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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↗
PubMed1996

Biomechanical effects of stress shielding of the rabbit patellar tendon depend on the degree of stress reduction.

A rabbit model was used to discover whether the effects of stress shielding on the mechanical properties of the patellar tendon depend on the degree of stress reduction. Ninety mature female Japanese White rabbits were divided into three groups: completely stress-shielded partially stress-shielded and sham-operation and contralateral controls. In the experimental groups, tension applied to the patellar tendon was 0%, approximately 30%, and 100% of the normal tension, respectively, with a polyester artificial ligament. Tensile tests were carried out on patella-patellar tendon-tibia complexes harvested 1, 2, 3, 6, or 12 weeks after surgery. The tensile strength decreased in comparison with the sham-operation group to 50.2, 13.5, 9.7, and 20.7% in the completely stress-shielded group and to 75.2, 57.6, 59.6, 57.3, and 72.9% in the partially stress-shielded group. The tensile strength in the completely stress-shielded group was significantly less than that in the partially stress-shielded group at 1, 2, 3, and 6 weeks. The cross-sectional area of the patellar tendon significantly increased to 132, 206, 237, and 136% in the completely stress-shielded group and to 136, 170, 175, 155, and 127% in the partially stress-shielded group compared with the sham-operation group. The cross-sectional area of the completely stress-shielded tendon was significantly larger than that of the partially stress-shielded tendon at 1, 2, and 3 weeks. This study demonstrated that effects of stress shielding on the mechanical properties of the patellar tendon were dependent on the degree of stress shielding.

Animals↗
PubMed2001

Chronic unpredictable stress, but not chronic predictable stress, enhances the sensitivity to the behavioral effects of cocaine in rats.

RATIONALE: Chronic unpredictable stress, in which the type and timing of stress exposures are varied, alters protein levels in the mesolimbic DA system in a manner previously shown to be associated with enhanced behavioral responsiveness to cocaine. Chronic exposure to the same or predictable stress (restraint) does not. Thus, we examined the effects of chronic unpredictable and chronic predictable (restraint) stress on the locomotor activating and place conditioning effects to low cocaine doses. OBJECTIVE: To test whether chronic unpredictable stress enhances the sensitivity to the behavioral effects of cocaine. METHODS: Rats were exposed to 10 days of chronic unpredictable stress, of chronic predictable (restraint) stress, or were not stressed. One day following cessation of stress exposure, locomotor activity to cocaine (0 or 7.5 mg/kg) was assessed for 4 consecutive days and corticosterone levels on the last day were determined. In other experiments, the effects of the chronic stress procedures on cocaine (0.5 and 7.5 mg/kg) place conditioning using an unbiased procedure were assessed. RESULTS: Chronic unpredictable, but not chronic predictable, stress transiently increased the locomotor activating effects of cocaine and this was correlated positively with corticosterone levels. Chronic unpredictable, but not chronic predictable, stress also enhanced the place conditioning effects of cocaine: increased place preference was seen with the low dose and a pronounced place aversion occurred with the high dose. CONCLUSIONS: These data demonstrate that chronic unpredictable stress enhances the behavioral effects of cocaine, including its aversive effects, whereas chronic predictable stress (restraint) is without effect.

Animals↗
PubMed1987

Effects of sequential acute stress exposure on stress-induced pituitary luteinizing hormone and prolactin secretion.

The present study was carried out to determine the effects of repetitive acute stress exposure on pituitary secretion of both luteinizing hormone (LH) and prolactin (PRL). Adult male rats were exposed to sequential episodes of acute novel environment stress separated by intervals of either 60 or 120 minutes. Serial blood samples were obtained from animals before, during and after each stress episode via indwelling intra-cardiac cannulas. The imposition of 10 minute episodes of novel environment stress on an hourly basis eventually rendered the hypothalamic-hypophyseal LH axis refractory to the stimulatory effect of stress. If sequential stress was imposed at 120 minute intervals, LH release was significantly enhanced during each exposure. A different pattern of PRL release was observed during the same sequential stress schedule. After an initial increase in hormone release in response to the first hourly stress episode, PRL levels were unaltered during the second and third hourly stress exposures. Thereafter, plasma PRL levels showed a trend toward a progressive increase in release during each successive episode, and were significantly elevated above preceding baseline levels during the fourth and fifth hourly stress exposures. In rats exposed to stress every two hours, a significant increase in PRL levels occurred following the first, but not the second stress episode. Hormone release was again enhanced in response to the third exposure to novel environment. The present results demonstrate that the repetitive exposure to acute novel environment stress results in differential alterations in pituitary LH and PRL secretion over time, and that the timing of repeated episodes is an important determinant of continued responsiveness to stress, particularly with regard to LH release. These findings suggest that the LH and PRL hormonal responses to at least this specific stressor are mediated by independent neural mechanisms.

Animals↗
PubMed1994

Neonatal chronic stress induces subsensitivity to chronic stress in adult rats: II. Effects on estrous cycle in females.

The purpose of the present report was to determine the effect of exposure of females rats to the unpredictable chronic stress model and two models of predictable chronic stress (cold and handling), from day 2-15 of life, on the estrous cycle alterations caused by the unpredictable chronic stress in adulthood. Adult control and neonatally stressed rats were submitted to estrous cycle analysis for 8 days through microscopic observations of vaginal smears. They were then exposed to chronic aleatory stress, and vaginal smears were analyzed daily throughout the stress period (17 days) up to day 5 after completion of the treatment. It was found that this treatment caused constant diestrus in a majority of control females. Such diestrus started at day 5.75 +/- 0.96 of stress administration and was maintained up to day 20.0 +/- 0.49 (i.e., about 3 days after interruption of stress). This effect was prevented by the neonatal aleatory stress and the neonatal cold stress. Neonatal handling only attenuated the estrous cycle alterations; this group showed a period of diestrus no longer than 4 days during the 17-day exposure to stress. The increased resistance of neonatally stressed rats to the estrous cycle effects of chronic aleatory stress in adulthood supports the speculation that neonatal manipulation can increase resistance of rats to stress-induced reactions throughout life.

Animals↗
PubMed2003

Chronic cold stress sensitizes brain noradrenergic reactivity and noradrenergic facilitation of the HPA stress response in Wistar Kyoto rats.

Many psychiatric disorders, including depression, post-traumatic stress disorder and other anxiety disorders, result from an interaction between genetic factors and exposure to a sufficiently sensitizing environmental stressor. The inbred Wistar Kyoto (WKY) rat strain has been proposed as a model of stress vulnerability, exhibiting an exaggerated hypothalamic-pituitary-adrenal (HPA) response to stress and susceptibility to gastric ulceration. Previously, we showed that stress-activation of the brain noradrenergic system was deficient in WKY rats, and they lacked noradrenergic facilitation of the HPA response in the lateral bed nucleus of the stria terminalis (BSTL), compared to outbred Sprague-Dawley (SD) controls. Deficient modulatory function of the noradrenergic system may contribute to the stress susceptibility of WKY rats. Thus, we investigated the influence of a sensitizing stimulus, chronic intermittent cold exposure, on neuroendocrine and noradrenergic stress reactivity, and on noradrenergic facilitation of the HPA response in these two strains. Chronic cold exposure (7 days, 4 h/day, 4 degrees C) potentiated activation of the HPA axis by acute immobilization stress, assessed by measuring plasma adrenocorticotropic hormone (ACTH), in both strains, although to a greater extent in WKY rats, and enhanced stress-induced norepinephrine (NE) release in BSTL of WKY but not SD rats. We then compared the influence of chronic cold exposure on noradrenergic modulation of the HPA stress response in BSTL, by measuring changes in acute stress-induced elevation of plasma ACTH after microinjecting the alpha(1)-adrenoreceptor antagonist benoxathian into the BSTL. As shown previously, benoxathian attenuated stress-induced ACTH secretion in control SD but not control WKY rats. After chronic cold, the ACTH response to acute stress was attenuated by benoxathian administration into BSTL of both strains, such that the WKY response was not different from that of SD rats. Thus, chronic cold not only sensitized the release of NE in BSTL of WKY rats, but also restored noradrenergic facilitation of their already-elevated HPA response. Such functional sensitization of a previously-deficient facilitatory system may be one mechanism whereby exposure to repeated or severe stress may induce pathologic dysregulation of the stress response in susceptible individuals, resulting in psychiatric illness.

Adrenergic alpha-Antagonists↗
PubMed2003

The stress experience dependent long-term depression disassociated with stress effect on spatial memory task.

Behavioral stress can either block or facilitate memory and affect the induction of long-term potentiation (LTP) and long-term depression (LTD). However, the relevance of the stress experience-dependent long-term depression (SLTD) to spatial memory task is unknown. Here we have investigated the effects of acute and sub-acute elevated platform (EP) and foot shock (FS) stress on LTD induction in CA1 region of the hippocampus of anesthetized rats and spatial memory in Morris water maze. We found that LTD was facilitated by acute EP stress, but not by sub-acute EP stress that may be due to the fast adaptation of the animals to this naturalistic mild stress. However, FS stress, an inadaptable strong stress, facilitated LTD induction both in acute and sub-acute treatment. In addition, with the same stress protocols, acute EP stress impaired spatial memory but the sub-acute EP stressed animals performed the spatial memory task as well as the controls, may due to the same reason of adaptation. However, acute FS stress slightly impaired learning but sub-acute FS even enhanced memory retrieval. Our results showed that SLTD was disassociated with the effect of stress on memory task but might be related to stress experience-dependent form of aberrant memory.

Adaptation, Biological↗
PubMed2003

Randomized controlled evaluation of the effects of cognitive-behavioral stress management on cortisol responses to acute stress in healthy subjects.

Psychosocial stress is a potent activator of the hypothalamus-pituitary-adrenal (HPA) axis. While neuroendocrine stress responses are essential for the maintenance of homeostasis, evidence suggests that excessive activation of the HPA axis constitutes a risk for disease and psychopathology. The purpose of the present study was to assess the effect of cognitive-behavioral stress management training on endocrine stress responses and cognitive appraisal under acute psychosocial stress among healthy young subjects. Forty-eight healthy, non-smoking male students without acute or chronic medical or psychiatric disorder on self report were randomly assigned to receive group-based cognitive-behavioral stress management training either before or after a standardized psychosocial stress test (Trier Social Stress Test, TSST). Endocrine and psychological stress responses were assessed with salivary free cortisol response and cognitive appraisal processes to the TSST. In comparison with the control group, subjects in the treatment group showed an attenuated endocrine response (F (2.55/117.41) = 3.81; P = 0.02; effect size f(2) = 0.35) to the TSST. In addition, subjects in the SIT group had lower stress appraisal and higher control expectancies (F (2/45) = 6.56; P = 0.003, effect size f(2) = 0.29) compared to controls. Short group-based cognitive-behavioral stress management training reduces the neuroendocrine stress response to an acute stressor in healthy subjects. Therefore, stress management training may prove useful in preventing detrimental effects of stress-induced neuroendocrine activation

Adult↗
PubMed2003

The effect of vitamin E on stress-induced changes in visual evoked potentials (VEPs) in rats exposed to different experimental stress models.

PURPOSE: The aim of the study was to investigate the effects of vitamin E on stress-induced changes in visual evoked potentials (VEPs) and lipid peroxidation. METHODS: Eight experimental groups of 10 rats per group were formed. These consisted of the control group (C); the group treated with vitamin E (E); groups exposed to cold stress (CS), immobilization stress (IS) and both cold and immobilization stress (CIS), and groups exposed to equivalent stresses and treated with vitamin E (CSE, ISE, CISE). Vitamin E was injected intramuscularly in a dose of 30 mg/kg/day. RESULTS: Following chronic stress (15 days), plasma corticosterone concentrations in all experimental groups were significantly increased over those in C group. Vitamin E significantly decreased corticosterone levels in all stress groups compared with their respective control groups. Brain nitrite levels were significantly more elevated in all stress groups than in the C group. Vitamin E reduced retina and brain nitrite levels in all stress and E groups compared with their respective control groups. Vitamin E decreased glutathione peroxidase (GSH-Px) activity in retina and brain tissues in the CSE group, but increased it in the ISE group compared with their respective control groups. Lipid peroxidation was increased in brain and retina tissues in all stress groups as indicated by the significant increase in thiobarbituric acid-reactive substance (TBARS) levels with respect to the C group. Vitamin E produced a significant decrease in brain and retina TBARS levels in all stress groups with respect to their corresponding control groups. The mean latencies of P1, N1, P2, N2 and P3 components were significantly prolonged in all stress groups compared with the C group. CONCLUSION: Vitamin E returned the VEP latencies in the stress groups to control values. Our findings clearly indicated that vitamin E has the potential to prevent VEP changes caused by stress.

Animals↗
PubMed2002

Combined dipyridamole-exercise stress echocardiography for detection of myocardial ischemia in hemodialysis patients: an alternative to stress nuclear imaging.

BACKGROUND: Stress nuclear imaging is the noninvasive technique currently used to detect coronary artery disease (CAD) in dialysis patients. Stress echocardiography is recognized as an alternative to stress nuclear imaging for the general population. The aim of this study is to assess the diagnostic accuracy of stress echocardiography for detecting myocardial ischemia in hemodialysis patients. METHODS: Stress echocardiography and stress technetium-99m-tetrofosmin (Myoview; Amersham International Plc) imaging were performed simultaneously for 66 asymptomatic hemodialysis patients in a single session, using a combination of high-dose dipyridamole and symptom-limited exercise. Coronary angiography was performed in 44 patients with at least one abnormal noninvasive test result or who were considered high-risk despite normal noninvasive test results. RESULTS: Results for stress echocardiography were abnormal in 15 patients (22%); stress Myoview, in 14 patients (21%); and coronary angiography, in 12 patients (18%). The sensitivity of stress echocardiography for detecting myocardial ischemia (defined as stress Myoview defect) was 86%; specificity, 94%; positive predictive value, 80%; negative predictive value, 96%; and overall accuracy, 92%. The sensitivity of stress echocardiography for detecting CAD (defined as abnormal coronary angiography result) was 83%; specificity, 84%; positive predictive value, 67%; negative predictive value, 93%; and overall accuracy, 84%. Stress echocardiography and stress Myoview did not differ significantly in overall accuracy for detecting CAD (84% versus 91%; P = not significant). CONCLUSION: In hemodialysis patients, combined dipyridamole-exercise echocardiography is an accurate method to detect both myocardial ischemia and CAD and represents an alternative to stress nuclear imaging.

Adult↗