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

The effects of various acute stressors on the activity of adult male rats in a holeboard and in the forced swim test were studied. When tested immediately or 24 h after 1 h exposure to noise, restraint in tubes or tail shock, no changes in either defecation rate or activity in the holeboard were observed. In contrast, immediately after 1 h immobilization in wood-boards, a reduction of the number of areas crossed and the number of head-dips was found. The inhibitory effect of immobilization on head-dips persisted 24 h later. The behavior of the rats in the forced swim test was classified into three categories: struggling, mild swim and immobility. The changes in behavior were critically dependent on the type of stressor, and more specifically on its intensity, that was evaluated with three different physiological parameters (serum prolactin, corticosterone and glucose levels). Thus, if tested immediately after stress, noise did not alter the response of the rats, restraint in tubes and tail shock-reduced immobility, and the latter stressor increased mild swim. In the second experiment, immobilization in wood-boards reduced struggling. Twenty-four hours after stress, noise, restraint in tubes or tail shock were without effect, but immobilized rats showed increased immobility and reduced mild swim activity. The present data clearly indicate that behavior of rats in a holeboard and in a forced swim situation are not related, and that acute stress could have a differential effect on the various categories of behavior in a forced swim situation.
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PMID:Influence of various acute stressors on the activity of adult male rats in a holeboard and in the forced swim test. 194 78

In man, acute stress, like extensive surgery, leads to a rapid and prolonged decrease in serum T3 concentrations. The present study was carried out to investigate the mechanisms that underly the abrupt decrease in T3-neogenesis that occurs in response to acute surgical stress. Male Sprague-Dawley rats, surgically thyroidectomized, and treated with 1.2 micrograms T4/100 g BW/day, underwent wide vertical and horizontal incisions extending into the abdominal cavity while receiving light ether anesthesia. Different dietary manipulations were performed to investigate the superimposed influence of reduced carbohydrate and caloric intake on T3-neogenesis. The metabolism of 125I T4 labeled in its outer (phenolic) ring was investigated in liver, kidney, and brain homogenates of animals killed 48 h after surgery. In liver, values for the proportion of T4 degraded and the percent generation of T3 and iodide were unaffected by laparotomy. The percent T3 generation in experiments with 25 nM T4 concentration was 3.7 +/- 1.24% (mean +/- SD) in fed control animals given free access to 5% glucose, 3.4 +/- 0.67% in unoperated controls given a restricted amount of chow and 5% glucose, and 3.8 +/- 0.67% in operated animals given free access to chow and 5% glucose. As expected, T3 neogenesis in livers from unoperated animals was significantly reduced in rats fasted for 48 h and this reduction was similar in laparotomized rats fasted for 48 h after surgery. As in the liver, no effect of laparotomy on T4 metabolism in kidney and brain homogenates was observed. Finally, serum total T4 and T3 concentrations were not affected by surgery. It is concluded that acute surgical stress in thyroidectomized T4 replaced rats does not influence T4 metabolism in liver, kidney, and brain homogenates or affect the serum T4 and T3 concentrations. Since thyroid secretion of T4 (and T3) was eliminated and careful attention was paid to caloric intake in this rat model, previously reported abnormalities in serum thyroid hormone concentrations and T3-neogenesis in various states of nonthyroidal illness in man and rat, including surgery, are probably contributed to by thyroid secretion of T4 (and T3) and caloric deprivation, especially carbohydrate.
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PMID:The effect of surgical stress on the in vitro metabolism of thyroxine by rat liver, kidney, and brain. 198 15

The reliability of serum glucose concentrations as an index of habituation to chronic stress was evaluated in adult male rats. The glucose response to immobilization was attenuated by six days of previous chronic exposure to the same stressor, the degree of reduction being related to the duration (15 min, 1 hr or 4 hr) of the daily exposure to immobilization. In another experiment, three groups of rats were exposed to one of three stressors (handling plus change of room, restraint in tubes, or immobilization by wood boards), 1 hr daily for 27 days. On day 28, when faced with the same acute stressor to which they were chronically exposed, the rats showed a consistent reduction in glucose response, regardless of the type of stressor used. In addition, in stress-naive rats serum glucose levels were related to the intensity of the stressor as assessed by three independent measures (food intake, body weight changes, and adrenal weight after chronic exposure to the stressor). These data indicate that, under appropriate conditions, glucose levels can be a good index of both the intensity of acute stress experienced by the rats and their habituation to repeated stress.
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PMID:The serum glucose response to acute stress is sensitive to the intensity of the stressor and to habituation. 210 60

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

In the experiments on rats acute stress is found to accelerate glucose resorption by isolated loop of small intestine in situ and it probably depends on increased level of corticosteroids. Glucose resorption changes in small intestine is of adaptable character during stress.
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PMID:[Effect of acute stress on glucose resorption by an isolated loop of the small intestine]. 232 54

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

Physiological responses to acute stress were assessed in alloxan diabetic, streptozotocin diabetic and control laboratory rats. Rats were prepared with indwelling tail artery catheters to allow for direct measurement of mean arterial pressure (MAP, mmHg) and heart rate (HR, beats per minute) and remote sampling of blood. Within 24 hours after surgery, basal values of MAP and HR were determined. Two days after surgery, rats were subjected to 5 minutes of intermittent footshock. Blood samples were collected before footshock stress and immediately and 15 minutes after termination of footshock. Plasma levels of norepinephrine (NE) and epinephrine (EPI) increased significantly above basal values in all animals exposed to acute footshock stress. However, in approximately one-half of alloxan and streptozotocin diabetic rats, plasma levels of EPI under basal conditions and following footshock stress were elevated significantly compared to controls and the remaining diabetic animals. We have denoted these subgroups of diabetic animals as reactive responders (plasma EPI greater than controls) and nonreactive responders (plasma EPI similar to controls), respectively. Plasma levels of NE under basal conditions and following footshock stress were similar in reactive responders and nonreactive responders compared to matched controls. Baseline blood glucose levels were elevated in alloxan and streptozotocin diabetic rats compared to controls. Blood glucose levels increased reliably in all animals following footshock stress. Basal MAPs were reduced significantly in both subgroups of alloxan and streptozotocin diabetic rats compared to matched controls. In contrast, resting HRs were similar between diabetic rats and their corresponding controls.(ABSTRACT TRUNCATED AT 250 WORDS)
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PMID:Physiological responses to acute stress in alloxan and streptozotocin diabetic rats. 252 54

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


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