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

Central noradrenergic pathways play a significant role in mediating blood glucose levels after neuroglycopenia. To further investigate hypothalamic noradrenergic neuronal activity (NNA) and sympathoadrenal influences in glucoregulation, we studied the effects of acute stress on glycemia and insulin release in normal and adrenalectomized (ADRX) rats. Within 5 min of exposure of rats to ether or cold-swim stress, significant positive correlations were evident between hypothalamic NNA and serum glucose levels (r = 0.70, P less than 0.001; at 15 min r = 0.78, P less than 0.0001). Five minutes after stress in the intact rat, insulin release was inhibited and serum insulin levels inversely correlated to hypothalamic NNA (r = 0.45, P less than 0.05). This relationship between insulin and NNA was no longer present 15 min after stress, but the levels of insulin remained inappropriately low with respect to the elevated serum glucose levels (approximately 30% above basal). Blockade of sympathetic noradrenergic pathways by treatment of intact rats with guanethidine prevented the rise in glucose after cold-swim stress but did not prevent the inhibition of insulin release. Fifteen minutes after exposure of ADRX rats to cold-swim stress their hypothalamic NNA and serum glucose levels were similar to intact animals. However, in contrast to their intact counterparts, serum insulin levels were significantly elevated (P less than 0.01). These data are consistent with central noradrenergic neural pathways directly mediating hepatic glucose release and indirectly inhibiting pancreatic insulin release via activation of adrenal medullary catecholamines.
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PMID:Hypothalamic noradrenergic and sympathoadrenal control of glycemia after stress. 264 83

To study the effect of acute stress on ACTH secretion and synthesis in rat pituitary and hypothalamus, ACTH content and POMC mRNA levels (measured by use of Northern blot analysis) in these tissues as well as the levels of ACTH in plasma and those of CRF in the hypothalamus were determined after insulin-induced hypoglycemia. Plasma ACTH levels increased at 30 and 60 min. ACTH levels in the anterior pituitary lobe (AP) decreased at 30 min, and then returned to control levels at 60 min. No change was seen in the intermediate-posterior pituitary (IP) or the hypothalamus after insulin injection. CRF levels decreased at 30 and 60 min, then returned to control levels at 90 min in the medial basal hypothalamus, including the median eminence. Hybridization with a cDNA probe revealed a single size class of POMC mRNA in AP, IP, and hypothalamus, and the size of POMC mRNA in these tissues did not change during the experimental period. POMC mRNA levels in AP increased at 60 min and reached a peak at 120 min, but those in IP and hypothalamus did not change. These results suggest that 1) insulin-induced hypoglycemia stimulates both secretion and synthesis of ACTH (at least by increasing POMC mRNA levels) in the AP, and 2) the levels of ACTH and POMC mRNA in the IP and hypothalamus are not affected by insulin-induced hypoglycemia.
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PMID:Insulin-induced hypoglycemia increases proopiomelanocortin messenger ribonucleic acid levels in rat anterior pituitary gland. 283 Oct 25

To study the effect of acute stress on CRF release and synthesis in rat hypothalamus, ACTH levels in plasma, CRF contents in the median eminence (ME), and CRF mRNA levels in the hypothalamus without ME and cerebral cortex were determined after insulin-induced hypoglycemia. Plasma ACTH levels increased at 30 and 60 min, while ME CRF content decreased at 30 and 60 min, then returned to the control level at 90 min. Hybridization with a cRNA probe revealed a single size class of CRF mRNA in the hypothalamus and cerebral cortex (approximately 1300 nucleotides), and the size of CRF mRNA in these tissues did not change during the experimental period. CRF mRNA levels in the hypothalamus increased to 130% of the control value at 30 min and reached a peak (186% of the control value) at 120 min, but these levels in the cerebral cortex did not change. These results suggest that insulin-induced hypoglycemia stimulates CRF synthesis by increasing CRF mRNA levels in the hypothalamus as well as CRF release, and that release and synthesis of CRF in the cerebral cortex are independent of those in the hypothalamus.
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PMID:Insulin-induced hypoglycemia increases corticotropin-releasing factor messenger ribonucleic acid levels in rat hypothalamus. 284 Oct 92

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

Intranasal infection of mice with a sublethal dose of Bordetella pertussis or the intravenous administration of purified pertussis toxin resulted in a marked increase in the serum immunoreactive insulin concentration following ether stress. This stress-induced hyperinsulinaemia was not modified significantly by blockade of alpha 2-adrenoceptors with idazoxan, beta-adrenoceptors with propranolol, autonomic ganglia with hexamethonium, opioid receptors with naloxone, muscarinic cholinoceptors with atropine or by adrenal demedullation. The effect of pertussis in promoting stress-induced hyperinsulinaemia was mimicked qualitatively by alpha 2-adrenoceptor blockade, adrenal demedullation or ganglionic blockade. However, the serum immunoreactive insulin response to ether stress was smaller in animals subjected to these procedures compared with the response seen in mice infected with B. pertussis or treated with pertussis toxin. Thus, in the mouse, acute stress produces hyperinsulinaemia under conditions in which the release of adrenal medullary catecholamines is prevented, or the inhibitory action on insulin secretion is blocked by alpha 2-adrenoceptor antagonists or by pertussis toxin.
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PMID:Role of the adrenal medulla in stress-induced hyperinsulinaemia in normal mice and in mice infected with Bordetella pertussis or treated with pertussis toxin. 304 44

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 opioid peptide methionine-enkephalin (Met-enkephalin) was measured in plasma and cerebrospinal fluid (CSF) of sheep in which the cisterna magna, carotid artery, and jugular vein were chronically cannulated. Venous blood plasma and CSF were collected before and after stress treatment and in control studies in conscious animals. Plasma and CSF were extracted with octadecylsilica and oxidized, and Met-enkephalin was measured as its Met-sulfoxide derivative by specific RIA. The molecular form of immunoreactive Met-enkephalin was characterized by peptide size exclusion chromatography of an octadecylsilica extract of sheep plasma through Bio-Gel P2, followed by reverse phase liquid chromatography, and was identical to Met-enkephalin and Met-sulfoxide-enkephalin. Insulin-induced hypoglycemia produced an elevation of plasma cortisol and an increase in the plasma concentration of Met-enkephalin. Acute hemorrhage led to an earlier and greater rise in plasma cortisol than that associated with insulin-induced hypoglycemia, but did not increase the concentration of Met-enkephalin in plasma. Neither form of acute stress increased the concentration of Met-enkephalin in CSF. These studies confirm that secretion of Met-enkephalin into blood can be dissociated from stimulation of the pituitary-adrenocortical system. They also show that circulating Met-enkephalin is elevated in conscious sheep during acute hypoglycemic stress, but plasma Met-enkephalin is unlikely to exert effects on the opiate receptors of periaqueductal or spinal nociceptive neurons under these conditions, since it does not enter cerebrospinal fluid in significant amounts.
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PMID:Immunoreactive methionine-enkephalin in cerebrospinal fluid and blood plasma during acute stress in conscious sheep. 327 39

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


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