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

Adaptation processes in an acute stress situation were investigated an compared in young and elderly subjects. Insulin hypoglycemia was used to provoke stress. The behavior of the blood sugar after administration of 0.1 U/kg old insulin shows a marked hypoglycemic state after 30 minutes, both in the young and in the older subjects. The rise into the normal range occurs considerably quicker in the young than in the elderly. Adrenaline excretion is distinctly lowered in older people. Measurement of hydrocortisone excretion also shows a lower reaction level and a delayed onset in the elderly. Growth hormone analysis shows a smaller production in advanced age. It is consequently established that adaptation potential decreases in old age.
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PMID:Altered adaptation behavior in the elderly (author's transl). 82 16

The effects of acute stress upon circulating triglyceride, glucose, insulin, free fatty acids, and glycerol were investigated in obese desert sand rats. Three groups of animals, designated "nonstress", "non-exertional stress", and "exertional stress", were studied. Acute stress, with or without accompanying exercise, was associated with significant decreases in circulating triglyceride; significant increases in circulating glucose, free fatty acids, and glycerol; and variable changes in circulating insulin. Since these data indicated that substrate availability and hepatic insulization were adequate and therefore could not explain the observed fall in circulating triglyceride, endogenous triglyceride secretion rates were examined by the Triton method. Compared to predicted rates based upon earlier studies, both nonexertional and exertional stress were associated with significantly decreased endogenous triglyceride secretion. Thus, acute stress in the sand rat, with or without accompanying exercise, appears to induce an immediate decrease in endogenous triglyceride secretion and circulating triglyceride.
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PMID:Stress-induced inhibition of triglyceride secretion in vivo sand rats (Psammomys obesus). 99 40

Four experiments examined the effects of stress on hypothalamic insulin and plasma hormones in rats. Two hours daily of immobilization (IM) stress for 2 and 4 days resulted in an increase in hypothalamic insulin. In contrast, 15 min of daily IM over 13 days or 48 h of continuous signalled shock avoidance did not alter hypothalamic insulin. These findings are interpreted to indicate that changes in hypothalamic insulin are part of the stress response. Possible reasons for the different effects of time and paradigm on the hypothalamic insulin responses to stress are discussed. Plasma insulin and glucose levels were not responsive to any of the stressors. Brief acute stress caused increases in the stress-responsive hormones ACTH, corticosterone, and prolactin, as expected, and these responses attenuated or disappeared with repeated or longer stress exposures.
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PMID:Effect of stress on hypothalamic insulin in rats. 132 77

The effect of hypoglycemic stress on the changes in water and electrolyte metabolism induced by head-down tilting (HDT) was studied. Six healthy men were subjected to postural changes (30 min standing, 2 h HDT, 1 h standing), with or without the intravenous administration of insulin at the beginning of HDT. When insulin was not given, antidiuretic hormone (ADH), cortisol, plasma renin activity (PRA), aldosterone, and catecholamine levels were decreased and atrial natriuretic polypeptide (ANP) levels increased during HDT. These changes were associated with 2.5- and 1.5-fold increases in urine flow and sodium excretion, respectively, when compared with the amounts before HDT. On the other hand, insulin-induced hypoglycemia during HDT produced increases in ADH, cortisol, PRA, aldosterone, and catecholamine levels. At the same time, an exaggerated ANP response by HDT was observed. These hormonal changes were associated with an abolishment of the increases in urine flow and sodium excretion. It is suggested that acute stress modifies the changes in fluid and electrolyte metabolism induced by HDT.
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PMID:Modification of water and electrolyte metabolism during head-down tilting by hypoglycemia in men. 147 52

The respiratory pathophysiology of placental insufficiency is well understood, whereas the metabolic effects of chronical or acute malnutrition still need further evaluation. In a comprehensive study of 20 deliveries respiratory parameters and substrates of carbohydrate- and lipid-metabolism were analysed simultaneously from maternal blood at 4 cm dilatation, at cord clamping immediately delivery and 2 hours post partum as well as from arterial and venous umbical blood samples. Normal deliveries were compared with cases of fetal retardation and moderate acute fetal acidosis. For glucose, insulin, c-peptide and pyruvate a strong rise in maternal blood during labour was observed as well as for the non-esterified fatty acids (NEFA), which have a high materno-fetal gradient. Arterio-venous differences of concentrations were found in the umbilical cord blood for glucose, pyruvate and NEFA. In cases of chronical insufficiency of the placenta especially elevated lactate levels were measured, whereas a moderate fetal acidosis obviously leads to an additional feto-maternal pyruvate transfer. The results lead to the conclusion that the fetal metabolism has considerable means of adaptation during delivery even under chronical or moderate acute stress conditions.
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PMID:[Maternal and fetal metabolic parameters in acute and chronic fetal malnutrition]. 188 57

It is clear that the sympathoadrenal system has a role in the regulation of endocrine pancreatic function and that the sympathetic nerves of the pancreas can change pancreatic hormone secretion to increase the availability of metabolic fuels. It seems likely that the classical sympathetic neurotransmitter, NE, acts in concert with peptide co-transmitters, such as galanin and NPY. Each is released during the stimulation of pancreatic sympathetic nerves and each is capable of influencing either islet function or pancreatic blood flow. There is considerable indirect evidence that the sympathetic innervation of the pancreas is activated during acute stress and influences the endocrine pancreas. However, proving such a physiologic role is difficult because of redundant mechanisms that influence the secretion of the metabolically-crucial hormones, insulin and glucagon. Such definitive proof therefore awaits the development of new techniques to dissect and dissociate these mechanisms.
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PMID:Neural control of islet function by norepinephrine and sympathetic neuropeptides. 192 79

In this study we examined the role of alpha and beta blockade on glucose and lactate metabolism during the acute stress of insulin-induced hypoglycemia. Three groups of conscious dogs with chronically fitted catheters in the femoral artery and in the femoral, portal, and hepatic veins were studied after an 18-hr fast. After a 1-hr basal period, hypoglycemia was induced with insulin infusion at 5 mU/kg.min for 3 hr. Group 1 received no other treatment. Groups 2 and 3 received, respectively, phentolamine (8 micrograms/kg.min) and propranolol (4 micrograms/kg.min) beginning 30 minutes before and throughout the experimental period. Despite similar hyperinsulinemia, plasma glucose dropped in Group 1 (from 115 +/- 10 to 40 +/- 3 mg/dl) and in Group 2 (from 110 +/- 4 to 60 +/- 3 mg/dl) but in Group 3 it was maintained at 45 +/- 4 mg/dl by exogenous glucose infusion at a rate of 2.2 +/- 0.4 mg/kg.min. Hepatic glucose production increased 50 +/- 13%, 127 +/- 30%, and 55 +/- 30% in Groups 1, 2, and 3, respectively, within 60 minutes and was 56 +/- 19%, 55 +/- 17%, and -0.04 +/- 12% during the last hour of the experiment. Glucose utilization did not change in Groups 1 and 2 but it increased in Group 3. Plasma lactate increased in Group 1 (from 850 +/- 190 to 1,980 +/- 450 mumol/L) and in Group 2 (985 +/- 180 to 4,785 +/- 500 mumol/L), while in Group 3 there was an early rise (to 695 +/- 120 mumol/L) within 30 minutes that gradually dropped to near basal.(ABSTRACT TRUNCATED AT 250 WORDS)
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PMID:Differential effects of alpha and beta adrenergic blockade on glucose and lactate metabolism during acute stress. 217 Jun 67

Stress has been implicated as an environmental factor that may accelerate the process of biological aging. However, this proposal has remained largely anecdotal due to relatively few studies that directly tested this hypothesis. In the present experiments groups of 6-month-old and 20-month-old male F-344 rats were chronically stressed for a six-month period. After the last stress session, when the animals were 12 months of age (adult) and 26 months of age (old), control and chronically stressed rats were tested for their ability to: (a) elicit glucose and insulin responses to an acute, novel stressor; (b) remove a circulatory glucose load elicited either by acute stress exposure or by injection of d-glucose; and (c) raise insulin levels after a glucose challenge. In control rats, we observed a deficit in each of these parameters in old compared to adult rats. Exposure to chronic stress did not exacerbate deterioration of these response mechanisms in either adult or old rats. In fact, the data showed a modest improvement in glucose tolerance in chronically stressed compared to age-matched control rats. We conclude that chronic stress did not exacerbate age-dependent decline of glucoregulatory capacity. From these results and from our earlier work, we speculate that the decline during aging of the functional integrity of systems involved in the response to stress may be sustained by periodic challenges from the organism's external environment.
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PMID:Glucoregulatory responses of adult and aged rats after exposure to chronic stress. 219 83

In this study aiming to clarify the relationships between beta-endorphin and glucose levels, beta-endorphin levels were determined in children in acute stress. The study was carried out on 32 critically ill children between 5 days and 12 years presenting with clinical symptoms of acute infectious conditions. 11 healthy children were taken as controls. The results showed that although beta-endorphin levels were elevated in all critically ill patients, these levels were significantly higher than control values in hyperglycaemic cases. The insulin levels were also elevated. A follow-up of nine of the hyperglycaemic cases showed a significant decline in beta-endorphin and insulin levels with recovery. Glucose tolerance was also normal. These results confirm the reports of many other studies on the role of beta-endorphin as a stress hormone.
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PMID:Beta-endorphin levels of children in acute stress. 222 24

Normoglycemic remission has been observed in black non-insulin-dependent diabetic individuals. Thirty-three patients presented with severe hyperglycemia (mean glucose 682 mg/dl) and were hospitalized for initial treatment. Following intensive outpatient therapy including insulin or sulfonylurea for 0.25 to 96 weeks, they became normoglycemic without pharmacologic treatment. This state was characterized by normal glycosylated hemoglobin levels in 29 of 30 patients and fasting plasma glucose levels of less than or equal to 115 mg/dl in 25 of 33 patients. During clinical remission these individuals were characterized as being lean to moderately obese (body mass index less than 30.5 kg/m), relatively young (45 years of age), and largely male (male:female ratio was 2:1). Thirty percent of the patients underwent normoglycemic remission after 3 months of treatment, 64% within 6 months, and 85% within 12 months. Normoglycemic remission was not related to weight loss or amelioration of stress and lasted from several months to as long 97 months. The results of the oral glucose tolerance test during remission showed that 9 had normal, 7 had impaired, and 17 had diabetic glucose tolerance. Thirteen of the 33 patients relapsed and developed hyperglycemia after a mean of 24.9 months. Relapse was not associated with weight gain or acute stress. Islet cell antibodies were uniformly absent, implying that these individuals did not have an autoimmune form of diabetes. It is not known if remission in non-insulin-dependent diabetes is unique to the black population. Neither the prevalence nor the mechanism of the development of remission is known at this time.
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PMID:Remission in non-insulin-dependent diabetes mellitus: clinical characteristics of remission and relapse in black patients. 234 23


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