Search PubMed⌕ Search

Biomedical subjects

P L Rayford

Publications and source records attributed to P L Rayford.

At least 55 records · Page 3Linked to original sources
PubMed1991

Tissue and plasma levels of immunoreactive gastrin and cholecystokinin in chickens with and without bombesin.

Immunoreactive gastrin and immunoreactive cholecystokinin were measured in chicken tissue extracts obtained from the gut and brain. In contrast to that found in mammals, immunoreactive gastrin found in chickens was higher in the brain than in gut tissues, and it was highest in the ileum when compared with other gut tissues. Dose-response curves of tissue extracts from the brain and ileum and of serum were parallel to the dose-response curve of synthetic human gastrin, suggesting the existence of gastrin or a peptide immunologically similar to gastrin in those chicken tissues. Immunoreactive cholecystokinin in tissues was highest in the duodenum, followed by the jejunum, ileum, and cortex; lesser amounts of cholecystokinin were found in other tissues. Influence of bombesin on the release of immunoreactive gastrin and immunoreactive cholecystokinin in the blood of chickens was also studied. Bombesin doses of 3 micrograms/kg per hour significantly increased immunoreactive gastrin in serum and immunoreactive cholecystokinin in plasma, whereas gastrin did not increase with a bombesin dose of 0.6 micrograms/kg per hour. The results confirm the existence of immunoreactive gastrin and immunoreactive cholecystokinin in the tissue of chickens and indicate that they are released into circulation in response to bombesin.

Animals↗
PubMed1990

Receptor binding of cholecystokinin analogues in isolated rat pancreatic acini.

The receptor binding of CCK analogues was determined in terms of the inhibition of [125I]CCK binding in isolated rat pancreatic acini. The inhibition curve produced by CCK-8 showed the same feature as that produced by synthetic human CCK-33. The relative potency values of CCK analogues to half-maximally inhibit specific CCK binding were calculated; CCK-8 was equal to human CCK-33, 3-fold stronger than natural porcine CCK-33 and 39, and 700-fold stronger than the unsulphated form of synthetic human CCK-33. Our data suggest that CCK-33, one of the longer molecular forms of CCK, is as important as CCK-8 in the mechanism of physiological actions of CCK.

Animals↗
PubMed1990

Effects of dietary protein alterations on circadian rhythms of gastrointestinal peptides in rats.

Altered protein diets and circadian rhythms of gastrin and cholecystokinin (CCK) were investigated in 126 male and 126 female Sprague-Dawley rats acclimated for two weeks to a 12:12 hr light-dark cycle. Rats were divided equally and fed low-protein (8%), high-protein (64%) or normal protein (27%) diets for four weeks. All animals were fasted for 24 hr prior to blood collections. Blood samples were collected at 4-hr intervals for 24 hr for determination of plasma gastrin and CCK using specific radioimmunoassays. A significant rhythm for gastrin was detected in males on normal and low-protein diets (P less than 0.03) and in females on low-protein diets (P less than .02). A significant rhythm for CCK was detected (P less than 0.05) in rats of both sexes fed normal and high-protein diets. Mean plasma levels of both peptides were lower in females than males. In a separate study, food intake and body weight were monitored in male rats receiving the three diets over 21 days. Animals on the low-protein diet exhibited reduced food intake and body weight compared to rats fed the normal or high-protein diets.

Animals↗
PubMed1990

Metabolic and pathologic effects of nicotine on gastrointestinal tract and pancreas of rats.

We examined in male Sprague-Dawley rats the effects of nicotine at doses of 50 (0.31 mM) and 200 mg/L (1.23 mM) given for a period of 16 weeks on body weight gain, food and fluid intake, plasma CCK, glucose and insulin levels, amylase secretory responses of isolated pancreatic acinar cells to CCK-8 and carbachol, and histopathology (gross and light microscopy) of stomach and pancreas. These parameters were re-examined further in animals treated with nicotine at doses of 200 mg/L (1.23 mM) for 12 weeks and given tap water for an additional 4 weeks to evaluate the effects of nicotine withdrawal. Metabolic data suggest that decreases in body weight gain, food and fluid intake, and plasma levels of glucose and insulin by nicotine are dose dependent. Endocrinological studies showed that the plasma levels of CCK were significantly increased with nicotine but the amylase secretory response of pancreatic acinar cells was inhibited in response to CCK-8 and carbachol. Histopathologic data revealed that treatment of animals with a high dose of nicotine enhanced the appearance of numerous vacuoles in the pancreatic acinar cell cytoplasm. When the pancreatic acinar cell morphology was closely examined, it showed evidence of pyknotic nuclei and fusion of vacuoles. Prominent loss of gastric mucosal surface was found in nicotine-treated animals with gross microscopic evidence of bleeding ulcers. All of the metabolic parameters except body weight gain were reversed upon nicotine withdrawal. In addition, plasma CCK levels and pancreatic enzyme secretion were reversed upon nicotine withdrawal.(ABSTRACT TRUNCATED AT 250 WORDS)

Amylases↗
PubMed1990

Effect of synthetic human cholecystokinin-33 on pancreatic blood flow in dogs.

We have examined the effect of synthetic human cholecystokinin (CCK-33 and CCK-8) on pancreatic blood flow and protein output in anesthetized dogs. Human CCK-33 and CCK-8 increased pancreatic blood flow and protein output in a dose-related manner. There were no significant differences in increasing pancreatic blood flow between human CCK-33 and CCK-8, and increases in blood flow were closely related to the increase of the pancreatic enzyme secretion. L-364,718 (20 nmol/kg) caused a potent inhibition of CCK-stimulated pancreatic blood flow as well as protein output. The degree of inhibition by L-364,718 was dependent on the amount of CCK infused. This study demonstrates that increasing effect on pancreatic blood flow may be one of the biological actions of CCK mediated via CCK receptor. The CCK-33, one of longer molecular forms of CCK, is an important biological stimulator of pancreatic blood flow as well as of exocrine pancreatic secretion.

Animals↗
PubMed1990

Hyperosmolal formula in neonatal piglets: effects on gastrointestinal hormone concentrations, enteric bacterial titers, and small intestinal histology.

Ingestion of hyperosmolal formula (HOF) by neonatal piglets has been shown to cause significant time-dependent reduction in phase 3 myoelectric activity, which persists in the terminal ileum. To determine whether a single hyperosmolal meal leads to elevated concentrations of gastrointestinal (GI) hormones that inhibit intestinal motility and/or promote bacterial proliferation and disruption of intestinal mucosa, we studied 20 healthy neonatal piglets following feeding with an increased HOF (872 +/- 32 mOsmol/kg, n = 10) and commercial pig milk formula (481 +/- 41 mOsmol/kg, n = 10). Gastrin, secretin, cholecystokinin, and motilin concentrations were determined by radioimmunoassay during fasting and postprandial periods (15, 30, 45, 120, 180, and 240 min). Gastrin concentrations were significantly increased at 15 and 30 min following a hyperosmolal meal (p less than 0.01), but there were no statistical differences in GI hormone concentrations between groups. These transient elevations of gastrin concentrations are associated with significant postprandial reductions in phase 3 small intestinal myoelectric activity (SIMEA) that we have observed. Aerobic bacterial titers were not significantly different between proximal and distal small intestinal segments or between experimental groups, and anaerobic bacteria were seldom recovered. Thus, SIMEA was not sufficiently altered to produce significant bacterial proliferation. Small intestinal histology, assessed by light microscopy, showed normal proximal and distal small intestinal mucosa in 8 of 10 piglets from each group. Therefore, orogastric instillation of a single hyperosmolal feed does not result in intestinal mucosal damage. Further studies are warranted to determine the effects of hyperosmolal feeds when additional risk factors exist in the neonate.

Animal Feed↗
PubMed1989

L-364,718, a new CCK antagonist, inhibits postprandial pancreatic secretion and PP release in dogs.

The effects of L-364,718, a new CCK receptor antagonist, on food-stimulated exocrine pancreatic secretion and plasma levels of PP, insulin, CCK, and gastrin were examined in four conscious dogs with pancreatic fistulas. Intravenous injections of L-364,718 (20 nmol/kg) significantly inhibited pancreatic protein and enzyme responses by food (33% inhibition) but not juice volume output. Both rapid and secondary prolonged postprandial rises of plasma PP were also significantly suppressed by L-364,718 (50% inhibition); however, plasma levels of insulin were not altered. Postprandial levels of gastrin were not affected by L-364,718 administration, whereas 3-hr integrated CCK response was significantly enhanced by L-364,718. This study indicates that L-364,718 inhibits pancreatic protein and enzyme secretion and the release of pancreatic polypeptide stimulated by food in conscious dogs. This inhibition might be due to the selective blockage of receptor binding of circulating CCK molecules. The results suggest that L-364,718 may be useful for the physiological and pathophysiological studies associated with CCK.

Animals↗
PubMed1989

Effect of natural peptide YY on pancreatic secretion and cholecystokinin release in conscious dogs.

The effects of natural peptide YY on pancreatic secretion under different stimulatory conditions and on fatty acid-induced cholecystokinin release were examined in five conscious dogs with pancreatic and gastric fistulas. Intravenous infusion of natural peptide YY at 1 and 0.2 microgram/kg/hr caused 60 and 40% inhibition of secretin- and cholecystokinin-stimulated secretion, respectively, and 40-50 and 20-40% inhibition of intraduodenal oleate stimulated secretion, respectively. A significant but transient decrease in the plasma cholecystokinin level was observed in response to peptide YY under oleate stimulation. The present study demonstrates that peptide YY has a potent inhibitory effect on both exogenously and endogenously stimulated pancreatic secretion and has a mild suppressive effect on fatty acid-induced cholecystokinin release suggesting that this peptide is an important colonic inhibitor of pancreatic secretion.

Animals↗
PubMed1989

Total small bowel resection inhibited bombesin-stimulated release of cholecystokinin and pancreatic polypeptide in anesthetized cats.

In anesthetized cats, immunoreactive cholecystokinin (CCK), pancreatic polypeptide (PP), and gastrin were released in response to bombesin both before and after small bowel resection. Total small bowel resection significantly decreased bombesin-stimulated release of cholecystokinin and pancreatic polypeptide without affecting the release of gastrin. Integrated analysis showed that CCK, pancreatic polypeptide, and gastrin were released in significant quantities after small bowel resection. The results show that total small bowel resection caused significant inhibition of bombesin-stimulated release of cholecystokinin and pancreatic polypeptide; in contrast, gastrin release remained unaffected. The data further indicate that extra bowel sources of cholecystokinin exist in cats and the release of CCK from those sources occurred following bombesin stimulation.

Anesthesia↗
PubMed1989

Inhibition of CCK or carbachol-stimulated amylase release by nicotine.

This study was undertaken to investigate the mechanisms of action of nicotine on receptor mediated enzyme secretion in isolated rat pancreatic acini. Acinar cells were isolated from untreated and nicotine treated rats by collagenase digestion and differential centrifugation. Cells from the untreated animals were incubated with either varying concentrations of nicotine (range 10 microM to 30 mM) or with a fixed dose of 10 mM nicotine with varying concentrations of carbachol(10nM to 100 microM). Cells from the nicotine treated animals(16 weeks in drinking water) were incubated with either a fixed dose of CCK-8(10(-10) M) or carbachol(10(-5) M). All incubations were conducted at 37 C for 30 min. Amylase released in the media was measured by spectrophotometry. In pancreatic acinar cells isolated from control rats, amylase release stimulated by carbachol was inhibited by nicotine. Acinar cells isolated from rats treated with nicotine at nicotine concentrations of 1.23 mM also showed significant inhibition of amylase release in response to CCK-8 and carbachol compared to their identical controls. Nicotine induced inhibition curves of amylase release stimulated by carbachol were non-parallel suggesting that the effect of nicotine on acinar cells is regulated by mechanisms other than carbachol receptors. Nicotine may have a direct inhibitory effect on the intracellular mechanisms of pancreatic enzyme secretion. We conclude that the mechanism by which nicotine inhibits pancreatic enzyme secretion is complex.

Amylases↗
PubMed1989

Photoperiod influences the growth of colon cancer in mice.

We have developed a mouse colon adenocarcinoma cell line that produces tumors in a dose-dependent manner when injected subcutaneously. Our previous work has demonstrated its sequential pattern of tumor area and weight under 12L:12D (12 hours light, 12 hours darkness) photoperiod. This study investigated whether shorter (6L:18D) or longer (18L:6D) photoperiods alter tumor growth. Significantly greater tumor area, weight, and group mortality were found in mice exposed to 12L:12D photoperiods as compared to either 6L:18D or 18L:6D photoperiods, and difluoromethylornithine (DFMO) was a more effective inhibitor of tumor growth under the 6L:18D photoperiod compared to 12L:12D. These results demonstrate an important role of photoperiod on tumor growth.

Adenocarcinoma↗
PubMed1989

Weight loss and altered circulating GI peptide levels of rats exposed chronically to nicotine.

This study was undertaken in male Sprague-Dawley rats to test the hypothesis that chronic ingestion of a low dose of nicotine suppresses body weight gain. The results from this study suggest that chronic nicotine ingestion induces weight loss in rats without the loss of their food intake. To determine whether the nicotine-induced body weight reductions are associated with endocrinological changes, the levels of gastrin and CCK in plasma were measured by specific radioimmunoassays and were found significantly elevated during chronic ingestion of nicotine. The data indicate that reduction of body weight mass by nicotine might be dependent on both hormonal and metabolic factors.

Animals↗
PubMed1989

Mechanism of action of nicotine on amylase release by isolated pancreatic acini.

The effects of nicotine on the pH of acinar suspension, amylase release and on amylase response stimulated by carbachol were examined in isolated rat pancreatic acini. Additions of nicotine at concentrations ranging from 10 microM to 30 mM caused dose-dependent increases in pH of acinar suspension with simultaneous amylase release (p less than 0.05). There was no increase in amylase release when acinar cells were incubated with nicotine adjusted to pH 7.40. Carbachol alone released amylase whereas nicotine (pH 7.40) at a concentration of 10 mM caused a significant and nonparallel inhibition of amylase release in response to graded doses of carbachol. At concentrations ranges between 3 microM and 10 mM, nicotine at pH 7.40 inhibited amylase release stimulated by 1 microM carbachol, with a half maximal inhibition at 0.8 +/- 0.2 mM. These results indicate that in isolated rat pancreatic acini nicotine at pH 7.40 has no effect on basal nonstimulated amylase release but it inhibits carbachol-stimulated amylase response in a noncompetitive manner. These observations may have direct implications in underlying mechanism of pancreatic disorders.

Amylases↗
PubMed1989

Effect of L-364,718 on GRP-stimulated pancreatic and gastric secretions and GI peptides in conscious dogs.

The effect of L-364,718, a cholecystokinin (CCK) receptor antagonist, on exocrine pancreatic secretion, gastric secretion, and plasma levels of gastrointestinal (GI) peptides stimulated by gastrin-releasing peptide (GRP) was examined in five conscious dogs. Intravenous infusion of graded doses of synthetic porcine GRP (18, 36, and 178 pmol/kg/h) caused significant and dose-dependent increases in pancreatic and gastric juice secretion and in plasma levels of pancreatic polypeptide (PP), CCK, and gastrin. Intravenous injection of L-364,718 (20 nmol/kg) significantly inhibited GRP-stimulated pancreatic outputs of juice volume, protein, and amylase and plasma PP release. L-364,718, however, did not affect gastric juice volume and plasma levels of CCK and gastrin. The results suggest that endogenously released CCK is, at least in part, responsible for GRP-stimulated pancreatic protein and enzyme secretions and PP release in dogs. The results further suggest that GRP-stimulated pancreatic secretion might be, in part, a direct response of GRP to exocrine pancreas.

Animals↗
PubMed1989

Neural mechanisms of pancreatic polypeptide release in conscious dogs.

L364,718, a potent and specific antagonist for peripheral cholecystokinin (CCK) receptors, was used to determine its effect on plasma levels of pancreatic polypeptide (PP) after administration of 2-deoxy-D-glucose (2-DG, a central vagal activator) and of bethanechol (a cholinergic receptor agonist). Six conscious dogs were used in this study. Intravenous injection of 2-DG (75 mg/kg) caused significant increases in plasma levels of PP and gastrin, but there was no significant rise in plasma levels of immunoreactive and bioactive CCK. Intravenous injection of L364,718 (20 nmol/kg) significantly inhibited the PP response stimulated by 2-DG injection by approximately 60% but did not affect gastrin. Plasma levels of PP were increased dose dependently by bethanechol infusion and were not altered significantly by injections of L364,718. The results indicate that L364,718 inhibits PP response stimulated by a central vagal activator (2-DG) but not by cholinergic receptor agonist (bethanechol). This study suggests that CCK might be involved in the neural control of PP release as a neurotransmitter but probably not as a final activator of PP cells in dogs.

Animals↗
PubMed1989

DNA synthetic activity in tumor-bearing mice.

The rate of DNA synthesis in normal tissues exhibits circadian rhythmicity. However, there have been conflicting reports of the effects of tumor burden on the circadian rhythm of DNA synthesis in non-cancer tissues. We have developed a mouse colon cancer (MC-26) that exhibits different growth under different photoperiods. The purpose of this study was to analyze DNA synthetic activity in tissues removed from tumor-bearing and tumor-free mice maintained under two different photoperiods. Two groups each of approximately 80 male Balb/c mice were acclimated to one of two light-dark cycles, 12L:12D or 6L:18D. Half of each group were injected with 5.0 x 10(4) MC-26 cells. Twenty-two days later, all mice were killed in subgroups at 4-6 hr intervals over one 24-hr period. Colons and tumors were removed for measurement of DNA synthesis. Results were analyzed by means of one-way analysis of variance (ANOVA) in order to determine whether DNA synthesis varied significantly within groups over the 24-hr period. The DNA synthetic activity, as measured by uptake of tritiated thymidine, exhibited significant temporal variation in the colons of control (tumor-free) mice under both the 12L:12D and 6L:18D photoperiods. The colons of tumor-bearing mice failed to exhibit a fluctuation under a 12L:12D photoperiod but did show a significant 24-hr rhythm under the 6L:18D photoperiod. The subcutaneously growing cancers did not exhibit a circadian variation in DNA synthetic activity under either photoperiod. Both photoperiod and the presence of cancer appear to affect the DNA synthetic activity observed in mice bearing the MC-26 colon cancer.

Animals↗
PubMed1989

Twenty-four-hour variations in ornithine decarboxylase and acid phosphatase in mice.

Polyamines are essential for cell growth and differentiation. Ornithine decarboxylase (ODC) is the rate-limiting enzyme in polyamine biosynthesis. Acid phosphatases (AP) are lysosomal enzymes that are important in normal intracellular metabolism. Twenty-four-hour variations in these enzymes may be important in understanding the temporal responses of different tissues to various stimuli. The purpose of this study was to examine a variety of tissues for fluctuations in the levels of ODC and AP over a 24-hr period. Significant circadian variations in the amount of ODC activity were observed in all tissues examined. Activity of AP varied with time of day in the liver, kidney, and heart. The highest and lowest measurements of ODC activity were as follows: liver, 81.5 +/- 7.0, 47.9 +/- 4.4; colon, 11.7 +/- 1.2, 3.1 +/- 0.7; stomach 3.1 +/- 0.4, 0.9 +/- 0.1; kidney, 420.9 +/- 0.9, 67.5 +/- 0.8; and heart, 4.7 +/- 1.0, 2.5 +/- 0.2. The highest and lowest measurements of AP activity were as follows: liver 3.8 +/- 0.1, 2.8 +/- 0.1; kidney, 3.4 +/- 0.1, 1.9 +/- 0.1; and heart, 2.6 +/- 0.1, 2.0 +/- 0.1. These findings suggest that rhythmic fluctuations in polyamine biosynthesis and lysosomal enzymes may influence other metabolic pathways differentially throughout 24 hr.

Acid Phosphatase↗