the lower hereditary stress resistance (Wistar rats) that sort of adaptation really rises this resistance. That is determined by changes in activity of the stress-limiting systems during repeated stress exposures. In the animals with the higher hereditary activity of the stress-limiting systems the adaptation reduces the activity of these systems. In the animals with the lower hereditary activity of the stress-limiting systems the adaptation rises this activity and the resistance of these animals to stress damages.

Adaptation, Physiological↗

PubMed1988

[Effects of cold acclimation and repetitive stress on stress-induced neuroendocrine response].

In order to elucidate the mechanism (S) involved in improved cold tolerance by means of enhanced non-shivering thermogenesis of the repetitively stressed rats, noradrenaline (NA) turnover of brown adipose tissue (BAT) and adrenocortical responses were investigated. (1) NA turnover of BAT in the cold-acclimated rats was greater than that in the resting controls. NA level of BAT in the cold-acclimated rats decreased to about 40% of the control level. It was thus inferred that this lower NA levels was induced by accelerated NA turnover. (2) NA turnover of BAT in the stressed rats after repetitive immobilization stress was higher than that of the non-stressed controls. Therefore, increased sympathetic activity of BAT would be one of the mechanisms of cross adaptation between cold and stress. (3) NA turnovers of BAT in the controls, the cold-acclimated rats and stressed ones were increased by acute cold exposure (-5 degrees C). NA turnovers of BAT in the controls and the stressed rats were increased by acute immobilization stress. (4) Plasma corticoids (corticosterone and deoxycorticosterone) in the cold-acclimated rats were higher than that of controls. Plasma corticoids in the controls, the cold-acclimated rats and stressed ones were increased by acute cold exposure (-5 degrees C, 15 min) and acute immobilization stress (30 min). The extents of increases in plasma corticoids in the stressed rats, but not in the cold-acclimated ones, were greater than those in the controls. It was suggested that repetitive immobilization stress could enhance nonshivering thermogenesis via an enhanced responsiveness of adrenocortical secretion to acute stress and cold. It would be concluded from these results that enhanced responses of corticoid secretion and accelerated sympathetic activity were associated with the establishment of cross adaptation between cold and stress. It was suggested that the extent of participation of these factors was not necessarily the same between the cold-acclimated and the stressed organisms.

Acclimatization↗

PubMed2002

Low-dose dobutamine stress gated SPET for identification of viable myocardium: comparison with stress-rest perfusion SPET and PET.

The detection of viable myocardium is important for the prediction of functional recovery after revascularisation. However, a fixed perfusion defect often includes viable myocardium, and perfusion imaging then underestimates myocardial viability. We previously reported that low-dose dobutamine stress gated single-photon emission tomography (SPET) provides similar findings to dobutamine stress echocardiography in the assessment of myocardial viability. The present study investigated whether low-dose dobutamine stress gated SPET is of additional value as compared with stress-rest technetium-99m tetrofosmin SPET for the detection of myocardial viability. Standard stress-rest perfusion SPET, low-dose dobutamine stress gated SPET and fluorine-18 fluorodeoxyglucose positron emission tomography (FDG PET) were studied in 23 patients (mean age 67+/-7.6 years) with previous myocardial infarction. Twenty-one of them were successfully studied with each technique. FDG PET viability (FDG uptake >/=50%) was employed as the gold standard. One-day stress-rest (99m)Tc-tetrofosmin myocardial SPET was performed. After the resting study, gated SPET was acquired following infusion of 7.5 microg kg(-1) min(-1) of dobutamine. Left ventricular wall motion in 16 segments was assessed by cine mode display using a four-point scale. Myocardial viability was considered present when there was improvement by one point. Of a total of 336 segments analysed, 53 had persistent defects on stress-rest perfusion SPET. FDG viability was seen in 16 of 17 dobutamine-responsive segments, but in only 11 of 36 dobutamine non-responsive segments ( P<0.01). Thus, in the segments with persistent defects, viability findings on low-dose dobutamine stress gated SPET were concordant with those on FDG PET in 77% of segments (kappa value =0.55). For the detection of FDG-viable myocardium, the combination of stress-rest perfusion SPET and low-dose dobutamine stress gated SPET achieved a better sensitivity than stress-rest perfusion SPET alone (35/46, 76% vs 19/46, 41.3%, P<0.001), with a similar specificity (25/29, 86% vs 26/29, 90%, P=NS). We conclude that in the identification of viable myocardium, low-dose dobutamine stress gated SPET may provide additional information missed on a routine stress-rest perfusion scan. Dobutamine stress gated SPET may provide new insights into myocardial viability on the basis of ischaemia and contractile reserve.

Aged↗

PubMed1999

Heat stress preconditioning does not protect renal epithelial Na(+),K(+),Cl(-) and Na(+),P(i) cotransporters from their modulation by severe heat stress.

This study compares the effects of heat and osmotic stress on heat stress protein (HSP) production while examining the putative protective action of HSPs on modulation of Na(+),K(+),Cl(-) and Na(+),P(i) cotransporters in Madin-Darby canine kidney (MDCK) epithelial cells by severe heat stress (46 degrees C, 15 min). Preconditioning heat stress (43 degrees C, 20 min) followed by 4 h recovery at 37 degrees C led to a 35-fold increase of HSP70 mRNA expression measured by Northern blot analysis. The protein content of HSP70 and HSP27, assessed by Western blots, was augmented by 5- and 2-fold, respectively, after 6 h of recovery. In contrast to preconditioning heat stress, hyperosmotic stress (520 vs. 320 mosm) elevated HSP70 mRNA content only by 7-fold and did not significantly affect the protein content of HSP70 or HSP27. Neither cell survival, assessed as lactate dehydrogenase (LDH) release, nor the basal activities of the ion transporters and their modulation by protein kinase C, P(2)-purinoceptor and cell volume were altered by preconditioning heat stress. Severe heat stress increased extracellular LDH content from 3+/-2 to 23+/-5% and enhanced Na(+),K(+),Cl(-) and Na(+),P(i) cotransport activity by 2-3-fold. The volume- and protein kinase C-dependent regulation of these carriers was abolished by severe heat stress while regulation by P(2)-purinoceptors was preserved. Preconditioning heat stress diminished severe heat stress-induced LDH release to 11+/-4% but did not protect Na(+),K(+),Cl(-) and Na(+),P(i) cotransporters from activation by severe heat stress and did not prevent severe heat stress-induced inactivation of protein kinase C- and volume-dependent signaling pathways. These results show that in MDCK cells, preconditioning heat stress-induced HSPs are not involved in the regulation of Na(+),K(+),Cl(-) and Na(+),P(i) cotransporters and do not protect them from modulation by severe heat stress.

Animals↗

PubMed1992

The concepts of stress and stress system disorders. Overview of physical and behavioral homeostasis.

OBJECTIVE: This article defines stress and related concepts and reviews their historical development. The notion of a stress system as the effector of the stress syndrome is suggested, and its physiologic and pathophysiologic manifestations are described. A new perspective on human disease states associated with dysregulation of the stress system is provided. DATA SOURCES: Published original articles from human and animal studies and selected reviews. Literature was surveyed utilizing MEDLINE and the Index Medicus. STUDY SELECTION: Original articles from the basic science and human literature consisted entirely of controlled studies based on verified methodologies and, with the exception of the most recent studies, replicated by more than one laboratory. Many of the basic science and clinical studies had been conducted in our own laboratories and clinical research units. Reviews cited were written by acknowledged leaders in the fields of neurobiology, endocrinology, and behavior. DATA EXTRACTION: Independent extraction and cross-referencing by the authors. DATA SYNTHESIS: Stress and related concepts can be traced as far back as written science and medicine. The stress system coordinates the generalized stress response, which takes place when a stressor of any kind exceeds a threshold. The main components of the stress system are the corticotropin-releasing hormone and locus ceruleus-norepinephrine/autonomic systems and their peripheral effectors, the pituitary-adrenal axis, and the limbs of the autonomic system. Activation of the stress system leads to behavioral and peripheral changes that improve the ability of the organism to adjust homeostasis and increase its chances for survival. There has been an exponential increase in knowledge regarding the interactions among the components of the stress system and between the stress system and other brain elements involved in the regulation of emotion, cognitive function, and behavior, as well as with the axes responsible for reproduction, growth, and immunity. This new knowledge has allowed association of stress system dysfunction, characterized by sustained hyperactivity and/or hypoactivity, to various pathophysiologic states that cut across the traditional boundaries of medical disciplines. These include a range of psychiatric, endocrine, and inflammatory disorders and/or susceptibility to such disorders. CONCLUSIONS: We hope that knowledge from apparently disparate fields of science and medicine integrated into a working theoretical framework will allow generation and testing of new hypotheses on the pathophysiology and diagnosis of, and therapy for, a variety of human illnesses reflecting systematic alterations in the principal effectors of the generalized stress response. We predict that pharmacologic agents capable of altering the central apparatus that governs the stress response will be useful in the treatment of many of these illnesses.

Adaptation, Physiological↗