Search PubMed⌕ Search

Biomedical subjects

G H Greeley

Publications and source records attributed to G H Greeley.

156 records · Page 9Linked to original sources
PubMed1978

Direct evidence that the arcuate nucleus-median eminence tuberoinfundibular system is not of primary importance in the feedback regulation of luteinizing hormone and follicle-stimulating hormone secretion in the castrated rat.

Adult rats which have received monosodium-L-glutamate (MSG, 4 mg/g BW) on alternate days for the first 10 days of life manifest central nervous system lesions largely restricted to the retina and the arcuate nucleus of the hypothalamus in which nearly 90% of the perikarya are destroyed, leaving axons in passage intact. In animals so treated, concentrations of dopamine within the arcuate nucleus and median eminence of the hypothalamus are reduced 52% and 57%, respectively, in males and 45% and 61% in females, whereas concentrations of norepinephrine in these same two areas are normal. Concentrations of both norepinephrine and dopamine in five other hypothalamic nuclei (dorsal septal, medial preoptic, suprachiasmatic, periventricular, and dorsomedial nuclei) are unchanged. Nevertheless, despite the destruction of the arcuate nucleus cell bodies of MSG-treated rats, postcastration levels of serum FSH and LH in males, and FSH in females were not significantly different from FSH and LH values in castrated controls. Serum LH in castrated, MSG-treated females was slightly but significantly lower than in castrated controls. It is concluded that the arcuate nucleus-median eminence tuberoinfundibular neurons are not of primary importance in the tonic, negative feedback regulation of gonadotropin secretion.

Animals↗
PubMed1978

Triiodothyronine (T3) modulation of gonadotropin secretion in the female rat.

The effect of T3 upon gonadotropin secretion was examined in ovariectomized (Ovarx), Ovarx thyro-parathyroidectomized (Ovarx-TxPx), or proestrus rats. T3 (50 microgram/-100 gBW), administered late diestrus-2, abolished the LH surge during the critical period of proestrus in 7 out of 9 rats; the rise in sera FSH was not inhibited, although a distinct peak was absent. Administration of 5 or 50 microgram T3/100gBW 2.5h before the critical period resulted in either a suppression or an alteration of the timing of LH release. In the 5 microgram T3/100gBW treated animals the sera FSH peak was delayed in timing, whereas in the 50 microgram T3/100gBW treated rats sera FSH demonstrated two separate peaks during the critical period. Treatment with various dosages of T3 of Ovarx-TxPx rats resulted in significant suppressions (p less than 0.05) of sera LH and FSH. Despite depressed concentrations of sera LH and FSH in T3-treated rats pituitary sensitivity to a challenge of 3LHRH was enhanced. Hence, the pituitary was not the site of T3 inhibition of gonadotropin secretion. Additionally, T3 did not modify pituitary LH content or hypothalamic LH3 releasing activity (LHRH). Since T3 did not inhibit gonadotropin secretion at the pituitary level, a neural site of T3 action is suggested.

Animals↗
PubMed1977

Ultrastructural and physiological studies of the stalk-sectioned rat pituitary gland.

A pituitary stalk-section rat model was prepared that would be suitable for the study of the direct effects of steroids on the pituitary gland. In this model, the hypophyseal stalk was severed surgically and metal foil was inserted to prevent regeneration of portal vessels. The major portion of the pituitary no longer had a direct communication with the hypothalamus, and the only blood supply was from short portal vessels that supply the dorsolateral part of the gland. The effectiveness of the lesion was demonstrated by very high levels of serum prolactin and very low FSH and LH. Light microscopic examination revealed a large infarct in the central region of the gland with stainable cells in the peripheral area. Fourteen days after stalk-section, the infarct had shrunken appreciably, and after 21 days it was replaced by a scar. Ultrastructural studies revealed the presence of functional mammotropes in the peripheral regions of the pituitary gland, while other cells were smaller, less active, and contained fewer secretory granules. After LHRH administration there was an increase in serum LH, thus indicating the presence of a substantial number of viable gonadotropes. This was confirmed by the ultrastructural findings which now showed the appearance of large, well-granulated gonadotropes. When LHRH was given to estradiol 17-beta primed ovariectomized stalk-sectioned rats, there was a great augmentation of LH release, and many castration cells were now apparent. Therefore, the administration of estrogen and LHRH was needed for the gonadotropes of the isolated pituitary to function optimally in the synthesis and secretion of FSH and LH. The stalk-sectioned animal model permits evaluation of pituitary function isolated from hypothalamic control while it leaves the surviving pituitary gland in its normal anatomical position.

Animals↗
PubMed1975

Potentiation of luteinizing hormone release by estradiol at the level of the pituitary.

The objective of this study was to determine the influence of estradiol-17beta and/or progesterone on gonadotropon secretion at the level of the pituitary. Female rats in which the hypothalamo-hypophyseal connections had been permanently interrupted after castration served as the experimental model in which the effect of estradiol and/or progesterone on LH-RH-induced gonadotropin release was examined. In out experimental animals, LH secretion was readily activated by LH-RH administration. LH release was greatly augmented by the prior administration of estradiol benzoate (1 mug/kg b.w./day). Progesterone (5 mg/day) in the absence of estradiol did not modify the 10-min responese to LH-RH but reduced the enhancement of LH secretion caused by estradiol pretreatment. Our findings suggest that estradiol potentiated the releasing effect of LH-RH at the level of the gonadotroph, whereas progesterone interfered with the potentiation effect. Plasma levels of FSH were not significantly elevated above the basal value by the administration of LH-RH alone, or in combination with estradiol and/or progesterone.

Animals↗
PubMedDate not supplied

Peptide YY inhibits gastric acid secretion stimulated by the autonomic nervous system.

Peptide YY (PYY), a new peptide found primarily in mucosal endocrine cells of the terminal ileum and colon, inhibits pentagastrin-stimulated gastric acid secretion in several species, including man. Several studies indicate that PYY can affect autonomic neurotransmission, and we have recently shown that PYY can inhibit neurally stimulated release of insulin. The purpose of the present study was to examine the effect of PYY on gastric acid secretion stimulated by the autonomic nervous system. On separate days, 6 dogs that were prepared with chronic gastric cannulas were given 2-deoxy-D-glucose (2-DG; 90 mg/kg, i.v.) for 6 min, either alone, or in combination with PYY (100, 200, or 400 pmol.kg-1.h-1, i.v.) for 60 min. The effect of PYY, at 400 pmol.kg-1.h-1, on gastric acid secretion stimulated by either 2-DG or PG (1 micrograms.kg-1.h-1, i.v.) was studied after treatment with propranolol (0.5 mg/kg, i.v. bolus) or phentolamine 1 mg/kg, i.v. bolus). PYY reduced the 2-DG-stimulated secretion of gastric acid in a dose-dependent manner. PYY, given at 100 pmol.kg-1.h-1, reduced gastric acid output by 29 +/- 17%; PYY, at 200, by 41 +/- 7% (p < 0.05), and PYY, at 400, by 52 +/- 8% (p < 0.05). The inhibitory action of PYY on 2-DG-stimulated secretion of gastric acid persisted after treatment with phentolamine (69 +/- 14%; p < 0.05), but it was blocked by treatment with propranolol.(ABSTRACT TRUNCATED AT 250 WORDS)

Adrenergic beta-Antagonists↗
PubMedDate not supplied

Inhibitory action of peptide YY on pancreatic secretion is independent of secretin.

The purpose of this study was to characterize the effect of peptide YY (PYY) on acid-stimulated pancreatic bicarbonate secretion and to determine whether PYY affects the release of secretin in response to intraduodenal infusion of acid. Six dogs were prepared with gastric and pancreatic cannulas. In study 1, graded doses of hydrochloric acid (HCl) (3, 6, 12, and 24 mEq/h) were given intraduodenally alone or in combination with intravenous PYY (400 pmol/kg.h). In study II, and ED50 of intraduodenal HCl (6 mEq/h) was given alone or in combination with graded doses of PYY (12.5, 25, 50, 100, 200, and 400 pmol/kg.h, i.v.). Bicarbonate output was significantly inhibited during PYY infusion at 200 and 400 pmol/kg.h, but plasma secretin levels were unchanged. The calculated maximal response for bicarbonate secretion (5.1 +/- 1.3 mEq/15 min) was significantly reduced by PYY (2.1 +/- 0.7 mEq/15 min). We concluded that PYY can inhibit acid-stimulated pancreatic bicarbonate secretion without affecting the release of secretin. The mechanism of the inhibitory effect of PYY on acid-stimulated pancreatic bicarbonate secretion is compatible with a noncompetitive type of inhibition.

Animals↗
PubMedDate not supplied

Effect of a cholecystokinin antagonist, proglumide, on cholecystokinin-8-induced gallbladder contraction in conscious dogs.

The objective of this study was to characterize the effect of proglumide, a cholecystokinin (CCK) antagonist, on gallbladder contraction stimulated by CCK in conscious dogs. The gallbladder contraction was monitored by a strain-gauge force transducer that was chronically sutured onto the serosal surface of the gallbladder. The results of this study show that proglumide, given as an intravenous bolus (2.5, 5, 10, 20, and 40 mg/kg) or as a continuous intravenous infusion (150 or 300 mg/kg/h, 10 min), can block the stimulatory action of CCK in a dose-related manner. Bolus administration of proglumide resulted in a transient inhibition, whereas continuous infusion of proglumide resulted in a prolonged antagonism of CCK-stimulated gallbladder contraction. Review of the data leads to the conclusion that the antagonistic action of intravenously administered proglumide on CCK-stimulated gallbladder contraction may be characterized as rapid and reversible.

Animals↗
PubMedDate not supplied

Neurotensin secretion in response to intraduodenal and intraileal administration of fat in dogs.

Release of neurotensin from the small intestine in response to administration of fat directly into the duodenum and ileum was examined in conscious dogs. The present results show that: (1) intraduodenal administration of fat causes a diphasic release of neurotensin which is mediated, at least in part, by cholinergic mechanisms, and (2) both a fatty acid (sodium oleate) and a triglyceride, when infused directly into an isolated ileal loop, stimulate a significant release of neurotensin. Our findings indicate that release of neurotensin is triggered by mechanisms originating in the proximal small intestine and by a direct contact of nutrients with the ileal mucosa.

Animals↗
PubMedDate not supplied

Serum thyroxine, triiodothyronine, and TSH levels and TSH release after TRH in aging male and female rats.

Serum levels of TSH, T3 and T4, pituitary responsiveness to TRH, and T3-resin uptake were examined in aging male and female rats. Despite normal serum TSH levels, serum T3 and T4 levels were significantly reduced in old male rats (19-26 months of age) when compared to young (120-150 days of age) and middle-aged males (12-1- months of age). In old female rats, serum TSH and T3 levels were not significantly (p greater than 0.05) different from those of young or middle-aged females. Serum T4 levels were significantly lower in old females when compared to younger rats. The T3-resin uptake of old rats was not significantly different from the value of young rats. Serum T4 levels, 3 hours after TRH induced TSH release, were significantly depressed in old male and female rats. Pituitary sensitivity to TRH was unaltered in old rats. These findings suggest that thyroidal release of T4 and T3 is depressed, and that the hypothalamic-pituitary axis is insensitive to diminished thyroid hormone feedback in old rats.

Age Factors↗
PubMedDate not supplied

Change in endocrine pancreatic function in short-term diet restriction.

Long-term diet restriction can retard the aging process. Lower sustained plasma glucose levels may be one of the key factors for prolongation of life. The purpose of this study was to determine the effects of short-term diet restriction on the endocrine pancreas in rats. One hundred 5-wk-old male Sprague-Dawley rats were fed ad libitum for 1 wk, and then 10 rats (5 fed, 5 fasted for 24 h) were killed. The remaining 90 rats were divided into two groups, either fed ad libitum or maintained on a restricted food intake (60% of control/day). At regular intervals after the start of food restriction, rats from each group were killed, and plasma and the pancreas were collected for measurements of glucose, insulin, and glucagon concentration and content. At the end of the study, isolated pancreatic perfusions were performed to examine dynamic insulin response to glucose. Throughout the study, plasma glucose and insulin levels were lower in fed rats from the diet-restricted group than in fed rats from the normally fed group. Furthermore, there were no differences in plasma glucose or insulin levels between fed and fasted rats in the diet-restricted group. Pancreatic perfusion showed that the second phase of insulin release was significantly lower in rats from the diet-restricted group than in rats from the normally fed group. Decreased content of spermine in the pancreas of the diet-restricted rats may correlate with a decreased second phase of insulin release. These findings may partly explain why lowered plasma insulin levels are observed in diet-restricted rats.

Aging↗