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

Acute exposure of male rats to cold (5C)leads to a rapid increase of plasma levels of thyrotropin (TSH), prolactin (PRL), corticosterone, and L-thyroxine. Exposure to ether is similarly followed by a rapid increase of plasma levels of PRL and corticosterone, while TSH release is inhibited. Acute treatment with dexamethasone (500 mug) inhibits almost completely the PRL response to both exposure to cold and ether stress, while the plasma TSH response to cold is only delayed and the decrease of plasma TSH observed after ether stress is unchanged. Basal plasma levels of both TSH and PRL are lowered after treatment with the steroid. Thyroxine treatment lowers the plasma TSH concentration to undetectable levels without affecting the plasma PRL response to cold or ether exposure. The present data suggest that the rise of plasma PRL observed after cold exposure is not related to TRH and may suggest that common mechanisms control ACTH and PRL secretion during acute stress exposure.
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PMID:Effect of pharmacological blockade of ACTH and TSH secretion on the acute stimulation of prolactin release by exposure to cold and ether stress. 18 Dec 37

In adult male rats, injection of TRH into a lateral ventricle of the brain 5 min prior to pentobarbital (PB) administration caused a significant dose-related inhibition of prolactin (PRL) release, in doses ranging from 500 to 5 ng. Among 8 TRH analogues devoid of thyrotropin-releasing activity, 6 were found to significantly suppress PB-induced PRL secretion at an intraventricular dose level of 10 microgram, and the 3 most effective in this respect were also able to counteract growth hormone (GH) release elicited by PB. The derivative [1,3'-DCM2]TRH was still potent enough to block PB-induced PRL secretion at an intraventricular dosage of 50 ng. The peptide ACTH 4--10 was ineffective, whereas another ACTH derivative H-Met(O2)-Glu-His-Phe-D-Lys-Phe-OH (Org 2766) reduced PRL release. TRH did not affect the increase of plasma PRL induced by acute stress. alpha-Methyl-p-tyrosine (alpha-MT) failed to influence the inhibiting effect of TRH on GH secretion but significantly reduced that on PRL release. p-Chlorophenylalanine (PCPA) completely blocked the antagonistic effect of TRH on all PB-induced hormonal changes, suggesting that serotoninergic mechanisms may be involved in the extra-pituitary effect of TRH.
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PMID:Antagonism of pentobarbital-induced hormonal changes by TRH in rats. 20 Apr 40

The effects of handling, ether vapor anesthesia and blood sampling on serum LH and prolactin were determined in intact, castrate and dexamethasone-treated male rats. Cage removal and transport to an adjacent room increased LH and prolactin levels by 10 and 15 min after the initial animal disturbance. Intact male rats subjected to repeated ether anesthesia and blood sampling showed a more rapid increase in serum LH and prolactin than the preceding rats, since serum LH and prolactin was increased by 4, 8 and 15 min after initial cage disturbance. In a group of rats subjected to serial blood sampling over a longer time interval, both prolactin and LH levels remained higher than 90 min after initial animal handling. At 90 minutes after a single blood sampling, blood prolactin concentration remained higher than in controls. Serum LH levels returned to control levels 90 min after the stress of a single blood sampling. Although serum prolactin was increased in the castrate group subjected to serial anesthesia and blood sampling, LH concentrations were reduced under the same conditions. Injection of 5 and 50 mug of dexamethasone/100 g body wt for 8 days markedly reduced adrenocortical responsiveness to the stress of serial anesthesia and blood sampling at 1, 4, 8 and 15 min after initial rat disturbance. The 50 mug dexamethasone treatment reduced the stress-stimulated increase in serum prolactin at all blood sampling intervals. The dexamethasone-treated groups also showed smaller increases in serum LH at 8 and 15 min after first animal handling than the control rats. These results indicate that serum LH and prolactin concentrations are consistently increased by acute stress in intact male rats, the duration of the stress stimulation of LH and prolactin is at least 90 min under the conditions of this study, serum LH levels of castrate male rats are decreased by acute stress and dexamethasone administration lowers stress stimulation of LH and prolactin release.
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PMID:Effects of acute stress on serum LH and prolactin in intact, castrate and dexamethasone-treated male rats. 110 6

Hypothalamic-pituitary control of prolactin and LH secretion was tested in young (4-6 months) and aged (22-30 months) male Long-Evans rats given L-dopa, methyl dopa, LHRH, or stress treatments. Pretreatment serum LH levels were consistently higher in young than in the aged groups. The increase in serum LH after LHRH injection was only about half as much in aged as compared to young control males. Although acute stress caused a prompt increase in serum LH in young male rats, this treatment was without effect in the aged group. Methyl dopa treatment stimulated serum prolactin secretion in both young and old rats. Although L-dopa treatment caused a reduction in serum prolactin in both age groups, the sensitivity, magnitude, and duration of the reduction was smaller in the aged rats.
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PMID:Effects of aging on LH and prolactin after LHRL L-dopa, methyl-dopa, and stress in male rat. 125 51

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

Since it has become possible to sample hypophysial portal blood from sheep without totally compromising pituitary function, several important features of the secretion of hypothalamic hormones have been elucidated. The secretion of gonadotropin-releasing hormone (GnRH) has been detailed most thoroughly with the important observation that each pulsatile discharge of luteinizing hormone (LH) is the direct result of a large secretory episode of GnRH from the hypothalamus. There is high fidelity in the GnRH relationship in terms of frequency and amplitude. During the LH surge, additional factors such as an alteration in the degree of enzymic degradation of GnRH may be important physiological mechanisms. The secretion of factors that control the release of growth hormone (GH), prolactin and adrenocorticotropic hormone (ACTH) have also been studied. Hypothalamic factors controlling GH and ACTH release do not bear such an explicit relationship to the secretory episodes of pituitary hormone as seen with the GnRH/LH axis. The factor involved in the acute stress-induced release of prolactin has not yet been identified in sheep.
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PMID:What can we learn from sampling hypophysial portal blood? 142 30

The present study was designed to evaluate the immunological outcome resulting from experimental conditions involving different corticosterone and prolactin ratios in rats. One set of experiments was conducted to assess the effects of prolactin and corticosterone on the in vitro mitogen-induced proliferation of spleen lymphocytes from animals previously submitted to the manipulation of their glucocorticoid status throughout adrenalectomy (ADX) and/or exposure to acute stress. The results indicated that prolactin (5 x 10(-9) M) induced a significant increase in concanavalin A- (ConA) induced proliferation of splenocytes only from ADX-control, unstressed, rats. However, a lower dose of prolactin (10(-9) M) failed to influence lymphoproliferation. Corticosterone (2 x 10(-8) and 10(-7) M) induced a dose-dependent reduction in lymphocyte proliferation in all experimental groups. Further experiments were conducted to study the relative potency of prolactin to antagonize the in vitro corticosterone-induced suppression of ConA-stimulated lymphocytes. The results showed, on the one hand, that higher doses of prolactin (10(-8) and 5 x 10(-8) M) were effective in stimulating ConA-induced lymphocyte proliferation in control, undisturbed, rats. They also showed that when prolactin and corticosterone are simultaneously added to the cultures, the immunostimulatory effect induced by a dose of 10(-8) M of prolactin can either predominate over a weak suppressive action of corticosterone (2 x 10(-8) M) or totally antagonize to normal values a marked immunosuppression induced by a higher dose of corticosterone (10(-7) M). These data support the view that different ratios between prolactin and corticosterone concentrations can result in differential immunological outcome.(ABSTRACT TRUNCATED AT 250 WORDS)
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PMID:Mutually antagonistic effects of corticosterone and prolactin on rat lymphocyte proliferation. 147 15

The effects of acute stress during a parachute jump on hormonal responses were studied in 12 experienced and 11 inexperienced military parachutists. Each subject performed two jumps. Prior to and immediately after each jump blood samples were drawn and analysed for plasma levels of cortisol, prolactin, thyrotropin (TSH), somatotropin (STH), and luteinizing hormone (LH). While there was a significant increase in cortisol, prolactin and TSH levels after both jumps, no alterations could be observed in STH and LH levels. Stress-induced hormonal responses were not affected by jump experience. There was also no association between the endocrine variables and anxiety scores.
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PMID:Acute psychological stress increases plasma levels of cortisol, prolactin and TSH. 156 28

In several diseases chronic pain is associated with long-lasting pathophysiological responses which differ strongly from those observed in acute situations. When persisting, acute pain often results in physical and psychological stress which may in turn aggravate the initial pathological state. In the present work we examined the secretory patterns of pituitary hormones related to acute stress (growth hormone (GH), prolactin (PRL) and beta-endorphin (beta-END)) in rats during the phase of Freund adjuvant-induced arthritis (AIA, a model used for chronic pain studies) when chronic pain is maximum (14 and 21 days, postinoculation (PI)). Using radio-immunoassay hormones were measured in plasma samples taken every 30 min for 7 h in free-moving rats 14 and 21 days after Freund adjuvant or vehicle injection and in control animals. The total amount of GH secretion was higher at 14 and 21 days PI in AIA rats as compared to vehicle-treated and control animals, and the pulsatility of GH secretory pattern was not modified by AIA. PRL and beta-END secretion were not significantly different in arthritic rats as compared to controls. These results show that GH, PRL and beta-END responses induced by acute stress are not observed during the AIA phase when chronic pain is maximum. Thus, in our experimental conditions, beta-END and PRL do not seem to be good plasma markers of chronic pain.(ABSTRACT TRUNCATED AT 250 WORDS)
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PMID:Chronic pain induces a paradoxical increase in growth hormone secretion without affecting other hormones related to acute stress in the rat. 159 79

Two male adult rhesus monkeys were used and caged individually. The room was temperature-controlled having a light-dark period of 12/12 hours. The animals were rapidly immobilized and immediately anesthetized with ketamine i. m. (10 mg/kg of body weight). They were bled four times at 15, 30, 45 and 60 mins after the ketamine injection, twice a week for 6 weeks. When necessary, maintenance doses of ketamine were administered. The serum levels of cortisol and prolactin after nasal instillation of a suspension of vaginal exudate showed lower values than in control conditions (nasal instillation of saline). The control levels of cortisol tended to increase up to 60 mins, whilst in experimental conditions (nasal instillation of female urine or vaginal exudate) did not show such an increase. Cortisol remained similar during the sampling and similar to the 15 mins control levels, but the difference is statistically significant only after instillation of vaginal exudate as compared with control. The levels of prolactin did not show significant variations during sampling either in control or after female urine instillation. However, the instillation of vaginal exudate decreased the prolactin levels at 15 mins which tended to recover the control levels up to 60 mins. These results support the hypothesis, discussed in a previous paper, that some chemical information from females suppresses or mitigates the effect of acute stress resulting from handling the animals before anesthesia.
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PMID:Effect of nasal instillation of female urine or vaginal exudate on serum cortisol and prolactin levels in isolated and anesthetized male rhesus monkeys (Macaca mulatta). 187 90


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