Effects of ECT on Pituitary Hormone Release: Relationship to Seizure, Clinical Variables and Outcome

1983 ◽  
Vol 143 (6) ◽  
pp. 618-624 ◽  
Author(s):  
J. F. W. Deakin ◽  
I. N. Ferrier ◽  
T. J. Crow ◽  
E. C. Johnstone ◽  
P. Lawler
Keyword(s):  
Growth Hormone ◽  
Serum Levels ◽  
Endogenous Depression ◽  
Pituitary Hormone ◽  
Cortisol Secretion ◽  
Hormone Release ◽  
Clinical Variables ◽  
Tsh Secretion

SummaryProlactin, Cortisol, growth hormone and TSH serum levels (before and 15 minutes after treatment) were measured in 62 patients with endogenous depression randomly allocated to real or pseudo-ECT. Prolactin increased significantly more in those receiving real ECT than in those receiving pseudo-ECT, but the size of this effect had diminished by the time of the last (8th) treatment in the trial. Cortisol secretion was also significantly increased following the first treatment by real ECT, but this increase was of significantly smaller size in patients with delusions. Tolerance to the effects of ECT on Cortisol secretion was not observed. No effects of ECT on growth hormone or TSH secretion were detected, and no clear evidence was obtained that endocrine responses can be used as a predictor of response to ECT.

scholarly journals Effects of 6-Methoxy-l,2,3,4-tetrahydro-b-carboline and Yohimbine on Hypothalamic Monoamine Status and Pituitary Hormone Release in the Rat

1983 ◽  
Vol 36 (4) ◽  
pp. 379 ◽  
Author(s):  
GA Smythe ◽  
M W Duncan ◽  
JE Bradshaw ◽  
MV Nicholson
Keyword(s):  
Growth Hormone ◽  
Neuronal Activity ◽  
Specific Effect ◽  
Thyroid Stimulating Hormone ◽  
Pituitary Hormone ◽  
Hormone Release ◽  
Tsh Secretion ◽  
Pituitary Prolactin ◽  
Hypothalamic Dopamine ◽  
Acth Release

Shortly after administration of 6-methoxy-1,2,3,4-tetrahydro-ft-carboline (6-MeOTHBC) and yohimbine to normal or hypothyroid rats [the latter exhibiting chronically elevated levels of serotonin (5-HT) neuronal activity in the hypothalamus] there was a highly significant increase in hypothalamic noradrenaline (NA) activity and in ACTH release concomittant with a reduction in hypothalamic 5-HT activity (P< 0'01) and in growth hormone (GH) (P<O'01) and in thyroid stimulating hormone (TSH) (P< 0'01) release from the pituitary. Both compounds caused an increase in hypothalamic dopamine (DA) metabolism and in pituitary prolactin (PRL) release in normal rats (P<0'01) but only yohimbine exerted this action in hypothyroid rats. Lower doses of 6-MeOTHBC exerted a relatively specific effect in hypothyroid rats, reducing (P< 0�01) 5-HT neuronal activity in parallel with pituitary TSH secretion (P<0�05). While gross effects of 6-MeOTHBC and yohimbine were similar with respect to their effects on NA and 5-HT status in the hypothalamus, there were quantitative differences. 6-MeOTHBC always caused a greater decrease in 5-HT turnover and a lesser increase in NA turnover than did yohimbine.

A comparison of the dynamics of secretion of human growth hormone and LH pulses

1988 ◽  
Vol 118 (2) ◽  
pp. 339-345 ◽  
Author(s):  
R. P. McIntosh ◽  
J. E. A. McIntosh ◽  
L. Lazarus
Keyword(s):  
Growth Hormone ◽  
Human Growth ◽  
Pituitary Hormones ◽  
Hypothalamic Stimulation ◽  
Target Organ ◽  
Pituitary Hormone ◽  
Hormone Release ◽  
Blood Samples ◽  
Gonadotrophin Releasing Hormone ◽  
Stimulation Current

ABSTRACT Patterns of hypothalamic stimulation causing pituitary hormone release cannot be studied directly in humans; one possible approach is to make inferences from the nature of the response of the target organ as revealed by patterns of pituitary hormones in blood. Replicated, precise assay of LH in frequently sampled blood of women at differing stages of the menstrual cycle has demonstrated previously that secretion of this hormone is compatible with a model of discrete, instantaneous episodes of LH output, which are assumed to be stimulated by isolated bursts of increased stimulatory hypothalamic gonadotrophin-releasing hormone. However, similarly detailed measurements of the dynamic secretion patterns of GH in women reported here, revealed much slower rates of increase of GH concentrations (median time to maximum concentration 38 min) in comparison with LH (13 min) assayed in the same blood samples. These rise rates of GH were uncorrelated with the final amplitude of the peak and were observably discontinuous in half the peaks. Simultaneous i.v. injection of a bolus of mixed GRF and GnRH produced similar dynamics of pituitary release of GH and LH. Thus differences in patterns of natural release of the two hormones appear to be contributed to by differences in the modes of hypothalamic stimulation. Current understanding of control of GH release in animal models suggests that the slow-rising, frequently discontinuous natural peaks of GH in human blood are likely to be caused by interaction between the withdrawal of inhibitory hypothalamic somatostatin and the increased secretion of stimulatory GRF. J. Endocr. (1988) 118, 339-345

scholarly journals Antagonism by Taurine of Morphine Induced Growth Hormone Secretion

1978 ◽  
Vol 5 (1) ◽  
pp. 139-142 ◽  
Author(s):  
R. Collu ◽  
G. Charpenet ◽  
M. J. Clermont
Keyword(s):  
Growth Hormone ◽  
Amino Acid ◽  
Hormone Secretion ◽  
Growth Hormone Secretion ◽  
Physiological Role ◽  
Pituitary Hormone ◽  
Hormone Release ◽  
Morphine Administration ◽  
Plasma Gh

SUMMARY:The intraperitoneal (IP) or intraventricular (IVT) administration of small amounts of taurine did not modify pentobarbital-induced sleep or pituitary hormone release. However, the drastic increment in plasma GH values induced by morphine administration was completely blocked by the IVT injection of the amino acid. Whether taurine plays a physiological role in the control ofGH secretion is highly speculative.

THE EFFECT OF INTRAVENOUS L-DOPA ON GROWTH HORMONE AND LUTEINIZING HORMONE LEVELS IN MAN

1973 ◽  
Vol 73 (2) ◽  
pp. 259-265 ◽  
Author(s):  
Athanasius Souvatzoglou ◽  
Klaus von Werder ◽  
Peter Bottermann
Keyword(s):  
Growth Hormone ◽  
Luteinizing Hormone ◽  
Normal Subjects ◽  
Serum Levels ◽  
Hormone Release ◽  
Growth Hormone Release ◽  
Serum Growth Hormone ◽  
Provocative Test ◽  
Hormone Levels ◽  
Serum Lh

ABSTRACT The effect of various intravenous doses of L-dopa on growth hormone and LH-serum levels in 25 normal subjects was investigated. Growth hormone increased 30–40 minutes following the injection of 25 mg and 100 mg L-dopa whereas doses of less than 25 mg had no significant effect on the serum growth hormone levels. The serum LH-level was not significantly altered by the intravenous administration of various doses (1 to 100 mg) of L-dopa. These findings, which are in agreement with the results obtained with L-dopa given orally, suggest that the intravenous injection of 25 mg L-dopa may be useful as a short provocative test for growth hormone release in man.

scholarly journals Growth hormone-releasing peptide-2 infusion synchronizes growth hormone, thyrotrophin and prolactin release in prolonged critical illness

1999 ◽  
pp. 17-22 ◽  
Author(s):  
G Van den Berghe ◽  
P Wouters ◽  
CY Bowers ◽  
F de Zegher ◽  
R Bouillon ◽  
...  
Keyword(s):  
Growth Hormone ◽  
Critical Illness ◽  
Cross Correlation ◽  
Pituitary Hormone ◽  
Hormone Release ◽  
Prolactin Release ◽  
Anterior Pituitary Hormone ◽  
Temporal Coupling ◽  
Pituitary Secretion ◽  
Design And Methods

OBJECTIVE: During prolonged critical illness, nocturnal pulsatile secretion of GH, TSH and prolactin (PRL) is uniformly reduced but remains responsive to the continuous infusion of GH secretagogues and TRH. Whether such (pertinent) secretagogues would synchronize pituitary secretion of GH, TSH and/or PRL is not known. DESIGN AND METHODS: We explored temporal coupling among GH, TSH and PRL release by calculating cross-correlation among GH, TSH and PRL serum concentration profiles in 86 time series obtained from prolonged critically ill patients by nocturnal blood sampling every 20 min for 9 h during 21-h infusions of either placebo (n=22), GHRH (1 microg/kg/h; n=10), GH-releasing peptide-2 (GHRP-2; 1 microg/kg/h; n=28), TRH (1 microg/kg/h; n=8) or combinations of these agonists (n=8). RESULTS: The normal synchrony among GH, TSH and PRL was absent during placebo delivery. Infusion of GHRP-2, but not GHRH or TRH, markedly synchronized serum profiles of GH, TSH and PRL (all P< or =0.007). After addition of GHRH and TRH to the infusion of GHRP-2, only the synchrony between GH and PRL was maintained (P=0.003 for GHRH + GHRP-2 and P=0.006 for TRH + GHRH + GHRP-2), and was more marked than with GHRP-2 infusion alone (P=0.0006 by ANOVA). CONCLUSIONS: The nocturnal GH, TSH and PRL secretory patterns during prolonged critical illness are herewith further characterized to include loss of synchrony among GH, TSH and PRL release. The synchronizing effect of an exogenous GHRP-2 drive, but not of GHRH or TRH, suggests that the presumed endogenous GHRP-like ligand may participate in the orchestration of coordinated anterior pituitary hormone release.

Bacteremia-induced changes in pituitary hormone release and effect of naloxone

1984 ◽  
Vol 247 (5) ◽  
pp. E585-E591 ◽  
Author(s):  
L. S. Leshin ◽  
P. V. Malven
Keyword(s):  
Growth Hormone ◽  
Luteinizing Hormone ◽  
Pituitary Hormone ◽  
Clinical Parameters ◽  
Plasma Prolactin ◽  
Hormone Release ◽  
E Coli ◽  
Opioid Mechanisms ◽  
Plasma Gh ◽  
Induced Changes

Acute bacteremia in sheep caused a surge of plasma beta-endorphin/beta-lipotropin (beta-EP/beta-LPH) associated with shivering behavior, tachycardia, hyperthermia, hemoconcentration, and decreased respiration rate. The surge of plasma beta-EP/beta-LPH was immediately followed by increases (P less than 0.05) in plasma prolactin and growth hormone (GH) concentrations and a depression (P less than 0.05) of plasma luteinizing hormone. These changes in pituitary hormone release were consistent with opioid-induced changes described in the literature. To examine possible opioid mediation, naloxone (2.5 mg X kg-1 X h-1) was continuously infused intravenously from 3 h before to 3 h after induction of an E. coli bacteremia. With the exception of plasma GH, naloxone failed to alter any of the hormonal or clinical parameters associated with bacteremia. For plasma GH, naloxone delayed (P less than 0.01) the increase but did not attenuate its magnitude, suggesting that an opioid mechanism may influence the timing of the pituitary GH release resulting from bacteremia. In general, opioid mechanisms sensitive to the present dosage of naloxone do not appear to mediate bacteremia-induced changes in hormonal or clinical parameters.

The effect of d-fenfluramine on anterior pituitary hormone release in the rat: in vivo and in vitro studies

1987 ◽  
Vol 65 (12) ◽  
pp. 2449-2453 ◽  
Author(s):  
O. Serri ◽  
E. Rasio
Keyword(s):  
Growth Hormone ◽  
Male Rats ◽  
Serum Prolactin ◽  
Pituitary Hormone ◽  
Pituitary Cells ◽  
Hormone Release ◽  
Growth Hormone Release ◽  
Serum Growth Hormone

Administration of d-fenfluramine, a serotonin-releasing drug, to male rats induced a dose-dependent increase in both serum prolactin and corticosterone concentrations. Serum growth hormone levels increased, but not significantly, at a dose of 1.25 mg/kg i.p. and decreased significantly at higher doses. When rats were pretreated with the serotonin uptake inhibitor fluoxetine (10 mg/kg i.p.) 30 min prior to injection of d-fenfluramine (5 mg/kg i.p.), the serum prolactin response to d-fenfluramine was partially inhibited, whereas the growth hormone response was not significantly modified. Fluoxetine pretreatment increased the serum corticosterone to the same level as did d-fenfluramine. d-Fenfluramine's effect on prolactin and growth hormone release was further tested in a hypothalamic–pituitary in vitro system. The addition of d-fenfluramine (5–500 ng/mL) for 30 min to rat hypothalami resulted in an enhancement of prolactin and growth hormone-releasing activities. These were expressed as the ability of the media in which the hypothalami had been incubated to stimulate prolactin and growth hormone release by cultured pituitary cells. The data suggest that the effect of d-fenfluramine on prolactin secretion is exerted through the hypothalamus and is probably mediated, at least partially, by a serotoninergic mechanism. The mechanism of d-fenfluramine's effect on corticosterone and growth hormone release needs further evaluation.

Altered release of growth hormone and thyrotropin induced by endotoxin in the rat

1982 ◽  
Vol 243 (4) ◽  
pp. E332-E337 ◽  
Author(s):  
N. W. Kasting ◽  
J. B. Martin
Keyword(s):  
Growth Hormone ◽  
Temperature Response ◽  
Hormone Release ◽  
Plasma Growth Hormone ◽  
Gh Secretion ◽  
Tsh Secretion ◽  
Initial Control ◽  
Freely Behaving ◽  
Tsh Levels

Plasma growth hormone (GH) and thyrotropin (TSH) levels were measured in freely behaving rats for 6 h on three consecutive days. On the 1st and 3rd days there was no treatment, and on the 2nd day endotoxin (150 mg/kg) was administered intravenously. Endotoxin causes a biphasic temperature response: an initial hypothermia persisting for 1 h, followed by hyperthermia evident from 5 to 8 h after injection. Normal pulsatile GH release observed on the 1st day was abolished on the 2nd day by the endotoxin treatment. On the 3rd day, however, GH secretion was greater than on the initial control day. TSH release was also suppressed by endotoxin and showed a rebound release on the subsequent day. The suppression of GH secretion by endotoxin was reversed in all animals by antisomatostatin serum, and the suppression of TSH secretion by endotoxin was reversed in some animals. These results suggest that endotoxin is a potent stimulus for hypothalamic somatostatin release in the rat. Endotoxin profoundly alters adenohypophyseal hormone release.

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