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Biomedical subjects

S H Shin

Publications and source records attributed to S H Shin.

At least 91 records · Page 5Linked to original sources
PubMed1988

Bovine 'neurophysin II' stimulates growth hormone release in the estradiol-primed male rat.

Basal plasma concentrations of growth hormone (GH) were monitored in both normal and estradiol-primed male rats by the collection of sequential blood samples from freely moving rats, via chronic intraatrial cannulae. Blood was sampled every 2 min for a period of 80 min and plasma GH levels determined by radioimmunoassay. The normal male rats displayed a pulsatile release of GH, while the estradiol-primed male rats exhibited a relatively steady level of plasma GH concentration. The rats exposed to high levels of estradiol (1.59 +/- 0.42 nmol/l plasma) also had a higher mean value of basal GH concentration. An injection of 100 micrograms/kg of bovine neurophysin II did not alter GH release in the normal male rats. However, it did significantly elevate GH levels in the estradiol-primed animals to a mean peak level approximately six times the mean basal level. The administration of 100 micrograms/kg of bovine neurophysin I to estradiol-primed male rats did not produce any change in plasma GH levels and thus eliminates the possibility of the nonspecific stimulation of neurophysin II on GH release.

Animals↗
PubMed1988

Pulsatile nature of luteinizing hormone release is maintained during luteinizing hormone-releasing hormone stimulation in normal male rats.

The plasma LH concentration is believed to be reasonably steady in normal male rats. We found that LH is released in a regular pulsatile fashion. The overall mean concentration of plasma LH in normal male rats was 46.6 +/- 4.4 (mean +/- SEM) ng/ml. The normal male rats showed periodic LH pulses: the mean pulse amplitude was 144.4 +/- 25.5 ng/ml and the inter-peak interval was 22.5 +/- 2.0 min. Each pulse lasted 9.7 +/- 0.8 min. When LH-RH (1 microgram/kg) was injected as a bolus, the peak concentration was attained in 10-30 min reaching a peak concentration of 279.4 +/- 39.6 ng/ml. Distinct pulsatile bursts of plasma LH were discernible during the period of elevated plasma LH concentration. When a higher dose of LH-RH (5 micrograms/kg) was administered, the LH concentration slowly increased to a peak concentration of 400.2 +/- 38.7 ng/ml in 20-40 min. The pulsatile nature of the LH concentration was recognizable with distinct bursts. We have observed that: (a) normal male rats release LH in a pulsatile fashion with an approximate 20-min inter-peak interval; (b) mean LH pulses last less than 10 min, and (c) the LH pulses are visible even with elevated LH and LH-RH concentrations in the general circulation.

Animals↗
PubMed1988

Ascorbic acid potentiates the inhibitory effect of dopamine on prolactin release in primary cultured rat pituitary cells.

The chemical structure of dopamine includes an ortho-catechol group which is labile to oxidizing agents. Ascorbic acid, a reducing agent, has in the past been added to the incubation medium in order to protect dopamine against oxidation. However, there has been no thorough examination of the biological effect of ascorbic acid on prolactin release. In this present study we have shown that ascorbic acid has neither a stimulatory nor an inhibitory effect on prolactin release but reduces by approximately two orders of magnitude the concentration of dopamine necessary to inhibit prolactin release from cultured anterior pituitary cells. The strong potentiation effect of ascorbic acid was reproduced using apomorphine. We compared the effect of ascorbic acid and isoascorbic acid on dopamine inhibition of prolactin release. Isoascorbic acid is an epimer of ascorbic acid, having the same reduction-oxidation potential as ascorbic acid, but is less biologically active. Isoascorbic acid was less effective in potentiating the dopaminergic effect than was ascorbic acid, which supports the notion that potentiation by ascorbic acid is not entirely due to its reducing property. In order to dissociate further the chemical protection of dopamine from the biological potentiation, the inhibitory effects of freshly made and 3-h-old dopamine solutions were compared. Neither one of the two solutions contained any ascorbic acid, yet the two solutions did not show any difference in their ability to inhibit prolactin release during the 3-h incubation period, indicating that no significant amount of dopamine was oxidized.(ABSTRACT TRUNCATED AT 250 WORDS)

Animals↗
PubMed1987

Current status of the rat prolactin releasing factor.

The release of prolactin is governed by both inhibiting and releasing factors. Basal plasma concentration of prolactin is controlled mainly through inhibition by a prolactin release-inhibiting factor (PIF), while acute stimulation of prolactin release is believed to be caused by a prolactin-releasing factor (PRF). It is the general consensus that PIF is dopamine. The PRF plays an important role in stimulation of prolactin release, and there are promising putative PRFs.

Animals↗
PubMed1987

Effect of catechol estrogens on prolactin secretion in the rat: lack of correlation with estrogenic activity.

Temporal changes in plasma prolactin (PRL) levels caused by the administration of a number of different catechol estrogens to freely-moving conscious male rats were determined. The steroids with a wide range of affinity for the estrogen receptor were given in a single bolus (100 micrograms/kg) into the right atrium via an indwelling cannula. Plasma PRL concentration was monitored by taking blood samples every 2 min. The effect on PRL secretion was found to be more pronounced when the catechol estrogens were administered to rats bearing implants of estradiol and could not be correlated with their Kd values for the estrogen receptor. The synthetic estrogen, diethylstilbestrol, behaved anomalously by producing an elevation in plasma PRL only in estradiol-primed animals or after prolonged infusion. Diethylstilbestrol-treated rats showed no PRL response to 2-hydroxyestrone unlike those bearing Silastic capsules of estradiol. The experiments support the hypothesis that catechol estrogens generally act as short-term dopamine agonists, lowering PRL, but that those which possess estrogenic activity also show a more prolonged PRL-elevating effect. Thus, the overall action of this group of steroids will be determined by factors which influence these two parameters.

Animals↗
PubMed1987

Epidemiological characteristics of ketoacidosis among Korean diabetic patients.

An epidemiological study on diabetic ketoacidosis (DKA) was done by analysis of 207 cases collected from the medical records of 6 major general hospitals in Seoul area during the period of 5 years between 1979 and 1984. There was female predominance in the occurrence of DKA (male/female ratio, 0.71) in spite of the male predominance in general prevalence of diabetes mellitus (1.80). This female predominance in DKA was most striking in the age group under 40. There was a significant seasonal variation in the occurrence of DKA. DKA occurred most frequently in colder season with the highest peak in December. In July and August, the hottest season in Korea, not even a single case of DKA was recorded in this series. No discernible precipitating factor was found in 39.3% of DKA cases and infections was present as a cause of DKA in 30% of cases. In 27.5%, DKA was the first clinical presentation of diabetes and in the remainders of cases, diabetes was known to be present for average of 6.4 years. Mortality of DKA was 13.2% in this series. As to the socioeconomic status, the education level, the style of living and the duration of diabetes, there were not ascertainable differences between the DKA cases and other diabetic cases. The prospective epidemiological study of diabetic population in Korea, especially in female group, would be necessary for elucidation of the characteristics of DKA in Koreans such as the female predominance and the seasonal difference of the occurrence.

Adolescent↗
PubMed1986

A possible phagocytic role for folliculo-stellate cells of anterior pituitary following estrogen withdrawal from primed male rats.

Ultrastructural changes suggesting a phagocytic role for the nongranular folliculo-stellate cells of the anterior pituitary are investigated in estrogen-primed male rats after withdrawal of estrogen. Morphological changes in mammotropes following the removal of a subcutaneous estradiol-containing Silastic implant include the formation of intracellular lipid bodies. These lipid bodies appear to be associated with enhanced estrogen-dependent prolactin secretion in mammotropes. Seven and 24 h after estrogen withdrawal intracellular lipid within mammotropes seems to be released into the intercellular space. Seventy-two h after estrogen withdrawal, lipid droplets are almost entirely cleared from mammotropes while folliculo-stellate cells become packed with lipid globules. Folliculo-stellate cells also undergo dramatic hypertrophy 7 and 24 h after the removal of E2-containing implants. Extensive intercellular junctions including zonulae adhaerentes, desmosomes, and putative gap junctions are formed. Intercellular junctions delineate extravascular channels into which numerous microvilli project. Folliculo-stellate cells appear capable of accumulating many lipid droplets, presumably related to mammotrope metabolism. What appear to be large secondary lysosomes as well as the lipid droplets are observed within folliculo-stellate cells; lipid, therefore, may be degraded through a lysosomal pathway in folliculo-stellate cells.

Animals↗
PubMed1986

Pulsatile release of immunoreactive luteinizing hormone (irLH) in hypophysectomized male rats.

The concentration of plasma luteinizing hormone (LH) was monitored every minute by radioimmunoassay in male rats that were either hypophysectomized, or castrated and hypophysectomized. Castrated rats showed a pulsatile fluctuation of plasma immunoreactive LH (irLH) concentration with an elevated basal level, confirming previous work. The hypophysectomized and castrated hypophysectomized rats also showed pulsatile changes in plasma irLH concentration. This unexpected result indicates that ectopic irLH is not only actively released after hypophysectomy, but is released in pulses. The pulse interval was approximately 20 minutes for all 3 groups. The slope of the rate of decline of plasma irLH in the castrated rats is parallel to a theoretical disappearance rate of 5 min, while these slopes in the hypophysectomized and castrated hypophysectomized rats correspond to a 1 to 2-min disappearance rate. The difference in these slopes implies that the two irLH molecules may not be identical.

Animals↗
PubMed1985

Dopamine-induced physical barrier to inhibit prolactin release in mammotrophs disappears during resumption of prolactin secretion.

After finding that dopamine can cause extensive changes in mammotroph ultrastructure within 2 min of administration, we further examined mammotrophs 20 and 40 min after dopamine injection when prolactin secretion had resumed. Dopamine (1,000 micrograms/kg) was injected into the right atrium of estradiol-primed male rats through indwelling cannulae. Rats were killed by decapitation 2, 20 and 40 min after dopamine treatment and their pituitaries were processed for electron microscopy. Within 2 min of administration, dopamine completely stopped prolactin release and significant changes in mammotroph ultrastructure were observed: peripheral relocation of rough endoplasmic reticulum (RER) ('dopamine barrier'); fewer secretory granules in close proximity to the cell membrane; fewer exocytoses, and increased numbers of 'intracellular bodies' associated with secretory granules (putative granule disposal system). 20 min following dopamine administration, when prolactin secretion had resumed, there appeared to be a breaking up of the 'RER barrier' in that more vesicular elements were seen and the amount of peripheral RER was reduced; more granules were adjacent to the cell membrane and exocytotic figures were more numerous. 'Intracellular bodies' decreased in number. By 40 min, mammotrophs appeared to resemble those of estradiol-primed controls with the RER stacked to one side of the cell and small numbers of 'intracellular bodies'. The correlation between ultrastructural changes in mammotrophs and prolactin release implies that the 'RER barrier' is part of a mechanism by which prolactin release is inhibited.

Animals↗
PubMed1985

Bovine neurophysin II has prolactin-releasing activity in the estradiol-primed male rat.

In the course of the search for the prolactin-releasing factor (PRF), we noticed that the posterior pituitary contained strong PRF activity and subsequently traced this activity to that of bovine neurophysin-II (NP-II). NP-II prepared in our lab was judged to be a homogeneous preparation according to Sephadex G-75 gel filtration, DEAE ion exchange chromatography and polyacrylamide gel electrophoresis. While neurophysin-I (NP-I) injections of 100 micrograms/kg and 1,000 micrograms/kg elevated plasma prolactin in estradiol-primed male rats to 30% and 50% over the control value, respectively, NP-II doses of 100, 1,000 micrograms/kg increased plasma prolactin concentration in estradiol-primed male rats to 130% and 170% over the control value, respectively. The lowest dose of NP-II needed to increase plasma prolactin concentration was 10 micrograms/kg. Since neurophysin does not stimulate prolactin release from the ectopic pituitary under the kidney capsule nor from lactotrophs in a primary monolayer culture system, neurophysin is believed to act indirectly on the pituitary, presumably through a neurotransmitter and/or hypothalamic releasing (or inhibiting) factor. We propose that NP-II may be one element in the complex chain of the prolactin-releasing mechanism.

Animals↗
PubMed1985

Surgery depresses pulsatile growth hormone release in rats for up to 2 days.

In order to study the pulsatile release of rat growth hormone in a stress-free environment, many investigators obtain sequential blood samples from individual rats bearing an indwelling, right atrial cannula. There has been little systematic study of the stressful effects of the cannulation procedure on the pulsatile release of rat growth hormone. We examined the acute and chronic effects of right atrial cannulation on growth hormone release in male rats by monitoring plasma growth hormone concentration at every 2 min. Right atrial cannulation was performed under ether anaesthesia. Blood was collected from the rats for a 2 h period (11.00-13.00 h), either immediately following, or 2, 3 or 7 days following the surgery. When blood was collected 7 days after surgery, growth hormone was released in large bursts. The amplitude of these bursts however, did not differ significantly from the bursts of growth hormone in rats cannulated 3 days prior to blood collection. On the other hand, the bursts of hormone release in rats cannulated immediately or 2 days before blood collection were significantly smaller in amplitude than those in rats cannulated 3 days before collection, but were not significantly different from each other. In many of the rats cannulated immediately before or 2 days before blood collection, pulsatile growth hormone release was completely suppressed. The results of the study suggest that blood sampling from right atrial cannulae to measure the plasma concentration of rat growth hormone should not be carried out until at least 3 days after the cannulation procedure.

Animals↗
PubMed1985

Pituitary gonadotroph adenomas in old Sprague-Dawley rats.

Light microscopic and immunocytologic investigation revealed focal or diffuse pituitary gonadotroph hyperplasia in 3/27 male and 3/39 female Sprague-Dawley rats over 2 years of age. Three male and 2 female rats exhibited proliferation of morphologically abnormal gonadotrophs which were described as nodules, and 4 male and 5 female rats possessed gonadotroph adenomas which contained both immunoreactive beta-LH and beta-FSH. On plastic sections at the ultrastructural level, a further female rat was found to possess focal gonadotroph hyperplasia, 2 male and 2 female rats, gonadotroph nodules and 2 male and 2 female rats gonadotroph adenomas. While extensive gonadotroph and thyrotroph hyperplasia was observed in the nontumorous portion of the 2 pituitaries harboring thyrotroph adenoma, widespread gonadrotroph hyperplasia was noted in only 2 of 13 pituitaries with gonadotroph adenoma. Gonadotroph adenomas appeared to develop from discrete foci of morphologically altered gonadotrophs. These foci probably then progressed to form nodules and subsequently adenomas. Gonadotrophs within the nodules were often similar in morphology to adenomatous gonadotrophs whereas the earlier, smaller lesions were pleomorphic or more commonly trabecular in appearance. Serum LH levels were measured in some animals. As a group, rats displaying changes in gonadotroph morphology had a higher mean serum LH level than those without these changes, however, the values ranging from 23-249 ng/ml were well within the normal serum LH levels reported in aging rats. Gonadotroph adenomas in human patients have only recently been identified with accuracy and are relatively uncommon. As in the case of rats, they do not appear to arise from a pre-existing end organ hypofunction or pre-existing gonadotroph hyperplasia. A suitable animal model, in the form of spontaneously occurring gonadotroph adenomas in aging rats, might be useful in establishing the etiology, biochemical properties and appropriate therapy for these tumors.

Adenoma↗
PubMed1984

Stability of dopamine in an in vitro incubation system using Medium 199.

This study investigated the stability of exogenous dopamine (DA) in vitro in a commercially available medium (Medium 199), with and without additional ascorbic acid, during incubation with pituitary halves in prolactin secretion experiments. After a 3-h incubation period, 26 and 15% of the starting concentrations of DA were degraded in the absence and presence of 1 mM ascorbic acid, respectively; in the absence of pituitary tissue, these reductions in DA concentration were 19% and 0%, respectively. In contrast, 98% of DA was degraded after 3 h of incubation in Krebs-Henseleit bicarbonate buffer which contained no tissue or no antioxidants. A number of antioxidants (including a low concentration of ascorbic acid) which are already present in Medium 199 are most likely responsible for the relative stability of DA in this medium. The loss of DA during incubation in Medium 199 is considered small for this type of study, and additional ascorbic acid only marginally improves DA stability in this medium. We have concluded that there is no need to be overly concerned about the degradation of exogenous DA in vitro for some incubation experiments using Medium 199, and the addition of extra ascorbic acid (which may be deleterious) is not necessary.

Animals↗
PubMed1984

Cysteamine acts immediately to inhibit prolactin release and induce cellular changes in estradiol-primed male rats.

Cysteamine (CSH) has an inhibitory effect on the secretion of PRL, GH and TSH. The purpose of the present study was twofold: (1) to examine the short-term effects of CSH on PRL secretion, and (2) to elucidate the mechanism of action of CSH. CSH (100 mg/kg) was injected as an intra-atrial bolus to both normal and estradiol-primed male Sprague-Dawley rats. Blood samples were drawn every 2 min for 1 h and assayed for PRL. To determine if the actions of CSH involved PIF release or PIF receptors, a dopamine receptor blocking agent, pimozide (100 micrograms/kg) was given intra-atrially 1 h after the CSH injection and PRL concentration was monitored. Within 6 min after the CSH injection PRL levels in estradiol-primed rats began to fall, and by 30 min postinjection the levels were well below baseline values. Blocking the dopamine receptors with pimozide did not result in increased PRL levels, indicating that CSH was acting through some mechanism not directly involving dopaminergic PIF receptors. In a separate study, 6 min after the injection of CSH the rats were decapitated and their anterior pituitaries were removed and processed for electron microscopy. Only mammotrophs from estradiol-primed rats treated with CSH showed an extensive rearrangement of rough endoplasmic reticulum (RER) in concentric whorls around the periphery of the cells. These studies show that the inhibition of PRL secretion by CSH begins within 6 min, and is appreciable only when basal PRL levels are increased by estrogen priming.(ABSTRACT TRUNCATED AT 250 WORDS)

Animals↗
PubMed1984

Gamma-aminobutyric acid is not likely a physiological prolactin-inhibiting factor.

Basal plasma prolactin concentration is controlled by tonic inhibition. The major prolactin-inhibiting factor (PIF) is believed to be dopamine. Factors other than dopamine have also been suggested as possible physiological PIF. One of the major candidates for the nondopaminergic PIF is considered to be gamma-aminobutyric acid (GABA). We have carefully examined the possible physiological role of GABA by monitoring, at every 2 min, the circulating prolactin concentration after GABA administration, in conscious freely moving rats. GABA (0.1 or 1 g/kg) had no significant direct effect on plasma prolactin in rats in which the dopaminergic receptors were completely blocked by pimozide, nor in hypophysectomized rats in which a pituitary had been grafted under the kidney capsule and was therefore removed from any hypothalamic influence. The effects of bicuculline, a GABA-receptor-blocking agent, was examined in order to find out whether a tonic inhibition is exerted by GABA after elimination of tonic dopaminergic inhibition on prolactin secretion. The pimozide-treated rat in which the dopaminergic tone is completely eliminated did not show any prominent elevation of plasma prolactin concentration after bicuculline (300 micrograms/kg) administration. However, GABA did have an inhibitory effect in a primary pituitary cell monolayer culture system. Therefore, we conclude that GABA does not play a significant role as a physiological PIF and that the inhibitory effect of GABA in vitro is of a pharmacological nature.

Animals↗