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Biomedical subjects

E H Mougey

Publications and source records attributed to E H Mougey.

At least 37 records · Page 2Linked to original sources
PubMed1990

The influence of fitness on neuroendocrine responses to exhaustive treadmill exercise.

Neuroendocrine and sympathoadrenal responses to exhaustive graded treadmill exercise were examined in 17 male subjects of varying degrees of fitness. The mean duration of exercise to exhaustion was 15.2 +/- 0.7 (+/- SE) min. Exercise duration was inversely correlated with baseline heart rate (P less than 0.05). Compared to standing baseline values, mean plasma norepinephrine and epinephrine levels increased 339% and 301%, respectively, in an integrated 2-min blood sample collected immediately after completion of exercise. Mean adrenocorticotrophic hormone (ACTH), beta-endorphin (beta-EP), beta-lipotropin (beta-LPH), and prolactin levels increased 282%, 720%, 372%, and 211%, respectively, in an integrated 4-min blood sample beginning 2 min after completion of exercise. Cortisol levels increased 183% in the sample collected 17-21 min after exercise. The magnitude of these neuroendocrine responses to exercise was similar among individuals at the same relative intensity of exhaustive exercise, regardless of the duration of exercise. The exercise-induced increases of the pro-opiomelanocortin (POMC)-derived peptides, ACTH, beta-EP, and beta-LPH, were highly correlated with each other (P values less than 0.001), and were correlated with prolactin increases, (P values less than 0.05). During a 20-min recovery period after exercise, changes in heart rate, ACTH, and beta-LPH levels were correlated with duration of exercise, (P less than 0.01, P less than 0.03, and P less than 0.03, respectively).(ABSTRACT TRUNCATED AT 250 WORDS)

Adrenocorticotropic Hormone↗
PubMed1990

Effects of social conflict on POMC-derived peptides and glucocorticoids in male golden hamsters.

The effects of fighting and footshock on circulating adrenocorticotropin-like immunoreactivity (ACTH-LI), cortisol, corticosterone, beta-endorphin-like immunoreactivity (beta-EP-LI), and beta-lipotropin-like immunoreactivity (beta-LPH-LI) were examined. In the first experiment, catheterized males were paired with large, ovariectomized females for 15 min. Submissive males exhibited significant increases in plasma ACTH-LI, cortisol, corticosterone, and beta-EP-LI. In the second experiment, two males were paired to determine whether the hormonal response in submissive animals was different from that in dominant hamsters. The pattern and magnitude of the hormonal response was also compared to that following a commonly used stressor-footshock. Footshock was associated with large increases in each of the plasma hormones measured. Submission, but not dominance, was associated with smaller, but still significant, increases in ACTH-LI, cortisol, beta-EP-LI and beta-LPH-LI. The data indicate that fighting is not a generalized stressor. "Losing," in particular, appears to be an example of a biologically relevant stressor.

Adrenocorticotropic Hormone↗
PubMed1990

Hyperresponsiveness of the rat neuroendocrine system due to repeated exposure to stress.

Sequential exposure to stressors may elicit a period of endocrine hyperresponsiveness during which plasma hormone concentrations reach higher levels after repeated exposure to a stressor compared to levels after initial exposure. The present study was designed to further characterize hyperresponsiveness to repeated stress and determine if hyperresponsiveness is dependent upon repeated exposure to the same stressful stimuli. In Experiment 1, rats were stressed by inescapable tailshock, immobilization or exposure to shock chamber without shock for one, two, three, four or five consecutive days (15 min/day). In rats exposed to tailshock, corticosterone (CS) levels in plasma collected on days 2, 3, 4 and 5 were higher than CS levels following acute tailshock on day 1, demonstrating hyperresponsiveness to repeated tailshock. Hyperresponsiveness of CS secretion also occurred in groups of rats restrained for four or five days. No changes occurred in the CS response of animals repeatedly exposed to immobilization. Prolactin (PRL) levels were not affected by repeated exposure to the stressors. However, PRL values were different between the stress conditions and indicated that the order of stressor severity was tailshock greater than immobilization greater than exposure to shock chamber without shock. In Experiment 2, rats were exposed to either one or two consecutive days of tailshock or immobilization. Other rats were exposed to either tailshock or immobilization on the first day, then switched to the other stressor on the next day. Hyperresponsiveness to repeated tailshock, but not immobilization, was reflected in plasma levels of CS and adrenocorticotropic hormone (ACTH), but not PRL. Hyperresponsiveness of CS and ACTH secretion also was found in rats first stressed by immobilization then switched to tailshock, demonstrating that hyperresponsiveness is not dependent upon reexposure to familiar stressful stimuli. However, hyperresponsiveness did not occur in rats first exposed to tailshock then switched to immobilization. The data suggest that both immobilization and tailshock primed the organism to hyperrespond, but only the more severe stressor (tailshock) elicited hyperresponsiveness of the neuroendocrine system.

Adrenocorticotropic Hormone↗
PubMed1989

Dexamethasone suppresses ACTH release without attenuating pituitary cyclic AMP response to stress in vivo.

Dexamethasone, a synthetic glucocorticoid, has been shown to decrease basal and stress-elevated levels of the pituitary hormone ACTH. Glucocorticoids are known to bind to multiple sites within the brain and pituitary and it is not known which site(s) is most important in mediating the observed inhibition of ACTH release. At the level of the corticotroph, there is contradictory data from in vitro studies regarding whether dexamethasone acts proximal or distal to the formation of the cyclic AMP second messenger that has been shown to be involved in CRF-stimulated ACTH release. In the present report, we have examined the effects of dexamethasone pretreatment on stress-induced elevations in pituitary cyclic AMP and the release of ACTH in vivo. Acute stress (15 min of intermittent footshock) elevated levels of pituitary cyclic AMP and plasma ACTH consistent with previous studies. Dexamethasone administration (0.4 mg/kg 24 hr prior to sacrifice plus 0.2 mg/kg 2 hr prior to sacrifice) inhibited stress-induced elevations in plasma ACTH but did not affect pituitary cyclic AMP response to acute stress. These findings suggest that dexamethasone inhibits the release of ACTH via an action distal to the generation of cyclic AMP.

Adrenocorticotropic Hormone↗
PubMed1989

ACTH, prolactin, corticosterone and pituitary cyclic AMP responses to repeated stress.

The present experiment was conducted to determine whether the plasma hormonal and pituitary cyclic AMP responses observed following a single exposure to an acute stressor would diminish following reexposures to the same stressor. Fifteen-min stress exposures (forced running) were separated by 45-min recovery periods. Separate groups of control and stressed animals were sacrificed before and after each of four 15-min stress periods and after each recovery period. The first exposure to 15 min of forced running raised plasma ACTH, corticosterone and pituitary cyclic AMP levels approximately 6-fold and more than tripled levels of plasma prolactin. Plasma ACTH and pituitary cyclic AMP responses to the second, third and fourth stress exposures were very similar to the responses to the first stress exposure, and levels of these substances returned to prestress levels during each 45-min recovery period. Plasma prolactin responses to the four stress sessions were somewhat variable but no significant trend among the responses was seen. Plasma prolactin levels also returned to prestress levels between stress exposures. Corticosterone levels were similar following each of the four stress sessions but levels remained elevated compared to prestress levels between stress exposures. These data suggest that pituitary responses to acute stress are rapid, that return to prestress levels is also rapid, with the exception of corticosterone, and that repeated responses of the same magnitude may be evoked when stressors are separated by short recovery periods.

Adrenocorticotropic Hormone↗
PubMed1988

Long-term sequelae of soman exposure: hormonal rhythms two weeks postexposure to a single dose.

Two weeks following a single exposure to either soman (100 micrograms/kg, sc) or saline, rats were sacrificed at 2-hr intervals over a 26-hr period. Trunk blood was collected and plasma was stored until assayed for corticosterone, prolactin, growth hormone, adrenocorticotropin, beta-endorphin, and beta-lipotropin. Rats surviving for 2 weeks following soman appeared well groomed and were gaining weight at a rate similar to saline-treated rats at the time of termination. Thus, they appeared to have recovered from the initial physiological effects of soman exposure. However, substantial differences in plasma levels of most hormones were seen in comparing soman- vs saline-treated rats. Levels of prolactin were suppressed at all time points in soman-treated rats. Growth hormone secretion was also suppressed and the normal episodic peaks of growth hormone were missing in soman-treated rats. Both soman- and saline-treated rats displayed circadian rhythms in levels of plasma corticosterone, but the usual late afternoon rise in plasma corticosterone levels was shifted to earlier time points in the soman-treated rats. Levels of beta-endorphin and beta-LPH were slightly but significantly suppressed in soman-treated rats at almost all time points. Levels of adrenocorticotropin were similar in control and soman-treated rats. The results of this experiment demonstrate that a single exposure to soman may have long-lasting effects on neuroendocrine function.

Adrenocorticotropic Hormone↗
PubMed1988

Neuroendocrine correlates of sustained stress: the activity-stress paradigm.

Rats sacrificed after 4 days in the activity-stress paradigm or after 4 days of food restriction had significantly elevated levels of plasma corticosterone as compared to control rats. The approximately 5 fold increase in corticosterone in the stressed treatment groups was consistently found in all experiments. ACTH levels were elevated in activity-stress and food-restricted groups in some experiments but these increases were not statistically significant. Prolactin levels were significantly elevated in food-restricted group rats as compared to controls or activity-stress group animals in one experiment but this finding was not repeated in further experiments. In a second series of experiments, rats from activity-stressed and food-restricted treatment groups and controls were exposed to an acute stressor for 15 min prior to sacrifice to assess the effects of prior sustained stress on hormonal responses to an acute stressor. Exposure to 15 min of immobilization or intermittent footshock immediately prior to sacrifice increased plasma levels of corticosterone, ACTH and prolactin in control, food-restricted and activity-stressed rats. Generally, hormonal responses to the acute stress were similar in all treatment groups. However, in two experiments where the resting levels of corticosterone were especially elevated in the activity-stress group, the acute stress-induced rise in corticosterone was less than that seen for the other two treatment groups. In another experiment, administration of dexamethasone suppressed acute stress-evoked levels of ACTH and corticosterone in control, activity-stressed and food-restricted rats. Thus, rats exposed to 4 days of sustained stress were found to have consistently elevated resting levels of corticosterone.(ABSTRACT TRUNCATED AT 250 WORDS)

Adrenocorticotropic Hormone↗
PubMed1987

Effects of chronic stress on plasma corticosterone, ACTH and prolactin.

Rats were placed in a stressful environment for 24 hr per day and levels of plasma hormones were measured after varying numbers of days in the environment. Rats were habituated to operant chambers placed in sound-attenuated enclosures. Food pellets were available by lever press on a FR1 schedule. After 3 days of habituation, rats in the "stressed" group were trained to pull a ceiling chain to avoid or escape shock. Following training, stress trials, consisting of a consecutive sequence of 5 sec each of a warning light, warning tone and 0.16, 0.32, 0.65, 1.3 and 2.6 mA of footshock, occurred approximately once per 5 min around-the-clock. For the first day, the sequence was terminated when the ceiling chain was pulled. On subsequent days, 90% of all shock presentations could be avoided or escaped by chain pull; the remaining 10% of trials were inescapable and the entire sequence was presented. Control rats lived in identical chambers without presentation of shock. Rats were sacrificed after 1, 2, 3, 4, 7 or 14 days in this environment and levels of plasma corticosterone, ACTH and prolactin were determined. Levels of plasma corticosterone were elevated during the first 7 days in the stressful environment, but returned to control values by day 14. Levels of plasma ACTH and prolactin were similar in stressed and control rats at all time points measured. These data suggest that stress-induced changes in glucocorticoids but not in ACTH or prolactin might mediate some of the physiological changes that occur as the result of chronic stress.

Adrenocorticotropic Hormone↗
PubMed1987

Paraventricular lesions abolish the stress-induced rise in pituitary cyclic adenosine monophosphate and attenuate the increases in plasma levels of proopiomelanocortin-derived peptides and prolactin.

Acute exposure to footshock stress increased the pituitary level of cyclic adenosine monophosphate (AMP) in vivo and sharply increased plasma levels of adrenocorticotropic hormone, beta-endorphin and beta-lipotrophic hormone, as well as prolactin. Seven days after bilateral lesions of the paraventricular nucleus of the hypothalamus, the pituitary cyclic AMP response to stress was totally eliminated and the increases in plasma levels of these pituitary hormones were blunted. We conclude that while the pituitary hormonal responses to stress might be mediated by several neurohumoral factors, the stress-induced increases in pituitary levels of cyclic AMP in vivo are mediated largely via corticotropin-releasing factor, released from neurons which project from the paraventricular nucleus to the median eminence.

Adrenocorticotropic Hormone↗
PubMed1986

Pituitary cyclic AMP and plasma hormone responses to epinephrine administration in vivo.

The present study was conducted to characterize the in vivo effects of epinephrine administration on levels of pituitary cyclic AMP and plasma hormones. Rats were injected with saline or epinephrine bitartrate (1 mg/kg lP) and sacrificed by decapitation 1, 5, 15, 30 or 60 min post-injection. Levels of pituitary cyclic AMP and plasma ACTH, beta-endorphin, beta-LPH, corticosterone and prolactin were determined by radioimmunoassays. The injection procedure itself was somewhat stressful as demonstrated by increased levels of plasma prolactin and ACTH 5 min following either saline or epinephrine injection. This "stress" response was rapid and short-lasting for the pituitary hormones. The response of the adrenal hormone, corticosterone, to saline injection was slower in onset and longer in duration. Pituitary cyclic AMP levels did not increase following saline injection. Epinephrine-injected animals displayed markedly elevated plasma levels of ACTH, beta-endorphin and beta-LPH at 15, 30 and 60 min as compared to control or saline-injected rats. In addition, levels of pituitary cyclic AMP were increased over 10 fold at these times. Levels of plasma prolactin, a stress-responsive hormone, were not significantly increased in epinephrine-injected animals as compared to saline-injected rats indicating that these later responses seem to be specific to epinephrine rather than to stress.

Adrenocorticotropic Hormone↗
PubMed1986

Hemorrhagic hypotension increases plasma beta-endorphin concentrations in the nonhuman primate.

The role which beta-endorphin plays in the pathogenesis of hemorrhagic hypotension is controversial. In the present experiment, 20 ml/kg of blood was bled from ten healthy male baboons (Papio anubis) over 60 min and then retransfused over the next 30 min. We found that the mean plasma beta-endorphin level increased 109% above baseline (p less than .05) within 15 min after starting hemorrhage, and rapidly returned to a baseline concentration with retransfusion. We conclude that in a primate species, circulating endogenous opioid peptide concentrations increase rapidly in response to sublethal hemorrhagic hypotension and normalize with restoration of the baseline intravascular volume. These findings support the concept that endogenous opioid peptides may mediate the hypotension of shock states.

Animals↗
PubMed1986

Diurnal variation in neuroendocrine response to stress in rats: plasma ACTH, beta-endorphin, beta-LPH, corticosterone, prolactin and pituitary cyclic AMP responses.

The effects of restraint stress applied at different times of the day on levels of five stress-responsive plasma hormones (ACTH, beta-endorphin, beta-LPH, corticosterone and prolactin) and pituitary cyclic AMP levels were assessed. Different groups of rats were subjected to 15 min of restraint stress at 2-hour intervals over a 24-hour period. Rats were sacrificed immediately upon removal from their home cage (controls) or immediately following restraint (stressed). The time of day of stress exposure markedly affected the stress responses measured. Generally, responses to stress applied at the beginning of the dark cycle (18:00) were less than those seen following stress applied at the beginning of the light cycle (06:00). Stress at 06:00 increased levels of pituitary cyclic AMP 10-fold, while stress applied at 18:00 did not significantly increase pituitary cyclic AMP levels. In stressed rats, high correlations were seen among levels of hormones derived from the common precursor, proopiomelanocortin (ACTH, beta-endorphin, beta-LPH) and between these hormones and levels of pituitary cyclic AMP. These findings support the hypothesis that pituitary cyclic AMP is involved in the stress-induced release or synthesis of the pituitary hormones ACTH, beta-endorphin, and beta-LPH.

Adrenocorticotropic Hormone↗
PubMed1985

Subsensitive pituitary cyclic AMP response to stress following adrenalectomy is not caused by loss of adrenal epinephrine.

We have previously reported that various stressors acutely elevate levels of pituitary cyclic AMP in vivo and that this stress response is not seen in animals tested 7 or 30 days post-adrenalectomy. In this report we present data that demonstrate that the loss of the pituitary cyclic AMP stress response following adrenalectomy is not the result of the loss of stress-induced adrenal epinephrine release. These data show that (1) although administration of epinephrine to intact rats does not elevate levels of pituitary cyclic AMP, administration of epinephrine to adrenalectomized animals does not elevate pituitary cyclic AMP levels in vivo; (2) splanchnic denervation prevents stress-induced adrenal epinephrine release but does not abolish stress-induced increases in pituitary cyclic AMP; and (3) the time course of the developing subsensitive pituitary cyclic AMP response to stress following adrenalectomy is much slower (2 to 3 days) than the loss of circulating epinephrine.

Adrenalectomy↗
PubMed1984

Adrenalectomy abolishes the stress-induced increase in pituitary cyclic AMP.

We have previously demonstrated that various stressors increase pituitary cyclic AMP in vivo in the rat. In the course of studying the mechanisms mediating this response, we examined the effect of bilateral adrenalectomy on footshock-induced increases in pituitary cyclic AMP. In unoperated rats, intermittent footshock markedly increased pituitary levels of cyclic AMP and plasma levels of corticosterone and prolactin. Adrenalectomy completely abolished the stress-induced increase in pituitary cyclic AMP. The marked increase in plasma prolactin following footshock was not affected by adrenalectomy. Our results indicate that adrenal factors are involved in the stress-induced increase in pituitary cyclic AMP.

Adrenalectomy↗
PubMed1984

Effects of 72 hour sleep deprivation on urinary cortisol and indices of metabolism.

Cortisol, urea, glucose, electrolytes, and other compounds were measured in five consecutive 24 h urine collections during a 72 h sleep deprivation study in six young men. Urine was collected during a 24 h predeprivation day, 3 days of sleep deprivation, and a recovery day. Whereas urinary cortisol decreased only slightly, marked changes in other urinary constituents were observed. During sleep deprivation, urinary urea rose markedly, glucose decreased, and urinary electrolytes decreased. These data indicate that sleep deprivation under ad lib food and water conditions can cause disturbances in normal metabolism.

Adolescent↗