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

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

We have tested the effect of physiological increases in plasma corticosteroids in conscious dogs on the levels of basal and hypoglycemia-stimulated adrenocorticotropic hormone (ACTH) 2 h later. Increases in plasma corticosteroids, produced by infusion of alpha-1-24 ACTH or corticosteroids for 40 min, suppressed basal and stimulated ACTH levels. The magnitude of inhibition produced by an increase in plasma corticosteroids induced by the infusion of ACTH was equivalent to the inhibition produced by the same increase in plasma corticosteroids induced by corticosteroid infusion. The infusions did not affect basal plasma glucose concentrations or the decrease in plasma glucose concentrations after administration of 0.1 U insulin/kg. Basal ACTH concentration was less sensitive than hypoglycemia-stimulated ACTH concentration to corticosteroid-induced suppression. Basal and stimulated secretion were significantly inhibited in all dogs after approximately half-maximal increases in plasma corticosteroids; maximum inhibition occurred after maximal increases in plasma corticosteroids. Therefore, physiological increments in plasma corticosteroids, similar to those produced by acute stress, are effective suppressors of subsequent stress-induced ACTH secretion.
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PMID:Feedback inhibition of adrenocorticotropic hormone by physiological increases in plasma corticosteroids in conscious dogs. 630 Jan 89

Reactions of adult rhesus monkeys to the glucose tolerance test and the insulin sensitivity test were examined during different exposures. It was found that both tests can be well used to evaluate responses to various environmental effects, psychoemotional strain, acute stress state and orthostatic effects. Orthostatics was shown to potentiate the inhibition of insulin secretion. The reciprocal relationship between glucose tolerance and insulin sensitivity was detected in the functional range of vago-insular regulation. The role of orthostatics in neurogenic disorders of the mechanism of glycemic regulation is discussed. The synergism of the combined effect of orthostatics and psychoemotional strain is described.
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PMID:[Adaptive mechanisms in the regulation of blood glucose levels in Macaca mulatta]. 639 37

Changes in plasma dopamine-beta-hydroxylase (DBH) activity were studied in rabbits subjected to two kinds of acute stress: insulin-induced hypoglycaemia and fatigue. A significant elevation of DBH levels was found both 30 minutes after fatigue-induced stress (p less than 0.001) and 90 minutes after insulin injection (p less than 0.01) when compared with the control values. Responses to these two kinds of stress are reported to be mediated by the sympathetic nervous system, mainly by the adrenal glands. Thus, these results suggest that plasma DBH level is a good index of acute alterations in sympathetic activity in rabbits.
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PMID:Plasma dopamine-beta-hydroxylase (DBH) activity in two kinds of acute stress in rabbits. 676 83

The effect of acute stresses on plasma norepinephrine, epinephrine and dopamine-beta-hydroxylase (DBH) were evaluated in control and 6-hydroxydopamine-treated, awake cannulated guinea pigs. Forced immobolization for 1 hr caused a 3- and 5-fold increase in plasma DBH and norepinephrine, respectively. Pretreatment with 6-hydroxydopamine (23 mg/kg b.wt.i.a., 72 and 48 hr before stress) reduced by 70% the increase in plasma DBH and totally prevented the rise in plasma catecholamines evoked by the restraining stress. Injection of insulin (5 U/kg b.wt.i.a.) induced a 60% decrease in blood glucose, a 1-fold increase in plasma DBH and a selective 4-fold increase in plasma epinephrine; these effects were not modified by chemical sympathectomy. Our results indicate that forced immobilization and hypoglycemia produce a preferential activation of the sympathetic postganglionic nerves and of the adrenal medulla, respectively, and that in guinea pigs both stresses increase plasma DBH. The kinetics of disappearance of plasma DBH were studied after subjecting the guinea pigs for 1 hr to forced immobilization. Although 7 of 12 animals showed a biphasic rate of fall of plasma DBH, in each case there was a rapid initial fall possibly due to the "distribution" of the enzyme with a T1/2 of 1.65 hr. Similar findings were observed in 6-hydroxydopamine-treated guinea pigs. These results suggest that the distribution of DBH is the most important process in reducing the augmented plasma DBH levels elicited by a short-term stress and that this process is not dependent on the integrity of the sympathetic nerves nor on the adrenal or sympathetic origin of the enzyme. This study supports the view that the ratio, content of releasable DBH present in sympathetic nerves and adrenal glands/total circulating pool of DBH, is the factor that determines whether an increase in plasma DBH would occur in animals exposed to an acute stress.
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PMID:Effects of chemical sympathectomy on the increases in plasma catecholamines and dopamine-beta-hydroxylase induced by forced immobilization and insulin-induced hypoglycemia: origin and fate of plasma dopamine-beta-hydroxylase. 704 31

A family physician is often the one who makes an initial diagnosis of diabetes. The physician must consider the impact of this diagnosis on both the patient and the patient's family members. Outpatient management is less costly and less traumatic for the patient than inpatient care. Initial management goals are control of hyperglycemia, correction of fluid and electrolyte imbalances, and avoidance of hypoglycemia. For patients with type I (insulin-dependent) diabetes, the initial insulin dosage ranges from 0.25 to 1.0 U per kg per day. For patients with type II (non-insulin-dependent) diabetes, standard therapy begins with dietary modifications, exercise and an oral hypoglycemic agent, if needed. Insulin is indicated in patients with type II diabetes during times of acute stress, infection, surgery and pregnancy, and if the patient is allergic to sulfonylureas. Initially, patients only need to have a basic understanding of glucose monitoring, medications, diet and symptoms of hypoglycemia. Simple instructions can help the patient achieve glycemic control without being overwhelmed with information. As the patient learns more about diabetes and the treatment regimen, therapy can become more intensive.
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PMID:Initial management of the patient with newly diagnosed diabetes. 748 1

The present study was undertaken to determine if acute stress induced by exposure to ether resulted in the presence of beta-cell-tropic factors in rat plasma and if this insulinotropic activity was increased by pertussis toxin. Rats pretreated with pertussis toxin (5 micrograms/kg, 5 days previously) showed marked hyperinsulinemia, but only after exposure to ether before blood sampling. This hyperinsulinemia was not modified by adrenal demedullation. Effects on insulin secretion were assessed by incubation of plasma (diluted with Krebs buffer) with collagenase-isolated rat pancreatic islets. When blood was collected by decapitation from normal rats, the subsequently prepared plasma (12.5% to 50%) profoundly inhibited insulin release from rat isolated islets. This inhibition was probably mediated by catecholamines, since it was not seen with plasma from adrenal-demedullated rats and was prevented by alpha 2-adrenoceptor-blocking drugs. Plasma from adrenal-demedullated, pertussis toxin-treated rats stimulated insulin secretion (by 60%) when the donor rats had been exposed to ether before blood sampling. It is suggested that stress may result in the presence of circulating beta-cell-tropic factors, which may contribute to the acute stress-induced hyperinsulinemia seen in pertussis toxin-treated animals.
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PMID:Acute stress-induced hyperinsulinemia in the pertussis toxin-treated rat: possible role of humoral beta-cell-tropic factors. 793 72

The levels of beta-endorphin, insulin, cortisol, GH, glucagon, prolactin and TSH were measured in serum samples of 9 hyperglycaemic patients (3 female, 6 male) with a mean age of 4.1 years admitted to the pediatric emergency unit. All patients were in acute stress due to severe diseases (acute gastroenteritis, bronchopneumonia, septicaemia, etc.). Initial and repeat blood samples for hormone determination were taken at admission and in the recovery phase (after 4-6 weeks of treatment). OGTT was also performed in the recovery phase. The hyperglycaemia, monitored hourly following the initial determination, returned to normal in all patients in 1-5 h without specific treatment. Mean serum glucose values at admission and in the recovery phase were 287.0 and 84.1 mg/dl. Concomitant to the hyperglycaemia encountered in these patients in the acute phase of stress, an increase was noted in all hormone levels excluding glucagon and cortisol. All elevated hormone levels fell to normal in 4-6 weeks with significant differences from initial levels for beta-endorphin (P < 0.05) and insulin (P < 0.01). OGTT gave a normal curve. These results indicate that stress hyperglycaemia, despite high insulin levels, is associated with an increase in beta-endorphin levels. The results also show that hyperglycaemia in acute disease does not alter OGTT in short-term follow up.
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PMID:beta-Endorphin and some hormonal levels in children with acute stress hyperglycaemia. 795 15

The neuropeptides enkephalin (ENK), galanin (GAL) and neuropeptide Y (NPY) are abundantly expressed in the paraaortic body (PAB) and adrenal glands of the newborn rabbit. To examine whether these neuropeptides are affected by acute stress, we exposed neonatal rabbits to asphyxia, insulin-induced hypoglycemia, and reserpine. Asphyxia, caused by rebreathing for 60 min in an airtight box, reduced the content of catecholamines (CAs) in the adrenal glands and increased ENK-like immunoreactivity (-LI) in the PAB. Insulin-induced hypoglycemia reduced the content of CAs as well as ENK-LI in the adrenal glands. Reserpine caused a marked depletion of the CAs both in the PAB and in the adrenal glands. In contrast, reserpine did not cause any change in the contents of the neuropeptides in either organ. These data indicate that tissue levels of the neuropeptides GAL-LI and NPY-LI, coexisting with CA in the PAB and the adrenal glands, are not biochemically affected by asphyxia, hypoglycemia or reserpine, whereas tissue levels of ENK-LI are reduced by hypoglycemia and, to some extent, are increased by asphyxia. Furthermore, even the CAs in the PAB were unaffected by asphyxia and hypoglycemia. Also, while reserpine reduces CA content, peptide levels are unaffected.
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PMID:Effects of acute stress on the contents of catecholamines and neuropeptides in chromaffin tissues of the newborn rabbit. 987 55

The effects of various stressors on insulin receptors in adipose, liver and skeletal muscle tissues were studied in rats exposed to acute or repeated stress. Adult male rats were exposed to immobilization (IMO) for 2.5 hours daily for 1, 7 and 42 days, or to hypokinesia (HK) for 1, 7 and 21 days. We determined the values of specific insulin binding (SIB) and insulin receptor binding capacity (IR) of plasma cell membranes from adipose, liver and muscle tissue (IMO groups), or insulin binding to isolated adipocytes and hepatocytes (HK groups). A significant decrease of SIB and IR was observed in rats exposed to acute stress (1x IMO) in muscle, adipose and liver tissues. However, in animals exposed to repeated stress (7x and 42x IMO), SIB and IR were diminished in the muscle tissue, whereas no significant changes were noted in the liver and adipose tissue. When tissue samples were collected 3-24 hours after exposure to IMO stress, no changes of SIB and IR were found in liver and adipose tissue, but insulin binding was lowered in skeletal muscles. In animals exposed to HK for one day, a decrease of SIB and IR was found in isolated adipocytes, but no changes in insulin binding were noted in the liver tissue. In rats exposed to HK for 7 and 21 days, values of IR were similar as in control group. Our results indicate a) the different changes of IR in the liver, fat and muscle tissues after exposure to stress situations, b) a long-term decrease of insulin binding in muscles of rats exposed to repeated IMO stress, and c) the return of reduced SIB and IR (induced by acute stress) to control values in the liver and adipose tissue after a short recovery period.
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PMID:Changes of insulin binding in rat tissues after exposure to stress. 1047 Aug 66


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