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

The present experiment was undertaken to study the metabolic response to stress of single or chronic ACTH-treated male rats. It was found that chronic ACTH-treated rats showed a slight reduction in food intake and a decrease in body weight gain. This treatment increased basal serum triglyceride and insulin levels. In addition, some differences in response to stress was found in chronic ACTH-treated rats. Thus, these latter animals, unlike the other two groups, showed a decrease in circulating triglyceride and insulin levels in response to short-term stress. Moreover, 24 h after onset of stress a more marked fall in liver weight and glucose levels were found in chronic ACTH-treated rats. It suggests that chronic ACTH treatment might alter the metabolic response to prolonged acute stress what could result in lower resistance to severe stresses.
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PMID:Metabolic effects of chronic ACTH administration, interaction with response to stress. 302 May 99

The concentration of ACTH, insulin, glucagon, glucose, epinephrine, norepinephrine, thyrotrophic hormone, thyroxine, and triiodothyronine was measured in plasma of the rats flown for 18.5 days on Cosmos-1129. As a result of the flight, the concentration of insulin, thyrotrophic hormone, and triiodothyronine increased and that of thyroxine decreased. It is suggested that the above changes have been induced by an acute stress associated with biosatellite reentry and touchdown.
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PMID:[Hormone content of the blood plasma of rats after a flight on the Kosmos-1129 biosatellite]. 315 31

The effect of age on the capacity of an organism to mobilize glucose and free fatty acids during stress and to adapt these responses from an acute to a chronic stress situation is not known. The purpose of this study was to determine whether aging impaired the capacity to 1) raise glucose and free fatty acid levels and suppress insulin release in acute stress situations and 2) develop adaptation of these responses to exposure to chronic stress. Our results indicate that 6-mo-old rats (young) trained to escape electric shock (short-term modulation) showed greater acute stress-induced hyperglycemic, hypoinsulinemic, and lipolytic responses than untrained young rats. By contrast, in 22-mo-old rats (old), responses of trained and untrained animals were not different. In the chronic stress (long-term adaptation) experiments, it was found that 1) adaptation of stress-induced hyperglycemia occurred at a faster rate in young than in old animals; 2) in young but not in aged rats, a strong positive correlation was observed between adaptation of stress-induced hyperglycemia and hypoinsulinemia; and 3) in young rats, stress-induced lipolytic responses declined proportionately to the duration of chronic stress exposure, whereas by contrast in chronically stressed aged rats steady-state levels of free fatty acids were not raised during exposure to stress. Thus we conclude that 1) glucose intolerance may play a key role in the altered stress-induced metabolic responses of aged rats; 2) with age, there is a loss of plasticity in physiological adaptive response mechanisms associated with metabolic responses to stress.
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PMID:Effects of age on metabolic responses to acute and chronic stress. 328 83

In a randomised controlled study in 16 orthopaedic patients, the influence of midazolam-fentanyl-N2O/O2 anesthesia (group A) resp. halothane-N2O/O2 anesthesia (group B) on the plasma concentrations of the endocrine parameters ACTH, aldosterone, cortisol, 17-DHEA, insulin, prolactin, T3, T4, TBG (thyroxine bounded globuline) as well as adrenaline, noradrenaline, and dopamine was investigated. Additionally the metabolites glucose, lactate, free glycerin, and acetacetate were measured. Beside prolactin values, only the values for ACTH, aldosterone, cortisol, and 17-DHEA differed with respect to both anesthesia methods. Under halothane-N2O/O2 anesthesia free T4 rose initially also, here represented by T4/TBG-ratio (= FTI). However, the fall of T3 concentration showed no phase - resp. anesthesia-specific changes. Catecholamine levels reached highest values towards the end of operation resp. one hour after extubation in both groups. The insulin secretion, however, was not significantly raised in either group during acute stress phases. As an expression of modified metabolic regulation comparable rises of plasma levels of glucose, lactate, free glycerin, and acetacetate were observed under midazolam-fentanyl-N2O/O2 anesthesia as well as under halothane-N2O/O2. According to presented data, both methods of anesthesia modulated the endocrine metabolic response of the organism to surgical stress, without showing any clinically relevant advantages or disadvantages attributable to either method.
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PMID:[Endocrine reaction pattern: midazolam-fentanyl anesthesia versus inhalation anesthesia]. 329 79

The opioid peptides beta-endorphin and [met]enkephalin are present in the peripheral circulation. Plasma beta-endorphin originates from the pituitary gland and its cosecretion with ACTH is stimulated by a variety of noxious stimuli. Although the adrenal medulla contains high concentrations of [met]enkephalin-containing polypeptides which are costored with catecholamines, and although the adrenal gland appears to secrete [met]enkephalin into the adrenal vein, the relative adrenal contribution to plasma [met]enkephalin appears to be negligible. Plasma concentrations of immunoreactive [met]enkephalin may be increased by insulin and by endotoxic shock, but they are not significantly altered by acute haemorrhagic stress nor by surgical stress. Thus blood plasma concentrations of beta-endorphin, but not of [met]enkephalin, are generally increased during acute stress. The physiological significance of endogenous opioids in the circulation is not known. It is unlikely that transient increases in the concentrations of opioid peptides in peripherally circulating blood modulate nociception, since the peptides do not enter ventricular cerebrospinal fluid in detectable amounts under these conditions. Recent evidence has raised the possibility that circulating opioids may be involved in regulating blood glucose and in activating the immune system. It is also possible that circulating beta-endorphin and related polypeptides have non-opioid actions on a variety of peripheral tissues.
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PMID:Opioid peptides in blood and cerebrospinal fluid during acute stress. 332 99

The effects of immobilization and femoral artery and vein cannulation on resting rates of local cerebral glucose utilization (LCGU) were measured in 35 brain regions of awake rats by using the quantitative, autoradiographic [14C]2-deoxy-D-glucose [( 14C]DG) technique. Three groups of rats were cannulated on the previous day, and LCGU was measured under conditions of no restraint, 4 h of hindlimb restraint, or acute, four-limb immobilization. A fourth group represented the conventional preparation for [14C]DG experiments, with same-day cannulation followed immediately by 4 h of hindlimb restraint. Plasma catecholamines, corticosterone, and glucose concentrations were measured in all groups; all were elevated significantly above values in unrestrained animals only during four-limb immobilization. LCGU was unchanged by same-day surgery, hindlimb restraint, or both. During four-limb immobilization, LCGU was reduced by 25% in the dorsal hippocampus, and to a lesser extent in the anteroventral thalamic nucleus. It was increased only in the lateral habenula (42%). We conclude that two stressors of the experimental preparation (same-day surgery and hindlimb restraint) do not influence LCGU measurements by the [14C]DG method. More severe, acute stress selectively alters LCGU in a few rat brain regions.
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PMID:Cerebral glucose utilization in rats is not altered by hindlimb restraint or by femoral artery and vein cannulation. 341 99

The study deals with the subject of exercise in diabetic patients, with particular emphasis on acute physical stress in type--I and type--II diabetics. The principal task was to define metabolic changes as they occur in the diabetic subjected to acute stress induced by exercise, in comparison with non-diabetics; metabolic changes during prolonged stress as well as during the period of rest; and finally, to propose, on the basis of authors' experimental results and detailed literature research, appropriate rules of procedure for prescriptive exercise for the individual patient. There were 120 subjects divided into 8 groups. Using primarily a bicycle ergometer, the members of the individual groups were subjected to physical stress of various intensity and duration. A detailed analysis of each subject's metabolic response was performed, involving an assessment of 35 physiological and biochemical parameters, with main focus on determining biochemical changes. The study results are presented in detail both with respect to the metabolic response to a given stress in individual groups and comparatively for individual parameters with regard to specific stress rates and groups. Significant differences were found in the metabolic responses concerning the following parameters: acid-base balance, potassium, triglycerols, glucose, cholesterol, FFA, free glycerol, lactate, uric acid. On the basis of the results of experimental measurements, the following algorithm has been designed for prescribing exercise to diabetics: appropriate motivation; determination of the type of exercise; determination of the intensity of exercise; determination of the duration of exercise; respecting related contraindications and complications. A conclusion has been made that provided all possible risks and contraindications as well as prescription guidelines are respected, exercise is to be considered one of the basic principles of diabetes management.
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PMID:Diabetes mellitus and exercise. 367 32

The effect of chronic noise, followed by acute noise and forced swimming, on basal glucose and insulin levels was studied in adult male rats. Chronic noise did not modify basal levels of either measured variable before or after the exposure of rats to acute stress. Acute noise decreased serum glucose and insulin levels, although hypoglycemia was transient. Forced swimming decreased insulin and increased glucose levels. Our results indicate that: serum insulin levels were sensitive to both physiological and psychological stresses, forced swimming caused more marked glucose and insulin responses than noise exposure, chronic intermittent noise did not alter pancreatic function, and no sign of adaptation was apparent after repeated exposure to noise.
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PMID:Chronic noise stress and insulin secretion in male rats. 389 57

1. Rhesus monkey (Macaca mulatta) foetuses were delivered by Caesarean section 3-10 days before term. Aortic blood and cerebrospinal fluid (c.s.f.) samples were taken, the latter from the cortical subarachnoid space and the cisterna magna. The umbilical cord was clamped and foetal breathing prevented for 14-17 min. Blood and c.s.f. were sampled further during this total asphyxiation and for up to 24 hr thereafter.2. The [K(+)] in the cortical subarachnoid fluid started to rise within 2-3 min after the onset of asphyxia and increased up to 7 times the normal level. The [K(+)] of blood plasma and cisternal fluid also increased, but much more moderately. All these effects reversed rapidly upon resuscitation of the foetus.3. A pronounced rise in the cortical subarachnoid fluid [glucose] and a lesser effect on cisternal fluid [glucose] were noted in most cases by the end of, or immediately following, the period of asphyxia. The onset, magnitude and reversal of these effects on [glucose] were less predictable than the observed effects on [K(+)].4. There were no significant changes in the [Mg(2+)], [Ca(2+)] or [Na(+)] of any of these fluids. The calculated total osmolarity of the cortical subarachnoid fluid and, to a much lesser extent, of cisternal fluid and plasma, increased during asphyxia mainly as a result of increased [K(+)].5. The results are interpreted as indicative of a rapid release of K(+) from cortical cells during total asphyxia. The (immature) haematoencephalic K(+) transport system becomes saturated and thus K(+) accumulates in the extracellular fluid (e.c.f.) whence it diffuses into adjacent regions of the c.s.f. system.6. The intracellular fluid of apical dendrites must become even more hypertonic than the e.c.f., since these cellular processes are known to swell during asphyxia at the expense of the e.c.f. space. This apparent increase in intracellular osmolarity could be accounted for by the release of normally bound intracellular cations.7. On the basis of our results and review of the relevant literature, the following sequence of events is proposed: the cortex responds to acute physiological stress (asphyxia, overstimulation, chemical or physical irritation, etc.) by releasing intracellularly bound cations (K(+) and possibly Na(+)). The increased intracellular osmolarity results in the absorption of water from the e.c.f. space. Passage of water across the blood-brain barrier is restricted; thus the e.c.f. space of the cortex does not swell, but becomes hyperosmotic. Under these circumstances, swelling of the cortical cells is limited by the volume of e.c.f. available.8. It is proposed that the release of intracellularly bound cations is a result of their displacement from their binding sites by NH(4) (+) which is released to, and recovered from, these cation binding sites by a glutamate-glutamine interconversion.9. It is concluded that the apparent organized ;shutdown' of the cortical cells in response to acute stress may contribute to the relative insensitivity of this area of the brain to permanent histopathological damage.
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PMID:On the physiological response of the cerebral cortex to acute stress (reversible asphyxia). 462 4

Hyponatraemia and hypoosmolality in patients with central nervous system (CNS) disease or trauma are often ascribed to inappropriate secretion of antidiuretic hormone. A "cerebral" aetiology has been postulated. A review of published reports and data from the present study indicate that the increase in antidiuretic activity in these conditions is generally to be expected and is therefore appropriate. It is suggested that the hyponatraemia observed is the result of excessive administration of fluids. In patients with CNS disease or injured brains intravenous fluid intake should be limited to about 1 litre (of 2.5% glucose in 0.45% saline for a 70 kg adult) per day during the acute stress.
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PMID:Is "cerebral hyponatraemia" iatrogenic? 612 62


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