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

Catecholamines (adrenaline, noradrenaline and dopamine) have been measured in specific areas of the rat brain stem after acute immobilization stress. Adrenaline levels were significantly decreased after 240 min of immobilization in all areas studied: A1 area, nucleus commissuralis (NCO), A2 area, anterior part of the nucleus tractus solitarii (NTS), and the locus coeruleus. Noradrenaline concentrations in stressed rats were significantly reduced only in the NTS area. In contrast, during stress there were no significant changes in dopamine concentrations with respect to control values in any of the areas studied. These results implicate the participation of central adrenaline neurons, localized in specific brain stem areas, and noradrenaline neurons innervating the rostral part of the nucleus tractus solitarii, in the mechanism of central response to acute stress.
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PMID:Adrenaline, noradrenaline and dopamine levels in specific brain stem areas of acutely immobilized rats. 76 Oct 66

1. The present study was carried out in order to elucidate the influence of the acute stress on alpha 1-adrenergic, serotonin-2 (5-HT2) and muscarinic cholinergic (M-Ach) receptors-mediated phosphoinositide (PI) hydrolysis in rat cerebral cortex slices. 2. In rat cerebral cortex slices, noradrenaline (NA), serotonin (5-HT) and carbachol stimulated [3H]inositol-monophosphate (IP1) accumulation in a concentration-dependent manner. 3. The forced swimming test (FST) for 15 min induced a significant reduction of 5-HT-stimulated [3H]IP1 accumulation, but this stress situation did not produce a significant alteration of NA- and carbachol-stimulated [3H]IP1 accumulation. 4. The FST for 15 min did not affect the density and affinity of alpha 1-adrenergic, 5-HT2 and M-Ach receptors. 5. In a mild acute stress situation, the intracellular signal transduction mediated by 5-HT was promptly inhibited as compared to the signal transduction mediated by NA or carbachol. This inhibition may be induced by an acute uncoupling of 5-HT2 receptor-mediated intracellular signal transduction.
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PMID:Influence of the acute stress on agonist-stimulated phosphoinositide hydrolysis in the rat cerebral cortex. 135 31

The effect of daily (2 h) exposure to immobilization (IMO) for 15 days on the behavioral and neurochemical responses of adult male rats to acute stress caused by 2-h IMO or 2-h tail-shock was studied. The brain areas studied were frontal cortex, hippocampus, hypothalamus, midbrain, and pons plus medulla. Chronic exposure to IMO did not alter noradrenaline (NA), 3-methoxy,4-hydroxyphenyletileneglycol-SO4 (MHPG-SO4), serotonin, or 5-hydroxindoleacetic acid (5-HIAA) concentrations in any brain area as measured approximately 20 h after the last exposure to IMO. Exposure to behavioral tests did not modify neurochemical variables except NA levels in the hypothalamus of nonchronically stressed (control) rats. Both exposure to 2-h IMO or 2-h shock significantly decreased NA levels in hypothalamus and midbrain of nonchronically stressed rats. These decreases in response to the two acute stressors were not observed in chronically stressed rats. However, MHPG-SO4 levels increased to the same extent in control and chronically stressed rats after exposure to the acute stressors. Likewise, increased 5-HIAA concentrations observed in response to acute stressors were similar in control and chronically stressed rats. The inhibition of activity (areas crossed and rearing) in the holeboard caused by acute IMO was less marked in rats previously exposed to the same stressor than in control rats, but the response to shock was similar. In the forced swim test, acute IMO decreased struggling in control rats but tended to increase it in chronically stressed rats. The response to shock followed the same pattern as that to IMO, although it was slight.(ABSTRACT TRUNCATED AT 250 WORDS)
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PMID:Behavioral and neurochemical changes in response to acute stressors: influence of previous chronic exposure to immobilization. 138 70

In Wistar male rats, 1-h acute immobilization stress resulted in the increased plasma adrenalin, noradrenaline and dopamine in approximately 13, 8 and 23 times, respectively. Plasma PGF2 alpha increased in 3.5 times while PGE remained unchanged; this resulted in the decreased PGE/PGF2 alpha relation in 2.8 times. The PGI2/TXA2 relation also decreased in 1.5 times due to a more pronounced growth of TXA2 than that of PGI2. In rats adapted to the repeated stress (12 sessions), the plasma catecholamine level was higher than that in control but 2-3 fold lower than in unadapted rats after acute single stress. In this situation, PGE was increased by 70% as compared to the control. This is why PGE/PGF2 alpha relation was similar to the control whereas the level of PGF2 alpha increased. PGI2 increased by 53% and TXA2--in two times as compared to the control. In these rats, acute stress induced neither plasma catecholamine enhancement nor PGE/PGF2 alpha relation decrease in comparison with the initial levels; the TXA2 content was increased but it was by 33% less than that in unadapted rats exposed to such stress. One can suggest that the decreased activation of adrenergic system respondent to acute stress in unadapted rats is associated with the increase in plasma PGE and PGI2 which are known to limit the catecholamine release from adrenergic terminals and their harmful effects.
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PMID:[Relations of catecholamine and prostaglandin contents in the blood of rats exposed to acute stress and during adaptation to stress]. 211 13

Foot-shock produced a more than 2-fold increase in noradrenaline (NA) release from the frontal cortex of freely moving rats. The effect of acute stress was almost completely prevented by the administration of diazepam (5 mg/kg i.p.). Diazepam alone inhibited cortical NA release, the maximal inhibition (-57%) being observed 90 min after the injection. Cortical NA release therefore appears to be a reliable index of central noradrenergic activity in response to stressful conditions.
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PMID:Stress increases noradrenaline release in the rat frontal cortex: prevention by diazepam. 231 68

The effects of 1 h/day restraint in plastic tubes for 24 days on the levels of serotonin (5-HT), 5-hydroxyindoleacetic acid (5-HIAA), tryptophan (TP), and noradrenaline (NA) in six regions of rat brain 20 h after the last restraint period were investigated. The levels of 5-HT, 5-HIAA, and NA but not TP increased in several regions. The effects of 1 h of immobilization on both control and chronically restrained rats were also studied. Immobilization per se did not alter brain 5-HT, 5-HIAA, and TP levels, but decreased NA in the pons plus medulla oblongata and hypothalamus. However, immobilization after chronic restraint decreased 5-HT, increased 5-HIAA, and decreased NA in most brain regions in comparison with values for the chronically restrained rats. We suggest that chronic restraint leads to compensatory increases of brain 5-HT and NA synthesis and sensitizes both monoaminergic systems to an additional acute stress. These changes may affect coping with stress demands.
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PMID:Chronic stress increases serotonin and noradrenaline in rat brain and sensitizes their responses to a further acute stress. 245 9

An acute form of "stress-analgesia" is evoked by allowing the smoke of a cigarette to envelope the nostrils of unanaesthetized rabbits. The response consists of an immediate and generalized arrest of spontaneous movements, including respiration and expiration, reduced muscular tone, and unresponsiveness to pinching. This motor "paralysis" is accompanied by a profound bradycardia. Attempts have been made to identify the neurotransmitters involved in "the smoke reflex" by the intervention of antagonists and psychopharmaca. The bradycardia was selectively blocked by atropine, leaving the somatomotor inhibition unaltered. All components of the response were abolished by approximately 60% by clonidine and by 40% by the tricyclic antidepressant amitriptyline, both of which are known to attenuate the release of noradrenaline as agonsits of alpha 2-adrenoceptors. Yohimbine blocked the clonidine effect. Naloxone (1-2 mg/kg), p-chlorphenylalanine and dexamethasone failed to influence the reflex response, suggesting that opiate, serotonergic and ACTH-systems do not play a critical role. The same applied to the benzodiazepine chlordiapoxide. The results suggest that this acute stress-induced analgesia is mediated via a noradrenergic system. The relationship of the smoke reflex to "the fear paralysis reflex", a possible trigger mechanism for the sudden infant death syndrome, is discussed.
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PMID:Neurotransmitters in "the smoke reflex" in rabbits. 288 36

Muscle thermogenesis was measured by direct microcalorimetry in hypertensive patients randomly treated with either metoprolol or placebo. Samples from rectus abdominis were taken after muscle relaxation during surgery, which was accompanied by a significant increase in arterial plasma noradrenaline. Thermogenesis was significantly lower in the metoprolol group compared with both the hypertensives given (p less than 0.05), and a normotensive group without treatment (p less than 0.005). Metoprolol also provoked a significant fall in body temperature in comparison with the two other groups (p less than 0.01). In the hypertensives given placebo, heat production was inversely related to plasma adrenaline (r = -0.89), indicating a role of the sympatho-adrenal system in muscle thermogenesis. No such correlation appeared during metoprolol treatment. In the present acute stress situation it is suggested that muscle thermogenesis was decreased indirectly by metoprolol via blockade of beta 1-receptors in adipose tissue, causing a relative inhibition of lipolysis with diminished substrate supply to the muscles.
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PMID:Selective beta 1-adrenoceptor blockade and muscle thermogenesis. 289 49

Ether-laparotomy stress produced a rapid increase in rat hypothalamic CRF concentration, followed by a rapid reduction and subsequent increase. Cold-restraint stress significantly reduced hypothalamic CRF concentration at 15 min after stress onset. Serum ACTH and corticosterone levels were significantly elevated at 15 min after the onset of both stresses. The CRF responses in the medulla oblongata were not similar to the hypothalamic CRF responses. Norepinephrine concentration in the hypothalamus was reduced, whereas dopamine concentration in the hypothalamus and medulla oblongata was significantly increased. Epinephrine concentrations in these tissues did not show any significant change throughout the stress period. The observations lead to the following conclusions: hypothalamic CRF plays a major role in stimulating ACTH secretion under acute stress; the reduction in hypothalamic CRF is due to an excess release in the early phase of acute stress; hypothalamic CRF and medulla oblongata CRF are controlled by different mechanisms; norepinephrine in the hypothalamus may not be involved in stimulating hypothalamic CRF secretion in the early phase of acute stress; and catecholamines are regulated differently in the hypothalamus and medulla oblongata.
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PMID:Brain corticotropin-releasing factor (CRF) and catecholamine responses in acutely stressed rats. 300 28

Because chronic infusions of adrenalin (A) produce hypertension in rats, it has been suggested that A is a mediator of stress-induced hypertension. In order to test the hypothesis that lowering A will attenuate stress-induced hypertension, rats who had their adrenal medullae removed (ADM) and sham-operated controls were subjected to chronic stress. All subjects were offspring of a cross between spontaneously hypertensive and Wistar-Kyoto rats. Prior to chronic stress, systolic pressures were the same in the two groups. The stress consisted of 60 2-h sessions of shock-shock conflict during 18 weeks. After conflict stress, the rats were implanted with arterial catheters and allowed two days to recover. The resting mean arterial pressure (MAP) was 141.2 mmHg in the ADM group and 142.3 mmHg in the Sham group. Cardiovascular responses to acute stress were then examined. The rats were transferred to a test-box and subjected to pulsed foot shocks (0.5-s duration, 5-s intervals) for 5 min. The MAP increase after transfer was 22.3% in the ADM and 4.2% in the Shams (P less than 0.001). After termination of the shocks, the MAP was elevated 22.2% above baseline in the ADM and 8.1% in the Shams (P less than 0.02). Five minutes after foot shocks the MAP increase was 21.6% in the ADM and 7.2% in the Shams (P less than 0.02). Adrenal demedullation was effective in attenuating plasma A during stress and reduced the plasma noradrenaline response. Therefore, the larger pressor responses of the ADM group seem to result from attenuation of beta-adrenoreceptor-mediated dilation of skeletal muscle vasculature.(ABSTRACT TRUNCATED AT 250 WORDS)
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PMID:Effects of adrenal demedullation on stress-induced hypertension and cardiovascular responses to acute stress. 322 33


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