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Query: UMLS:C0432222 (SEM)
 47,337 document(s) hit in 31,850,051 MEDLINE articles (0.00 seconds)

The mean fasting serum secretin level determined in newborn swine was found to be 298.0 +/- (SEM) 5 pg/ml, significantly higher than that in the adult animal. Intraduodenal infusion of 0.1 N HCl produced dramatic elevation of the mean serum secretin level to 2,090 +/- 340 pg/ml. The tissue secretin concentration of duodenal mucosa as well as the molecular species of tissue secretin were found to be identical to that of the adult swine. The mean disappearance half-life of exogenously administered secretin in the newborn swine was significantly prolonged over adult values, to 3.6 min. These data suggest that delayed secretin degradation can be implicated as a factor in the etiology of the hypersecretinemia in the newborn swine.
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PMID:Secretin levels in plasma and tissue of the neonatal swine. 712 6

Immunoreactive plasma motilin concentrations were studied following a variety of stimuli in 24 healthy fasting subjects. Plasma motilin was measured by a radioimmunoassay using antibody GP 71 (J. C. Brown) and natural porcine motilin as standard. Basal motilin levels ranged from undetectable to 365 pg/mL. Antral and intraduodenal infusion of 50 mL o.1 N HCl (pH 1.2) at 5 mL/min failed to alter significantly plasma motilin levels but duodenal acid infusions at 17 mL/min caused a significant increase (70.8 +/- 29.5 pg/mL, mean +/- SEM; n = 6), maximal at 40 min. Duodenal alkalinization with 50 mL 0.3 M Tris buffer (pH 8.0) infused at 5 mL/min produced no change in plasma motilin. A mixed meal did not affect plasma motilin levels. Ingestion of 60 g fat significantly increased plasma motilin (n = 13; maximal increase 150.3 +/- 43.3 pg/mL at 30 min) but duodenal infusions of fat failed to increase plasma motilin levels. These results suggest that motilin secretion induced by fat requires that the fat be present initially within the stomach for secretion to occur. We conclude that ingested fat is a potent stimulus of motilin release. As duodenal acidification (50 mL 0.1 N HCl over 10 min) induces duodenal activity resembling migrating motor complexes but does not release motilin, our data argue against the release of motilin following duodenal acidification as a trigger for the initiation of these complexes in man.
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PMID:Changes in plasma motilin concentration in response to manipulation of intragastric and intraduoduenal contents in man. 722 46

Our aim was to determine whether endogenously released gastrin inhibits cyclic interdigestive motility in the proximal stomach. In 4 dogs with chronic duodenal electrodes and isolated innervated antral pouches, we constructed proximal gastric pouches, the external neural connections of which were completely severed by autotransplanting the pouches to the left pelvis. After recovery, the antral pouch was irrigated with 0.2% acetylcholine for 3.7 hr at 90 ml/hr, while intraluminal pressure was monitored in the proximal gastric pouch and myoelectric activity was recorded from the duodenum. Blood was collected concurrently for radioimmunoassay of gastrin. The antral irrigations increased serum gastrin from a mean +/- SEM of 85 +/- 14 pg/ml before irrigation to a mean +/- SEM of 350 +/- 54 pg/ml after 30 min of irrigation (P less than 0.001), and the increased levels continued throughout the remaining 3.2 hr of irrigation. The irrigations also suppressed the cycles of interdigestive motor activity in the proximal gastric pouch and the cycles of interdigestive myoelectric activity in the duodenum. The cycles had a mean duration +/- SEM of 105 +/- 5 min before irrigation in both the proximal gastric pouch and duodenum, but were abolished in every test during irrigation. Irrigation inhibited the cycles even when cimetidine was given intravenously at 200 mg/hr to block gastrin-stimulated secretion of HCl, duodenal acidification, and subsequent release of duodenal hormones. However, cimetidine alone had no effect on the interdigestive cycles. We concluded that antral irrigation with acetylcholine inhibited interdigestive cyclic motility in the proximal stomach via a hormonal mechanism and that gastrin was likely the hormone involved.
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PMID:Can endogenous gastrin inhibit canine interdigestive gastric motility? 735 58

Studies were initiated to determine whether resident nuclear estrogen receptors with unfilled binding sites existed in the nuclear fraction of uteri from untreated immature rats. These studies revealed a small population (mean +/- SEM, 0.087 +/- 0.017 pmol/uterus) of unfilled estrogen-binding sites in the uterine nuclear fraction from untreated immature rats, which bound [3H]estradiol in the absence of added cytoplasmic receptor. These nuclear estrogen-binding sites occurred in addition to the 0.60--1.2 pmol estrogen-binding activity/uterus in the uterine cytoplasmic fraction of these animals. [3H]Estradiol bound reversibly with high affinity (apparent Kd = 1.4 x 10(-10)M to these binding sites, and only estrogenic compounds competed for this binding. Binding studies done at a variety of temperatures (0--37 C) showed that there were no estradiol-filled receptor sites associated with the nuclear fraction. In addition, these unfilled nuclear estrogen-binding sites remained unfilled 15 min after injections of either 1.0 or 0.1 micrograms estradiol/rat. Extraction of these sites was achieved with 0.4 M KCl, and when this extract was centrifuged on a 5--20% linear 0.010 M Tris-HCl, 0.0015 M Na2EDTA, and 0.40, M KCl sucrose gradient, the binding activity exhibited a sedimentation coefficient of 3.6S. These unfilled nuclear estrogen-binding sites did not appear to have arisen as a contaminant from the estrogen-binding proteins present in either uterine cytoplasm or serum during tissue homogenization. The existence of these unfilled nuclear estrogen-binding sites does not represent a major exception to the classical two-step theory of estrogen action; instead, they seem to be novel forms of the estrogen receptor whose physiological role has not been determined.
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PMID:Characterization of a unique population of unfilled estrogen-binding sites associated with the nuclear fraction of immature rat uteri. 737 93

Trifluoroacetate (TFA), the major metabolite of halothane, was assayed by a newly developed isotachophoretic technique. This technique has several advantages over the presently used methods of analysis. It requires no special preparation of urine or blood samples. The sample volume is small (5--100 microliters) and the analysis time is short (30--90 min per sample). In addition, the method provides an analysis that is both qualitative and quantitative over a wide range of concentrations (from 2 nanomoles in 200 microliters to 200 nanomoles in 5 microliters). In this study, the assay was performed using HCl (0.001 M) in 1 per cent Triton X-100, titrated with beta-alanine to a pH value of 3.6--3.9 as the leading electrolyte and n-caproic acid (0.01 M) as the terminal electrolyte (50--100 muA migration current). Using this technique, daily urinary TFA excretion of seven patients was measured during halothane anesthesia and for 14 days postoperatively. The TFA values were highest on the second postoperative day (317--1,259 mg). The mean values of the urinary TFA excreted during the entire study (2,501 +/- 493 mg, mean +/- SEM) were much higher than those reported previously. The isotachophoretic technique provides a sensitive assay for future research into the biotransformation of halothane.
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PMID:Quantitative analysis of trifluoroacetate in the urine and blood by isotachophoresis. 738 9

Ischemia of the gastric epithelium has emerged as one of the more likely mechanisms for gastric ulceration. Radiolabeled microspheres (15 mu) were used to measure blood flow to exteriorized, chambered stomach segments in eight dogs during the development of aspirin erosions. Flow determinations were made before aspirin (20 mM in 140 mM HCl) exposure and at 2, 10, and 20 minutes after the initiation of the chemical insult. Lesions formed at 30 minutes of acetylsalicylic acid exposure. The epithelium was separated into normal and injured, based on gross discoloration caused by intramucosal hemorrhage. The calculated blood flows to the abnormal and normal mucosa were identical at 2 minutes (0.22 +/- 0.04 versus 0.15 +/- 0.03, NS) and at 10 minutes (0.39 +/- 20 versus 0.17 +/- 0.04, NS) after initiation of aspirin injury (all values in ml/gram-wet weight/min, mean +/- SEM). By 20 minutes of aspirin exposure, mucosal blood flow to areas that eventually became injured was greater than the blood flow to areas that remained normal (0.45 +/- 0.12 versus 0.13 +/- 0.05 P less than 0.05). The data suggest that ischemia does not play a role in chemical erosive gastritis.
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PMID:Focal microcirculatory changes during the production of aspirin-induced gastric mucosal erosions. 746 23

To evaluate the possibility that insulin-like growth factors (IGFs) and their binding proteins (BPs) in bone play a role in regulating cortical bone formation in growing animals, we compared changes in IGF and IGF BP levels with changes in bone mineral density (BMD) at three different regions (proximal, middle, and distal) along the rabbit femoral shaft. BMD measured by dual-energy x-ray absorptiometry decreased progressively from proximal to distal regions of the shaft, from 0.449 +/- 0.005 to 0.354 +/- 0.002 g/cm2 (mean +/- SEM; n = 9), respectively; total protein concentrations also decreased toward the distal region. We extracted the IGFs and their BPs from bone by demineralization in 10% EDTA and 4 M guanidine-HCl (pH 4.5). The IGFs were then separated from their BPs by size exclusion HPLC. The pH of the extraction buffer profoundly influenced the recoveries of the IGFs and, to a lesser extent, the total protein; at least 100% more IGFs were recovered at acid (4.5) pH than at neutral (7.5) or basic (10.5) pH. The levels of IGF-I decreased markedly from proximal to distal regions, from 273 +/- 27 to 100 +/- 38 ng human IGF-I equivalent/g bone (or 103 +/- 10 to 52 +/- 11 ng human IGF-I equivalent/mg protein), respectively. IGF-II was uniformly distributed (385 +/- 17 ng human IGF-II equivalent/g bone; mean of all three regions). Levels of the predominant 28-32 kD IGF BP doublet increased by about 100% from proximal to distal segments, regardless of whether the data were expressed per unit mass or protein.(ABSTRACT TRUNCATED AT 250 WORDS)
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PMID:Differential distribution of insulin-like growth factors and their binding proteins within bone: relationship to bone mineral density. 753 48

The ontogenic destruction of dopamine (DA) neurons in rat brain is associated with supersensitization of DA D1 receptors. This effect is attenuated when rats are cotreated in ontogeny with the serotonin (5-HT) neurotoxin, 5,7-dihydroxytryptamine (5,7-DHT). In an attempt to determine whether 5-HT fibers might have a similar modulatory role on the sensitivity of the DA D2 receptor complex, we pretreated rats with desipramine HCl (20 mg/kg, IP, base), 1 h before the DA neurotoxin, 6-hydroxydopamine (6-OHDA; 134 micrograms ICV, base) and/or 5,7-DHT (75 micrograms ICV) and/or vehicle. At about 3 months after birth dose-effect curves for quinpirole-induced oral activity were constructed for each group of rats. We found that quinpirole, an agonist for the DA D2 receptor complex, produced a dose-related increase in oral activity in all groups of rats. After a 200 micrograms/kg dose of quinpirole HCl, however, neonatal 5,7-DHT-lesioned rats had a peak oral response of 54.4 +/- 5.1 (mean and SEM) vs. 22.6 +/- 4.8 for control rats (p < 0.01). In neonatal 6-OHDA-lesioned rats this dose of quinpirole increased oral activity to 36.8 +/- 5.8 oral movements (p < 0.05 vs. control). In rats lesioned with both 5,7-DHT and 6-OHDA, the oral response was not different from control. The enhanced oral response to quinpirole in 5,7-DHT-lesioned rats was attenuated by spiperone, an antagonist for the DA D2 receptor complex.(ABSTRACT TRUNCATED AT 250 WORDS)
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PMID:Enhanced quinpirole response in rats lesioned neonatally with 5,7-dihydroxytryptamine. 761 14

The selective muscarinic M1 receptor antagonist, pirenzepine, considerably stimulates duodenal mucosal bicarbonate secretion in the rat and increases gastric luminal release of prostaglandin E2 (PGE2) in humans. This study, therefore, looked at the effect of pirenzepine on bicarbonate secretion and luminal output of PGE2 into the stomach and the duodenum of nine healthy volunteers using a new technique permitting simultaneous measurements. In the stomach modified sham feeding increased bicarbonate secretion from 382 (62) mumol/h (mean (SEM)) to 959 (224) mumol/h (p < 0.02). In the duodenum modified sham feeding and acid exposure (HCl 0.1 M; 20 ml; 5 min) of the duodenal bulb increased mucosal bicarbonate secretion from 191 (14) mumol/cm x h to 266 (27) mumol/cm x h (p < 0.02) and 634 (157) mumol/cm x h (p < 0.01), respectively. Pirenzepine (10 mg/h intravenously) reduced basal and vagally stimulated gastric and basal duodenal bicarbonate secretion by about 50% (p < 0.03). In the stomach, but not the duodenum, basal and vagally stimulated PGE2 output increased significantly (p < 0.05) in response to pirenzepine. In conclusion, human gastroduodenal mucosal bicarbonate secretion is regulated by a pirenzepine sensitive mechanism, which is probably cholinergic. The rise in gastric PGE2 output seen in response to M1 receptor inhibition by pirenzepine suggests the existence of a feed back loop secondary to the decrease seen in bicarbonate secretion.
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PMID:Muscarinic M1 receptor inhibition reduces gastroduodenal bicarbonate secretion and promotes gastric prostaglandin E2 synthesis in healthy volunteers. 773 58

In the present publication we report mainly electrophysiological studies on oxyntopeptic cells of frog gastric mucosa which aim at clarifying a possible involvement of these cells in the process of resting gastric alkali (HCO3-) secretion, described in the preceding publication. The experiments were performed on intact gastric fundus mucosa of Rana esculenta mounted in Ussing chambers. After removal of the muscle and connective tissue layer oxyntopeptic cells were punctured from the serosal surface with conventional or pH-sensitive microelectrodes to measure, besides transepithelial voltage and resistance, the basolateral cell membrane potential, the voltage divider ratio, and the cell pH in response to secretagogues and/or changes in serosal ion concentration. Carbachol (10(-4) mol/l), which transiently stimulated HCO3- secretion by 0.22 mumol.cm-2.h-1, transiently acidified the cells by 0.09 +/- SEM 0.03 pH units (n = 6) and transiently induced an apical cell membrane anion conductance. According to the model of gastric HCO3- secretion presented in the preceding publication, this anion conductance could be involved in gastric HCO3- secretion, mediating, besides Cl- efflux, also apical HCO3- efflux. In addition carbachol stimulated basolateral Na+(HCO3-)n-cotransport, which according to the results from the preceding publication mediates basolateral HCO3- uptake for secretion. By contrast, cAMP-mediated secretagogues, such as histamine or others, which stimulate HCl secretion and transiently alkalinize the oxyntopeptic cells, were found to down-regulate the basolateral Na+(HCO3-)n-cotransporter.(ABSTRACT TRUNCATED AT 250 WORDS)
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PMID:Model of bicarbonate secretion by resting frog stomach fundus mucosa. II. Role of the oxyntopeptic cells. 783 89


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