To determine whether exocrine pancreatic secretion is regulated by endogenous somatostatin, somatostatin deficiency was induced by cysteamine. Rats were subcutaneously administered a single dose of cysteamine (30 mg/100 g body weight) 12 hr before experiment. Anesthetized rats were prepared with cannulation into bile duct, pancreatic duct, duodenum, and jugular vein and pancreatic juice was collected. For in vitro study, isolated pancreata of rats, pretreated with cysteamine, were perfused with an intraarterial infusion of Krebs-Henseleit solution (37 degrees C) at 1.2 mL/min, and pancreatic juice was collected in 15-min samples. In vivo experiment of the rat, the mean basal pancreatic secretions, including volume, bicarbonate, and protein output were significantly increased from 18.4+/-0.5 microL/30 min, 0.58+/-0.05 microEq/30 min, and 214.0+/-26.1 microg/30 min to 51.6+/-3.7 microL/30 min, 1.52+/-0.11 microEq/30 min, and 569.8+/-128.9 microg/30 min, respectively (p<0.05). In the isolated perfused pancreas, cysteamine also resulted in a significant increase in basal pancreatic secretion (p<0.05). Simultaneous intraarterial infusion of octreotide (10 pmol/hr) to isolated pancreata partially reversed the effect of cysteamine on basal pancreatic secretion. These findings suggest that endogenous somatostatin play an important role on the regulation of basal pancreatic exocrine secretion.
Animal ; Cysteamine/pharmacology* ; Hormone Antagonists/pharmacology* ; Hormones, Synthetic/pharmacology ; In Vitro ; Male ; Octreotide/pharmacology ; Pancreas/secretion ; Pancreas/drug effects* ; Perfusion ; Rats ; Rats, Sprague-Dawley ; Somatostatin/antagonists & inhibitors*

OBJECTIVETo evaluate the application of gonadotrophin-releasing hormone antagonist (GnRH-ant) in patients with risk of poor response to controlled ovarian stimulation in IVF-ET.

METHODSClinical data of 48 patients undergoing IVF with or without ICSI were retrospectively analyzed. Among them 24 patients were allocated to the GnRH-ant protocol and 24 to the long gonadotrophin-releasing hormone agonist (GnRH-a) protocol. The duration of down-regulation, duration of stimulation, amps of gonadotropin estradiol level on hCG day, number of oocytes retrieved, fertilization rate, total embryos obtained, high quality embryo obtained, embryos transferred, embryos frozen, implantation rate per transfer, clinical pregnancy rate per transfer, embryo survival rate, clinical pregnancy rate per frozen embryos transfer and per cycle were compared between two groups.

RESULTThe duration of down-regulation, duration of stimulation, the amps of gonadotropin were significantly lower in the antagonist group than those in agonist group (P <0.001, <0.05, <0.05), the estradiol level on hCG day, the number of oocytes retrieved were significantly lower in the antagonist group than those in the agonist group (P<0.05, <0.05). No significant differences were noted in fertilization rate, total embryos obtained, high quality embryo obtained, embryos transferred, embryos frozen, implantation rate per transfer, clinical pregnancy rate per transfer, embryo survival rate, clinical pregnancy rate per frozen embryos transfer and per cycle.

CONCLUSIONCompared with long GnRH-a protocol, the GnRH-ant protocol in patients with risk of poor response can reduce the dosage of gonadotropin and shorten the duration of stimulation, although the estradiol level on hCG day and the number of oocytes retrieved are lower, which does not affect the implantation rate and clinical pregnancy rate.

Adult ; Embryo Transfer ; Female ; Fertilization in Vitro ; Gonadotropin-Releasing Hormone ; agonists ; antagonists & inhibitors ; Hormone Antagonists ; pharmacology ; therapeutic use ; Humans ; Infertility, Female ; therapy ; Ovulation Induction ; methods ; Retrospective Studies

AIMIn order to explore the mechanism of central motilin-induced feeding behavior, the effects of erythromycin, a motilin receptor agonist, on glucose responsive neurons in hypothalamus were observed.

METHODSExtracellular recordings were made from single neurons in region of lateral hypothalamic area (LHA) and ventromedial hypothalamic nucleus (VMH) in anesthetized rats. On the basis of their responsiveness to intracarotid injection of 0.58 mol/L glucose solution 0.2 ml, glucose-sensitive neurons (GSNs) in LHA and glucoreceptor neurons (GRNs) in VMH were recognized. Effects of intracerebroventricularly (i. c. v.) administration of 4 microg erythromycin on neural activities of glucose responsive neurons and non-glucose responsive neurons were examined. The mixture of EM and GM-109 1 microl were used to GSNs and GRNs which were sensitive to i. c. v. administration of EM.

RESULTSIn LHA, EM increased activity of GSNs significantly (P < 0.05 vs non-glucose-sensitive neurons group). Whereas in VMH, EM significantly decreased the activities of GRNs (P < 0.01 vs non-glucoreceptor neurons group). The mixture of EM and GM-109 had no effect on GSNs and GRNs.

CONCLUSIONEM, a motilin receptor agonist, can stimulate GSNs in LHA and suppress GRNs in VMH and this may contribute to central motilin's effect on feeding behavior.

Animals ; Erythromycin ; pharmacology ; Hypothalamus ; cytology ; Neurons ; cytology ; drug effects ; Rats ; Rats, Wistar ; Receptors, Cell Surface ; metabolism ; Receptors, Gastrointestinal Hormone ; antagonists & inhibitors ; Receptors, Neuropeptide ; antagonists & inhibitors

OBJECTIVETo investigate the effect of the non-PLC-dependent protein kinase C (PKC) pathway of parathyroid hormone (PTH) on the apoptosis and proliferation of osteoblast MC-3T3E1 cells.

METHODSMC-3T3E1 cells were seeded in 96-well plates at the density of 1.5×10(4) cells/mL and incubated for 3 day. The cells were then exposed to 100 nmol/L of [Gly(1), Arg(19)]hPTH(1-28), 100 nmol/L of [Gly(1), Arg(19)]hPTH(1-34), 100 nmol/L of [Gly(1), Arg(19)]hPTH(1-34)+1 µmol/L Go6983, 1 µmol/L Go6983, or deionized water (control) for 1, 24 or 48 h. After the treatments, cell counting kit-8 (CCK-8) and Caspase-Glo® 3/7 Assay (Caspase-3) were used to examine the proliferation and apoptosis of MC3T3-E1 cells.

RESULTSCCK-8 results showed that hPTH(1-34) increased the number of MC3T3-E1 cells compared with hPTH(1-34)+Go6983 at 1 h and 24 h, but this difference was not statistically different. At 48 h, treatment with hPTH(1-34), as compared with hPTH(1-28), significantly increased the number of MC3T3-E1 cells (P<0.05), and this effect was blocked by the PKC inhibitor Go6983 (P<0.05). hPTH(1-34) did not result in significant inhibition of MC3T3-E1 cell apoptosis at 1 h and 24 h as compared with hPTH(1-34)+Go6983, but significantly inhibited the cell apoptosis as compared with hPTH(1-28) (P<0.05); this inhibitory effect was blocked by Go6983 (P<0.05).

CONCLUSIONs A relatively long time (for 48 h) of exposure to PTH can inhibit apoptosis and promote the proliferation of MC3T3-E1cells through a non-PLC-dependent PKC pathway.

3T3 Cells ; Animals ; Apoptosis ; Cell Proliferation ; Indoles ; pharmacology ; Maleimides ; pharmacology ; Mice ; Osteoblasts ; Parathyroid Hormone ; pharmacology ; Protein Kinase C ; antagonists & inhibitors ; metabolism ; Signal Transduction

Aged ; Aged, 80 and over ; Androgen Antagonists/pharmacology* ; Androgens/blood* ; Cohort Studies ; Gonadotropin-Releasing Hormone/antagonists & inhibitors* ; Hormones/blood* ; Humans ; Luteinizing Hormone/blood* ; Male ; Middle Aged ; Orchiectomy ; Prostatic Neoplasms/surgery* ; Toremifene/therapeutic use*

To determine the adequate models for studying the functions of pancreatic acinar cells, secretory responses to CCK and to CCK receptor antagonist, L-364, 718 were examined in freshly isolated cells and confluent monolayer cells. The results showed that as CCK concentration increased, releases of amylase and lipase increased dose-dependently reaching a maximum at 10(-9) M in acinar cells cultured in serum-containing media as well as in serum-free media. Acinar response to CCK was partially inhibited by L-364, 718, L-364, 718 itself had no effect on the releases of both amylase and lipase. Confluent monolayer of acinar cells released relatively low levels of enzymes and exhibited less response to CCK. In conclusion, short-term culture of acinar cells would be suitable to study the regulation of pancreatic enzyme secretion, and serum factors do not influence acina response to the secretagogues. However, confluency of the acinar cells resulted in the loss of their secretory potential in the aspect of amylase and lipase release.
Amylases/secretion ; Animal ; Benzodiazepinones/pharmacology ; Cells, Cultured ; Cholecystokinin/*pharmacology ; Devazepide ; Dose-Response Relationship, Drug ; Hormone Antagonists/pharmacology ; Lipase/secretion ; Male ; Pancreas/cytology/*drug effects/*secretion ; Rats ; Rats, Sprague-Dawley ; Receptors, Cholecystokinin/antagonists & inhibitors ; Support, Non-U.S. Gov't

OBJECTIVETo study the effect of purariae isoflavone on estrogen level in ovariectomized rats.

METHOD80 rats were divided into four groups randomly, every group with 20 rats: 1. Control group; 2. Normal + purariae isoflavone group; 3. Ovariectomized group; 4. Ovariectomized + purariae isoflavone group. Estrogen level and gonadotropin-releasing hormone level of all rats were measured.

RESULTThirty days after being ovariectomized, E2, E3 level was significantly lower than that of the first group(P < 0.05). But Testerone, FSH, LH, PRL and GH increased(P < 0.05). After being gastrogavaged with purariae-isolfavone for thirty days, Estrogen level and gonadotropin-relasing hormone level of the second group were significantly lower in various degree than those of normal control group (P < 0.05). But in ovariectomized rats, the estrogen level was recovered (P > 0.05). The gonadotropin-releasing hormone level was increased (P < 0.05).

CONCLUSIONPurariae-isoflavone can increase estrogen level to normal in ovariectomized rats by way of increasing the level of gonadotropin-releasing hormone. In normal rats, it has anti-estrogen effect.

Animals ; Estradiol ; blood ; Estriol ; blood ; Estrogen Antagonists ; pharmacology ; Female ; Gonadotropin-Releasing Hormone ; blood ; Isoflavones ; isolation & purification ; pharmacology ; Ovariectomy ; Plants, Medicinal ; chemistry ; Pueraria ; chemistry ; Rats ; Rats, Sprague-Dawley

OBJECTIVETo observe the role of NB127914, a CRF R1 receptor antagonist, in the regulation of neonatal sleep/wake cycle.

METHODSRat pups were surgically implanted with electrodes at postnatal day(PN) 13. At PN 14, 6 hours polysomnographic recording data were continuously collected before and after administration of various doses of NBI 27914, atropine and the same amount of saline.

RESULTSCompared with baseline, rapid eye movement (REM) sleep was significantly reduced and was replaced primarily by non-REM (NREM) sleep in all groups treated with NBI, but not with dimethyl sulfoxide/saline. Atropine suppressed REM sleep significantly and increased wakefulness simultaneously.

CONCLUSIONBlockage of corticotropin-releasing factor (CRF) R1 receptors deprives neonatal rat REM sleep.

Aniline Compounds ; pharmacology ; Animals ; Female ; Male ; Polysomnography ; Pyrimidines ; pharmacology ; Rats ; Rats, Sprague-Dawley ; Receptors, Corticotropin-Releasing Hormone ; antagonists & inhibitors ; Sleep, REM ; drug effects ; physiology ; Wakefulness ; drug effects ; physiology

The effect of electroacupuncture (EA) on experimental colitis was investigated in Sprague-Dawley rats. Colitis was induced by intracolonic instillation of 4% acetic acid. EA (2 Hz, 0.05 ms, 2 V for 20min) was applied to bilateral Hoku (LI-4) and Zusanli (ST-36) on 12 hrs and 36 hrs after induction of colitis. EA-treatment significantly reduced the macroscopic damage and the myeloperoxidase activity of colonic samples at 3 days post-induction of colitis. Colitic colon showed a decreased in vitro motility. However, colonic motility of EAtreated group was not significantly different from that of normal group. The anti-inflammatory effect of EA was not inhibited by a glucocorticoid receptor antagonist, RU-486, but suppressed by a beta-adrenoceptor antagonist, propranonol. These results suggest that EA-treatment has a beneficial effect on colitis, and its anti-inflammatory effect is mediated by beta-adrenoceptor activation but not by endogenous glucocorticoiddependent mechanism.
Acetic Acid ; Adrenergic beta-Antagonists/pharmacology ; Animals ; Carbachol/pharmacology ; Cholinergic Agonists/pharmacology ; Colitis/chemically induced/enzymology/pathology/*therapy ; Electroacupuncture/*veterinary ; Enzyme Inhibitors/metabolism ; Gastrointestinal Motility/physiology ; Hormone Antagonists/pharmacology ; Male ; Mifepristone/pharmacology ; Muscle Contraction/physiology ; Muscle, Smooth/drug effects/physiology ; NG-Nitroarginine Methyl Ester/pharmacology ; Peroxidase/metabolism ; Propranolol/pharmacology ; Rats ; Rats, Sprague-Dawley

Corticotrophin-releasing factor (CRF) plays a major role in coordinating stress responses. We aimed to test whether blocking endogenous CRF activity can prevent the stress-induced dilation of intercellular spaces in esophageal mucosa. Eighteen adult male rats were divided into 3 groups: 1) a non-stressed group (the non-stressed group), 2) a saline-pretreated stressed group (the stressed group), 3) and an astressin-pretreated stressed group (the astressin group). Immediately after completing the experiments according to the protocol, distal esophageal segments were obtained. Intercellular space diameters of esophageal mucosa were measured by transmission electron microscopy. Blood was sampled for the measurement of plasma cortisol levels. Mucosal intercellular spaces were significantly greater in the stressed group than in the non-stressed group. Mucosal intercellular spaces of the astressin group were significantly smaller than those of the stressed group. Plasma cortisol levels in the stressed group were significantly higher than in the non-stressed group. Pretreatment with astressin tended to decrease plasma cortisol levels. Acute stress in rats enlarges esophageal intercellular spaces, and this stress-induced alteration appears to be mediated by CRF. Our results suggest that CRF may play a role in the pathophysiology of reflux-induced symptoms or mucosal damage.
Animals ; Corticotropin-Releasing Hormone/*antagonists & inhibitors/metabolism/pharmacology ; Esophagus/anatomy & histology/*drug effects ; Extracellular Space/*drug effects ; Hydrocortisone/blood ; Male ; Mucous Membrane/anatomy & histology/*drug effects ; Neuroprotective Agents/pharmacology ; Peptide Fragments/*pharmacology ; Rats ; Rats, Wistar ; *Stress, Psychological/blood/physiopathology