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Biomedical subjects

P L Rayford

Publications and source records attributed to P L Rayford.

At least 73 records · Page 4Linked to original sources
PubMed1989

[The effect of gastrectomy on cholecystokinin (CCK) release and gallbladder contraction in patients with early gastric cancer--preliminary report].

Gastrectomy has been implicated in cholelithiasis. Impaired gallbladder motor function after the operation has been thought to be one of the major mechanisms. This study was undertaken to determine the effect of gastrectomy on release of cholecystokinin and contractile motility of gallbladder in five patients with early gastric cancer. After 14 hours fast, the gallbladder area was estimated by ultrasonography every 10 minutes for 120 minutes both before and after oral administration of 200 ml of Clinimeal. Blood samples were collected simultaneously via a peripheral vessel for measurement of plasma CCK levels by radioimmunoassay. Gallbladder contraction correlated well with the elevation of plasma CCK levels indicating that CCK might be one of the major factors governing gallbladder contraction both in pre- and post-gastrectomized conditions. Compared with preoperative cases, the postgastrectomized patients showed a significantly exaggerated postprandial response of CCK release in the initial 60 minutes, however, their gallbladder, responding to rapid reduction of plasma CCK levels, refilled significantly earlier. Postprandial rapid gastric emptying was thought to be related to the exaggerated postprandial CCK release, and the early refilling of the gallbladder might be attributed to the indefinite vagal or sympathetic denervation that might occurs during the necessarily wide lymph node dissections for gastric cancer operations.

Aged↗
PubMed1988

Circadian rhythms in gastrin receptors in rat fundic stomach.

Circadian rhythmicity in the number of gastrin receptors in rat fundic mucosa was characterized and was related to the concentrations of gastrin in serum and in antrum. Male Sprague-Dawley rats were acclimated to 12 hr light alternating with 12 hr darkness. Subgroups of six rats each were killed at 4-hr intervals. Fundic mucosa was collected for measurement of gastrin receptors; serum and antral tissues were collected for measurement of gastrin levels by radioimmunoassay. Circadian periodicity in the data was determined by cosinor analyses. In both freely fed and fasted rats, gastrin receptors showed circadian variation (range 2.5-10 fmol/mg protein), as did serum gastrin concentrations (range in fed rats 195-407 pg/ml). The phasing of the intrinsic circadian variation in gastrin receptor level that was observed in the fasted rats was advanced by a few hours in fed rats. This shift is probably due to food-induced gastrin release, resulting in gastrin-mediated down-regulation of gastrin receptors, followed by up-regulation of gastrin receptors. Food-related effects were thus superimposed upon the intrinsic circadian rhythms in gastrin receptor levels, causing the circadian variation in gastrin receptor levels in the fed rats to be shifted forward compared to that in the fasted rats. No significant circadian rhythms, on the other hand, were found in concentrations of gastrin in the antrum. These results suggest that changes in sensitivity of target tissues to hormones are related to both intrinsic circadian rhythms in levels of hormone receptors and also to food-related changes in hormone-receptor levels mediated by changing serum hormone levels.

Analysis of Variance↗
PubMed1988

Daily variations in the formation of gastric ulcers caused by cervical cord transection in the rat.

Cervical spinal cord transection is used as a model of mammalian stress ulcerogenesis. Circadian variations in gastric ulceration have been demonstrated in other animal models. We investigated whether gastric ulceration changed after cervical cord transection throughout a 24-h period by subjecting different groups of rats to cord transection. Ulcers were quantitated using an index described by Szabo and colleagues. Ulcer formation showed significant variation as a function of time of lesioning, with least severe ulceration at 8 AM. We found that cord transection, like other models of gastric ulceration, is also influenced by the circadian system.

Animals↗
PubMed1988

Restricted feeding schedules alter the circadian rhythms of serum insulin and gastric inhibitory polypeptide.

Insulin and gastric inhibitory polypeptide (GIP) have a circadian rhythm of secretion that is altered by various feeding schedules. We acclimated rats over 3 weeks to one of 6 different feeding schedules. They were then killed at intervals over one feeding cycle. Blood was collected, and their stomachs were weighed. Hormones in the serum were measured by radioimmunoassay. When highest and lowest measured concentrations were compared in ad libitum fed rats, insulin more than doubled (445 +/- 50 to 993 +/- 180 pg/ml) and GIP more than tripled (682 +/- 108 to 1964 +/- 145 pg/ml) during a 24-h period. With restricted schedules, concentrations correlated with the feeding schedule, not the light-dark cycle. Hormone levels rose higher during feeding and fell lower with fasting than in ad lib fed rats. For example, GIP in one study fluctuated from 468 +/- 22 to 6433 +/- 432 pg/ml. In another example, insulin ranged from 30 +/- 5 to 2259 +/- 406 pg/ml during a 24-h period. However, insulin did not always correlate well with stomach weight. Circadian rhythms occurred for insulin with all feeding schedules and for GIP with all schedules except fasted rats. This finding implies an endogenous insulin rhythm, whereas food intake controls GIP secretion. Thus, disruption of normal circadian cycles of feeding may yield misleading information about gut hormone secretion.

Animals↗
PubMed1988

Effect of L364718, a new CCK antagonist, on amylase secretion in isolated rat pancreatic acini.

We examined the effect of L364718, a new cholecystokinin (CCK) receptor antagonist, on amylase release stimulated by CCK or different secretagogues in isolated rat pancreatic acini. L364718 caused a parallel rightward shift of the dose-response curve of CCK8. Schild plots showed a slope of 1.05 +/- 0.15 and a pA2 value of 10.01 +/- 0.31. L364718 inhibited maximally stimulated amylase release by CCK in a dose-dependent manner, with half maximal inhibition (ID50) at 1.7 nM and complete inhibition at 30 nM. Asperlicin, a prototype compound of L364718, also caused dose-dependent inhibition, but L364718 was approximately 400 times more potent than asperlicin (ID50 = 761 nM). L364718 significantly inhibited amylase release in response to CCK33 and CCK8 but had no effect on amylase release stimulated by other receptor secretagogues or agents by passing receptors. The results indicate that L364718 acts as an extremely potent, competitive, and specific antagonist of CCK's action on pancreatic acini.

Amylases↗
PubMed1987

Synthetic neuromedin C stimulates exocrine pancreatic secretion in dogs and rats.

We have examined the effect of neuromedin C on exocrine pancreatic secretion both in vivo and in vitro, and compared its bioactivity with those of related peptides. In anesthetized dogs, neuromedin C caused a dose-dependent initial reduction of pancreatic blood flow and an increase in secretin-stimulated exocrine pancreatic secretion, and had almost the same potency as gastrin-releasing peptide (GRP) in decreasing pancreatic blood flow. A potent stimulatory effect on exocrine pancreatic secretion was found in conscious dogs accompanied by a significant elevation in the circulating cholecystokinin (CCK) levels. In isolated rat pancreatic acini, amylase was released dose-dependently in response to neuromedin C. This study demonstrates that neuromedin C (a smaller molecular form of GRP) possesses potent bioactivity on exocrine pancreas and suggests that two factors may be involved in the mechanism by which this peptide effects exocrine secretion, namely; direct stimulation on acinar cells and stimulation of CCK release.

Amino Acid Sequence↗
PubMed1987

Circadian rhythms of serum gastrin and plasma cholecystokinin in rodents.

Fluctuations in serum gastrin and plasma cholecystokinin (CCK) over a 24-hr period were examined in fasted and freely fed adult BALB/c mice and Sprague Dawley rats. Eighty-four mice and 84 rats were caged in groups of (six) each and placed in separate isolation chambers with light from 0600 to 1800 hr (CST) daily (LD 12:12). After standardization for 30 days, one-half of the animals were fasted 24 hr prior to circadian sampling, and the remainder were allowed continuous access to food. Animals were removed and killed by rapid cervical dislocation every 4 hr beginning at 0800 hr for seven time points. Blood was collected and serum gastrin and plasma CCK were measured by specific radioimmunoassays. The data document a circadian bioperiodicity for serum gastrin and plasma CCK. The parameters of the rhythms, evaluated by cosinor rhythmometric methods, are characterized by an acrophase that occurs in the dark period for both fed and fasted rodents and a mesor that is higher in fed than fasted animals. Circadian sampling time and nutritional status appear to be important in studies involving serum levels of gastrin and plasma CCK in rodents.

Animals↗
PubMed1987

Release of cholecystokinin and gallbladder contraction before and after gastrectomy.

The contraction of the gallbladder by ultrasonography and release of cholecystokinin (CCK) by specific radioimmunoassay in response to the ingestion of oral fatty meal before and 1 month after gastrectomy in five patients with early gastric cancer was studied. Before gastrectomy, basal concentrations of CCK (13.4 +/- 2.3 pmol/L) rose significantly to a maximum of 23.3 +/- 3.6 pmol/L at 20 minutes after ingestion of oral fatty meal, and remained significantly elevated during the study. Gallbladder contraction began as CCK concentrations rose, demonstrating significant correlation with plasma CCK. One month after gastrectomy, CCK showed a rapid and greater response to the ingestion of fatty meal, attaining a maximum of 53.7 +/- 7.3 pmol/L at 10 minutes, then gradually falling to basal level. The maximal contraction of the gallbladder after gastrectomy was almost the same as before gastrectomy (62.7 +/- 4.0% of original area), showing a significant correlation with plasma CCK, but refilling of the gallbladder was induced earlier with corresponding reduction of plasma CCK. Simultaneous measurement of plasma concentrations of pancreatic polypeptide revealed a fairly similar response to plasma CCK before and after gastrectomy. The release of CCK is the chief mechanism by which the ingestion of a fatty meal causes contraction of the gallbladder even after gastrectomy as well as before gastrectomy.

Aged↗
PubMed1986

Influence of obstructive jaundice on pancreatic growth and on basal plasma levels of cholecystokinin and gastrin in rats.

Obstructive jaundice was produced in rats by ligation and transection of bile duct outside the liver; the control group underwent laparotomy alone. Pancreatic wet weight, amylase, lipase, protein, DNA, RNA, RNA/DNA ratio, and weight/100 micrograms DNA were significantly increased in jaundiced rats when compared to control rats. Histologic evaluation of pancreatic tissue obtained from jaundiced rats revealed the appearance of large or multiple nuclei in pancreatic acinar cells. Basal plasma levels of immunoreactive CCK were significantly increased in jaundiced rats at two weeks and four weeks but, when compared to the levels obtained in laparotomized controls at those time intervals, CCK levels were not significantly different. In jaundiced rats, plasma immunoreactive gastrin was found to be significantly decreased at two and four weeks. Plasma gastrin levels were also found significantly decreased when the jaundiced group was compared with laparotomized control group. The results suggest that obstructive jaundice induced enlargement of the pancreas, probably due to hyperplasia and hypertrophy of pancreatic cells. Whether or not this phenomenon is related to changes in gastrin and CCK is not known.

Amylases↗
PubMed1986

An antiserum that recognizes mesotocin and isotocin: development of a homologous radioimmunoassay for plasma mesotocin in chickens (Gallus domesticus).

This report presents characteristics of an antiserum raised in a rabbit immunized with synthetic mesotocin (MT) conjugated to bovine thyroglobulin. Cross-reactivity studies indicate that the antiserum (Kl-II) recognizes the carboxyl-terminal "tail" of MT and isotocin (IT). A homologous, disequilibrium radioimmunoassay (RIA) for MT has been developed that can detect less than 1 pg of peptide. Plasma was extracted with octadecasilyl-silica. Recovery of MT from plasma was correlated with the amount added and averaged 70%. Different volumes of plasma and posterior pituitary extract, when measured in the assay system, yielded inhibition curves that were parallel with standard MT. Immunoreactive MT and AVT of plasma and neural lobe coeluted with synthetic standards after gel filtration. The ED50 of a heterologous, sequential saturation RIA for IT was 17.4 pg, suggesting that the MT antiserum may be useful for measuring the oxytocin-like principle in bony fishes. Immunoreactive MT in plasma of cockerels increased and decreased with iv infusion of hypo- and hyperosmotic saline, respectively. The changes in plasma MT were inversely related to osmolality. Hyperosmotic saline infusion resulted in correlated increases in plasma AVT and osmolality. The data suggest that MT may be released by dilution and/or expansion of extracellular fluid in chickens.

Animals↗
PubMed1986

Cholecystokinin-destroying activities of canine tissue homogenates.

We have studied the capacity of different canine tissue homogenates to destroy cholecystokinin in vitro. Tissues from the kidney cortex, lung, pancreas, and small bowel contained significant cholecystokinin-destroying activity. Only small amounts of activity were found in the liver, and no activity was detected in the kidney medulla, the gastric antrum, gallbladder, spleen, or in serum or plasma. The kidney cortex was the richest source of activity. The cholecystokinin-destroying enzyme isolated from the kidney cortex was heat-labile, non-dialyzable, and trypsin-resistant, with an optimum pH between 7 and 7.4. The enzyme was inhibited by chelating agents and by phenylalanine amide, although it was little affected by phenylalanine itself or proteinase inhibitors. The enzyme required divalent cation cofactors for its activity. After inhibition by EDTA, the enzyme could be reactivated completely with Mn2+, but not with Ca2+ or Mg2+ alone. The cholecystokinin-destroying enzyme was bound strongly to membranes, and during differental centrifugation, was sedimented with mitochondrial fractions of kidney cortex. The supernatant fraction of the solubilized enzyme obtained at 105,000 X g had a molecular weight of about 480,000 dalton. Since the enzyme could be inhibited by phenylalanine-amide, it would appear to act at the C-terminal end of the cholecystokinin molecule.

Animals↗
PubMed1986

Relationship of omeprazole-induced hypergastrinemia to gastric pH.

The increase in gastrin caused by the gastric proton pump inhibitor, omeprazole, is presumably secondary to inhibition of gastric acid secretion but could also be due to a direct effect on the gastrin cells. This experiment was designed to determine whether gastrin elevations caused by omeprazole are related to intragastric pH. We studied gastrin release and acid output in response to 10% peptone broth (400 ml) in five dogs with gastric fistulas. The broth, at pH 5.5 or 2.5, was instilled into the stomach through the cannula, and the desired pH was maintained by intragastric titration with 0.1N NaHCO3 for 2 hours. Studies at each pH level were performed on separate days before, during, and after omeprazole (10 mumol/kg daily for 20 days). Omeprazole increased intragastric pH to greater than or equal to 3.5 for 24 hours. At pH 5.5 omeprazole inhibited acid secretion and increased gastrin levels; however, setting the intragastric pH at 2.5 completely blocked omeprazole's effect on gastrin release. Therefore these data support the hypothesis that the hypergastrinemia caused by omeprazole is dependent on gastric pH and gastric acid suppression.

Animals↗
PubMed1984

Specificity of cholecystokinin antibody may influence choice of tracer for radioimmunoassay.

When CCK33 was iodinated at His 20 with lactoperoxidase, the labelled hormone was less immunoreactive under radioimmunoassay conditions than CCK39 which is readily iodinated at Tyr 1. Since the difference in immunoreactivities could not be due to different degrees of oxidative damage, the regional specificity of the assay antibody (UT122, from the laboratory of J.C. Thompson, University of Texas) was re-examined. A synthetic parital sequence, CCK33 6-16, which had similar conformation to the same sequence in the intact peptide, as shown by CD analysis, was devoid of immunoreactivity. Results with sulphated and non-sulphated C-terminal octapeptides of the hormone, CCK8 (CCK33 27-33), indicate limited dependence of the C-terminal region for binding to antibody. Thus, the lower binding with 125I-CCK33 than with 125I-CCK39 indicates that His 20 is an important feature of the immunogenic site and that the iodine atom is large enough to cause steric hindrance. This explains why the method of iodination might have to be varied depending on the regional specificity of antibodies.

Amino Acid Sequence↗
PubMed1983

Biologic and radioimmunologic activity of cholecystokinin in regions of mammalian brains.

The distribution and heterogeneity of cholecystokinin (CCK) in different regions of the central nervous system (CNS) of 12 adult rats and six cows was determined by means of specific radioimmunoassays. In addition, the biologic activity of immunoreactive material was evaluated in a bioassay that used a rabbit gallbladder-strip preparation. High amounts of immunochemically detectable CCK-8 (20.2 +/- 1.5 pmol/g) and CCK-33 (33.7 +/- 3.3 pmol/g) and of biologically active CCK were found in the telencephalon, although concentrations decreased progressively from the rostral to the caudal portions of the brain. The distribution and biologic activity of CCK was similar in rat and cow brain. Ratios of biologic to immunologic activity ranged from 1.0 to 8,0 and were higher for CCK-8 than for CCK-33. The results indicate that (1) CCK-8 and CCK-33 immunoreactivity are widely distributed throughout the CNS in a unique and differential manner; (2) CCK is biologically active in all the regions of the brain, with a pattern of distribution similar to that found with radioimmunoassay; (3) measurable bioactivity was equal to or greater than measurable immunoreactivity in all areas of the brain in rat and cow; and (4) CCK is present in tissues without significant species differences between rat and cow.

Animals↗
PubMed1983

Potentiation of Cd-induced pulmonary injury in alpha 1-antitrypsin suppressed rats.

The interrelationship of alpha 1-antitrypsin (alpha 1-AT) or serum trypsin inhibitor capacity (TIC) level and cadmium exposure in the induction of pulmonary lesions was investigated. Sprague-Dawley rats were exposed to CdCl2, galactosamine, or galactosamine + CdCl2 for 24 hr. Biochemical study indicated a 20% reduction of serum TIC in animals exposed to galactosamine. A marked, 50%, reduction of serum TIC was induced in animals exposed to galactosamine + CdCl2. Histopathological study revealed no major morphological lesions in lungs of animals exposed to either CdCl2 or galactosamine. However, extensive lesions, including polymorphonuclear leukocyte (PMN) infiltration, distortion and distention of the alveolar spaces, and massive hemorrhages were observed in the lungs of animals exposed to galactosamine + CdCl2. It is believed that cadmium can induce rapid lesions in the pulmonary tissues when the alpha 1-AT is significantly suppressed. The present investigation has provided direct evidence on the importance and interrelationship of cadmium and alpha 1-AT in pulmonary lesion development.

Animals↗