Gene/Protein Disease Symptom Drug Enzyme Compound
Pivot Concepts:   Target Concepts:
Query: UMLS:C0848237 (acute stress)
 4,619 document(s) hit in 31,850,051 MEDLINE articles (0.00 seconds)

Groups of female rats were injected daily for 14 days with 10 mg of cortisone acetate subcutaneously, to study the mechanisms of glucocorticoid suppression on the hypothalamic-pituitary-adrenal axis. Pituitary adrenocorticotropic hormone (ACTH) content, plasma ACTH, adrenal venous corticosterone, adrenal weights, and the catabolic effects on body weight were studied simultaneously (under stressful and non-stressful conditions) before, during, and up to six weeks after cortisone. This study confirmed the results of other investigators that cortisone acetate caused catabolic weight loss and adrenal atrophy, but it was noted to persist up to six weeks after the injections. Glucocorticoid acetate was more effective in causing ACTH-axis suppression than succinate or phosphate preparations, and the effects were dose and time related. Significant depletion of pituitary ACTH content, suppression of plasma ACTH, and corticosterone secretion occurred five to seven days after beginning cortisone acetate (p=<0.001); it was continuous throughout the injection schedule (p=<0.001); it remained for two to four weeks after the cortisone was discontinued (p=<0.001). The animals showed minimum plasma ACTH responsiveness to severe acute stress during this two to four-week suppression phase, but rapid recovery occurred thereafter. Plasma ACTH was undetectable up to six weeks post-cortisone when the animals were not under stress. This may be related to residual cortisone acetate found at the injection sites, or to an altered or different ACTH-axis control mechanism. The sequence of events during recovery from cortisone suppression appeared to be (1) repletion of corticotrophin-releasing hormone (by inference), (2) repletion of pituitary ACTH content, (3) secretion of plasma ACTH, (4) reversal of adrenal atrophy, and (5) subsequent secretion of corticosterone.
J Natl Med Assoc 1977 Dec
PMID:Suppression of the hypothalamic-pituitary-adrenal axis after subcutaneous cortisone acetate administration in rats. 22 95

1. Haemodynamic effects of adrenaline were studied in 27 hypertensive patients, succesively during treatment with propranol and metoprolol. In 12 patients beta-adrenoreceptor blockade was combined with diuretics and in 15 patients the blockade was combined with vasodilators. 2. During propranolol adrenaline caused a marked pressor effect: there was a considerable rise in systolic as well as in diastolic blood pressure and a marked fall in heart rate. During metoprolol there was only a slight rise in blood pressure and an increase in heart rate. 3. Forearm blood flow was decreased by adrenaline during propranolol and was increased during metoprolol. Calculated vascular resistance showed opposite changes. 4. Results were essentially the same when beta-adrenoreceptor blockade was combined with diuretics or with vasodilators and did not differ from previous results obtained in patients treated by blockade alone. 5. If adrenaline infusion can be considered as a model for acute stress, our results seem to favour a selective beta 1-adrenoreceptor blocking agent over a non-selective one, even when the blocker is combined with a diuretic or a vasodilator.
Clin Sci (Lond) 1979 Dec
PMID:Influence of selective and non-selective beta-adrenoreceptor blockade on the haemodynamic effect of adrenaline during combined antihypertensive drug therapy. 23 27

Autoanalgesia (behaviorally-induced antinociception) may be elicited by acute stress or clasically conditioned fear. Antinociception within both of these paradigms is reportedly associated with increased CNS opioid peptide activity. Large doses of naloxone (20 mg/kg) failed to modify antinociception elicited by acute footshock or conditioned fear in rats. Naloxone (4 mg/kg) was also ineffective against antinociception following footshock in mice. These data suggest that if an endorphin does mediate autoanalgesia, the affinity of its receptor for naloxone is very low. Alternatively, parallel opioid and non-opioid systems may be activated by autoanalgesic procedures, with antagonism of the opioid component being insufficient to reduce the antinociception.
Pharmacol Biochem Behav 1979 Dec
PMID:Lack of effect of naloxone on autoanalgesia. 53 54

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.
Metabolism 1976 Dec
PMID:Stress-induced inhibition of triglyceride secretion in vivo sand rats (Psammomys obesus). 99 40

Intragastric glucose prevents acute stress-induced gastric mucosal injury in the restrained rat. Because increased gastric contractions contribute to mucosal injury in this model and because parenteral glucose infusions have been shown to suppress gastric contractility, we hypothesized that centrally mediated responses to hyperglycemia might contribute to the cytoprotective effect of intragastric glucose. We compared intragastric and intravenous 25% glucose with saline infusions during cold restraint and measured their impact on gastric lesions, serum glucose levels, gastric residual volume (an indirect indicator of net gastric contractility), acidity, and mucin concentration. We found that both intravenous and intragastric glucose infusions increased serum glucose to over 500 mg/dl after 4 hr of stress. Intragastric glucose increased residual volume and gastric pH, as well as decreased gastric mucosal injury, but intravenous glucose had no effects on gastric function. We found that none of the potentially protective effects of intragastric glucose are mediated by central responses to hyperglycemia, and likewise that intravenous glucose has no effect on gastric mucosal injury.
Dig Dis Sci 1992 Dec
PMID:Effects of intragastric and intravenous glucose on restraint model of stress ulceration. 147 35

In this study we have used the rainbow trout as a model animal to study the biological consequences of stress in terms of gamete quality and quantity. Groups of 30 mature male and female rainbow trout were subjected to repeated acute stress during the 9 mo prior to spawning. Time of ovulation, fecundity, and egg size were recorded in mature females, and sperm counts were carried out on the milt from the male fish, from both the stressed and control groups. Eggs from ovulated females were fertilized with milt from males subjected to the same treatment regime. Approximately 300 eggs from each female were fertilized with a sperm dilution of 10(-3) in diluent. Subsequent development of the fertilized eggs was then monitored. There were no differences in somatic weight or length between the two groups at the end of the experiment, but exposure of rainbow trout to repeated acute stress during reproductive development resulted in a significant delay in ovulation and reduced egg size in females, significantly lower sperm counts in males, and, perhaps most importantly, significantly lower survival rates for progeny from stressed fish compared to progeny from unstressed control fish. Hence, stress reduces the quality of gametes produced by rainbow trout.
Biol Reprod 1992 Dec
PMID:Stress reduces the quality of gametes produced by rainbow trout. 149 80

Diazepam binding inhibitor (DBI) acts in brain by binding to GABAA/benzodiazepine receptors (GBR) and to mitochondrial benzodiazepine receptors (MBR). Because DBI acting at MBR, has been shown to be an effector of ACTH-induced steroidogenesis and stress is known to change the level of GBR and MBR, the model of acute noise stress in rats was used to study modifications of DBI and GRB or the content of MBR in various areas of the brain and adrenal gland. It was found that, in the brain of stressed rats, DBI and its processing products (ODN-like immunoreactivity), increased selectively in the hippocampus. This increase in the content of DBI was preceded and followed by a net decrease of GBR and an increase of MBR. Similarly, in adrenal cortex, the content of DBI and MBR increased during the first hour, following acute stress and this increase paralleled the increase in plasma corticosterone. These data suggest that DBI, acting on MBR may regulate steroidogenic function in stress.
Neuropharmacology 1991 Dec
PMID:Diazepam binding inhibitor (DBI) increases after acute stress in rat. 166 70

Many immigrants to Australia are refugees, some of whom have experienced acute stress and trauma, including torture, prior to or during their escape from their home countries. In response to a growing recognition that the health care services may not be meeting the needs of these people the NSW Department of Health funded the establishment of a community-based rehabilitation service for traumatised refugees. This paper provides an overview of the recent history of the service, some of the organisational and staffing issues faced during its first year, some characteristics of the first 200 clients, principles of treatment, clinical, nosological and therapeutic issues and relationships with other agencies.
Aust N Z J Psychiatry 1990 Dec
PMID:The development of the New South Wales Service for the Treatment and Rehabilitation of Torture and Trauma Survivors (STARTTS): the first year. 207 24

This study evaluated the role of stress disregulation in tension headache. Two headache groups, a low-life stress group (N = 12) and a high-life stress group (N = 12), that represented different probable etiologies within the disregulation model were compared to analogous control groups. Subjects were selected after screening 441 undergraduate students. Measures of frontalis EMG and self-report acute stress were obtained at multiple intervals during a series of four laboratory stress tasks. Data supported the disregulation model as determined by replication of the significantly different correlations between self-report acute stress and EMG for the headache versus control groups reported by Hovanitz and co-workers (1989), and by several new within-group and within-individual analyses. Curiously, disregulation was found for acute and life stress but not for the intermediate level of daily hassle stress. These data are presented as support for a reformulation of Schwartz' disregulation model.
J Behav Med 1990 Dec
PMID:Tension headache: disregulation at some levels of stress. 207 38

The ability of selective and nonselective 5-HT1A agonists, nondirect 5-HT agonists and 5-HT2 antagonists influence on the L-DOPA-disturbed rats behaviour were studied. The results indicate that agonists 5-HT1A like receptors largely than 5-HT2,3 agonists, 5-HT2 antagonists and nondirect 5-HT agonists promote restoration of the L-DOPA disturbed escape behaviour in acute stress situation.
Biull Eksp Biol Med 1990 Dec
PMID:[The agonists of I-A serotoninergic receptors restore in rats behavior impaired by L-dihydroxyphenylalanine]. 208 66


1 2 3 4 5 6 7 8 9 10 Next >>