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Biomedical subjects

L R Johnson

Publications and source records attributed to L R Johnson.

At least 253 records · Page 14Linked to original sources
PubMed1977

New aspects of the trophic action of gastrointestinal hormones.

This paper deals with several new findings regarding the trophic action of gastrointestinal hormones. Naturally occurring gastrins (G-17 I, G-17 II, G-34 II) stimulated DNA synthesis and increased total DNA content of gastric mucosa. These were several times more potent than pentagastrin on a molar basis. In a survey of various tissues from the gastrointestinal tract, pentagastrin exerted trophic effects on mucosa of the oxyntic gland area, duodenum, and colon; it had no effect on the esophagus, antrum, or diaphragm. Maximal stimulation (200% of control) of colonic DNA synthesis was produced by 250 mug of pentagastrin per kg. Vasoactive intestinal peptide did not stimulate DNA synthesis when given alone and inhibited the trophic effect of pentagastrin when administered simultaneously. Glucagon stimulated DNA synthesis in both colon and oxyntic gland mucosa to 40% of the increase caused by pentagastrin and did not inhibit the effects of pentagastrin when administered concurrently.

Animals↗
PubMed1976

Relationship between the changes in gastrin levels and intestinal properties in the starved rat.

Intestinal DNA, RNA, and protein content were decreased to a greater extent than was body weight when rats were starved for 3 days. Specific lactase and maltase activity increased with progressively longer periods of starvation. Antral and serum gastrin concentration significantly decreased during the 3 days of starvation. Pentagastrin (250 mug/kg 3 times daily) was injected into a group of rats for the duration of a 3-day starvation period and caused a small but significant increase in the relative intestinal RNA and protein content and decreased lactase and maltase specific activities in comparison with the levels of 3-day starved controls. Pentagastrin thus partially reversed some of the starvation-induced changes toward fed levels. Thus, a deficiency in the trophic hormone gastrin may be partially responsible for the disproportionate changes in intestinal tissue during starvation.

Animals↗
PubMed1976

Serum and antral gastrin levels in rats infected with intestinal parasites.

Serum and antral gastrin were measured in rats infected with either Trichinella spiralis or Hymenolepis diminuta as a step in testing the hypothesis that parasites change certain aspects of host physiology by altering gastrointestinal (GI) hormone levels or responses to GI hormones. Parasitism with T. spiralis was associated with inflammatory changes in the small bowel mucosa and with a significant increase in serum gastrin. Neither changes in hormone level nor inflammation were induced in tapeworm-infected rats. These results reveal the capacity of tissue penetrating parasites to alter the level of circulating gastrin. This finding coupled with considerable indirect evidence suggests that some of the pathologic changes induced in hosts by enteric parasites may be due to changes in functions that are regulated by GI hormones.

Animals↗
PubMed1976

Effect of cholecystokinin and 16,16-dimethyl prostaglandin E2 on RNA and DNA of gastric and duodenal mucosa.

Fasted rats were injected with either cholecystokinin-octopeptide (CCK-OP), 20 mug per kg; 16,16-dimethyl prostaglandin E2 (16,16-dimethyl PGE2), 0.2 mg per kg; pentagastrin, 250 mug per kg, or saline every 8 hr for 48 hr. The rats were killed and the incorporation of [3H]thymidine into DNA as well as the total DNA and RNA content of the mucosa of the oxyntic gland area and the duodenum were determined. Pentagastrin increased DNA synthesis 60% (P less than 0.001) in gastric mucosa and 90% (P less than 0.001) in duodenal mucosa when compared with rates for saline controls. Neither CCK-OP nor 16,16-dimethyl PGE2 altered gastric mucosal DNA synthesis. Pentagastrin significantly increased the DNA and RNA content of both the gastric and duodenal mucosa. CCK-OP and 16,16-dimethyl PGE2 caused a slight but significant increase in duodenal DNA synthesis, CCK-OP did not significantly increase duodenal DNA content, and 16,16-dimethyl PGE 2 increased duodenal RNA but not DNA content. CCK-OP (20 mug per kg) in combination with pentagastrin did not alter the stimulation of gastric DNA synthesis but significantly decreased the effect of pentagastrin on duodenal DNA. A dose of CCK-OP (370 mug per kg) equimolar to 250 mug per kg of pentagastrin did not stimulate DNA synthesis in either tissue and significantly inhibited stimulation by pentagastrin in both tissues. Low doses of CCK-OP (2.5, 5.0, 10.0, 20.0 mug per kg) caused statistically significant increases in DNA synthesis and DNA content of the pancreas, but had no effect on either mucosa of the oxyntic gland area or duodenum. 16,16-Dimethyl PGE2 did not inhibit the stimulation of DNA synthesis or the increases in DNA and RNA content stimulated by pentagastrin. From these results it appears that: (1) moderate doses of CCK have a weak trophic effect in the duodenum but not in the stomach, (2) physiological doses of CCK-OP stimulated pancreatic DNA synthesis and increased pancreatic DNA content without affecting these parameters in the oxyntic gland area or duodenum in the same animals, (3) in the stomach and duodenum CCK is not as potent a trophic hormone as gastrin and inhibits, probably competitively, the trophic effects of gastrin, (4) 16,16-dimethyl PGE2 does not stimulate growth and does not interfere with the trophic response to gastrin even though it inhibits acid secretion, and (5) 16,16-dimethyl PGE2 increased the RNA content of duodenal mucosa indicating that it may stimulate activity resulting in hypertrophy.

Animals↗
PubMed1976

Effect of hypophysectomy and growth hormone on serum and antral gastrin levels in the rat.

The effects of hypophysectomy and subsequent replacement therapy with growth hormone on serum and antral gastrin levels was investigated in both fasted and nonfasted pair-fed rats. Hypophysectomy caused a 57% decrease in serum and 47% decrease in antral gastrin content in 18-hr fasted animals. In nonfasted animals, hypophysectomy resulted in a 42% fall in serum gastrin and a 76% fall in antral gastrin. Animals were given injections of growth hormone over a 10-day period, then fasted 16 to 18 hr before being killed. Doses of 100 to 200 mug per 100 g of body weight were ineffective, but a dose of 500 mug per 100 g was sufficient to restore completely serum gastrin levels to intact control values. In nofasted rats this same dose raised serum gastrin to intact levels and increased antral gastrin significantly over hypophysectomized levels, but did not increase it to control values. When given to pair-fed intact animals, growth hormone caused slight but not significant elevations in serum and antral gastrin. The effect of growth hormone on gastrin secretion and /or synthesis may be a significant physiological factor in the regulation of normal gastrointestinal function and growth.

Animals↗
PubMed1976

Course of infection with enteric parasites in hosts shifted from enteral to total parenteral nutrition.

UNLABELLED: Two groups of rats were kept on an oral diet after infection with 10(4) Trichinella spiralis or 10 Hymenolepis diminuta larvae. Sixteen days and 2 days after infection with H. diminuta and T. spiralis, respectively, 8 rats from each group were switched to intravenous (iv) alimentation, while the remaining animals were retained on oral nutrition as controls. Rats were killed during the following 21 days. The number of T. spiralis recovered from iv-fed rats was significantly higher than in controls, whereas the sex ratio and worm size were similar. Disaccharidase deficiencies normally associated with either infection or parenteral feeding were additive in the infected, parenterally nourished rats. The rise in peroxidase activity normally associated with intestinal trichinosis was not as great (P less than 0.05) in iv-fed rats. Intravenous feeding did not affect tapeworm number, but caused destrobilization. This was followed by secondary proglottization that led to development of worms of normal length and with gravid segments, but with an increased length: weight ratio. CONCLUSIONS: oral food deprivation in the host does not adversely affect development of established T. spiralis. The larger worm burden in iv-fed rats may be due to reduced inflammation normally involved in worm expulsion. Exogenous food in the gut is not necessary for maintaining established H. diminuta; factors necessary for sustenance and growth can be acquired by the worm entirely from the exocrino-enteric circulation.

Animals↗
PubMed1976

Stimulation of DNA synthesis by big and little gastrin (G-34 and G-17).

Fasted rats were injected six times over a 48-hr period with G-17 I, G-17 II, G-34 II in doses doubling from 3.38 nmoles per kg to 54 nmoles per kg. Twelve rats were studied at each dose. NaCl-injected animals were used as controls. The rats were killed and the in vitro incorporation of [3H]thymidine into DNA as well as the total DNA content of the mucosa of the duodenum and oxyntic gland area of the stomach were determined. All gastrins, as well as pentagastrin, stimulated DNA synthesis. Peak stimulation occurred at 13.5 nmoles per kg for G-17 I and G-17 II and at 6.75 nmoles per kg for G-34 II. Pentagastrin's peak trophic effect was produced by 325 nmoles per kg. In order to compare the efficacies of the various types of gastrins, 60 rats were divided into groups of 12. One group received saline and the other four groups received the maximally effective dose of one of the four types of gastrins. The responses to each of the gastrins were not significantly different, and DNA synthesis was doubled in each tissue. Total DNA content increased slightly, but significantly, in response to each gastrin. Several conclusions can be drawn from these data: (1) G-17 and G-34 possess trophic activity; (2) the efficacies of pentagastrin, G-17 I, G-17 II, and G-34 II for the stimulation of DNA synthesis are not significantly different; (3) sulfation of G-17 has no significant effect on its trophic activity; (4) based on the effects of exogenous molar doses and their respective half-lives, both G-17 and G-34 would be expected to contribute to the trophic effect of endogenous gastrin; and (5) G-17 and G-34 are at least as effective in stimulating DNA synthesis as they are in stimulating gastric acid secretion.

Animals↗
PubMed1975

Stimulation of human pepsin output by tropical hydrochloric acid.

Pepsin secretion is stimulated by the back-diffusion of acid across the mucosa of the vagally denervated canine pouch. If back-diffusion is enhanced by damage, pepsin secretion increases. The current study investigates whether this mechanism exists in man. The stomach of normal human volunteers were irrigated for 1 hour with either buffer of 0.01 N HCl, 1 hour with 0.2 N HCl, and a final hour with buffer or 0.01 N HCl. During the middle hour both the concentration and output of pepsin increased three- or fourfold. From these studies it appears that the human gastric mucosa contains a mechanism similar to the dog's which results in the stimulation of pepsin secretion when exposed to acid. This mechanism could be of etiologic significance in gastric ulcer disease, which has been shown to be associated with increased gastric-mucosal permeability.

Adolescent↗
PubMed1975

Intestinal disaccharidase and peroxidase activities in parenterally nourished rats.

The importance of the presence of food in the gastointestinal (GI) tract in maintaining normal enzyme activity in the small intestine was investigated in rats that were kept from eating for as long as 2 weeks. During this time animals were sustained on a nutrient solution administered intravenously. Enzyme activity and small bowel mass in these animals and similiar parameters in rats that were administered the same solution orally were compared with control groups fed an essentially isoenergetic diet of stock rat food and water. Disaccharidase and peroxidase levels in mucosal scrapings expressed as activity/milligram protein, activity/intestine, and activity/100 g body weight, were significantly reduced in intravenously nourished rats but not in rats receiving the solution orally. In addition to changes in enzyme activities, parenteral feeding was accompanied by a significant reduction in the small bowel weight:body weight ratio as compared with that of rats fed the stock diet or nutrient solution orally. Results support the conclusion that normal activity of intestinal enzymes spatially distributed with regard to depth within the mucosa depends on the presence of food in theGI tract and cannot be maintained at normal levels by total intravenous nutrition.

Animal Nutritional Physiological Phenomena↗
PubMed1975

Effect of vagotomy on electrical activity of the small intestine of the dog.

The effect of bilateral thoracic vagotomy on the myoelectric activity of the small intestine was determined in conscious dogs. Animals were implanted with electrodes spaced 25 cm apart along the serosal surface of the small intestine, and a cannula was placed in the most dependent portion of the stomach. Recordings were made with dogs in the fasted and fed states. Two distinct patterns of myoelectric activity were recorded: one typical of the fasted state (the interdigestive myoelectric complex) and one typical of the fed state. After completion of the control recording periods, a truncal vagotomy was performed on each animal. Completeness of vagotomy was confirmed by lack of a gastric secretory response to insulin. Gastric stasis occurred after vagotomy; therefore, the animals' stomachs were emptied via the gastric cannula to obtain a fasted condition. Vagotomy had little to no effect on the fasted pattern of myoelectric activity. The fed pattern was significantly altered in two of the three animals. This alteration could be due to the effect of vagotomy on gastrin release. We conclude that nervous pathways within the vagus may exert some influence on intestinal myoelectric activity but that other neural-humoral pathways are probably involved.

Animals↗
PubMed1975

Effect of secretin on electrical activity of small intestine.

The effect of intravenously administered secretin (0.5, 2.0, 6.0 U/kg-h) and intraduodenal acidification (13.2 meq/h HCl) on the electrical activity of the small bowel of three conscious dogs with gastric and duodenal cannulas was observed. Electrical activity was recorded in fasted as well as fed conditions through silver wire electrodes implanted along the entire length of the small bowel. Intravenous infusion of secretin in all dosages and in all dogs delayed the onset of the interdigestive myoelectric complex and reduced the total percentage of slow waves with superimposed spike potentials. Intraduodenal acidification also inhibited the interdigestive myoelectric complex, which developed incompletely with fewer action potentials on slow waves. Secretin did not produce any alteration in the fed pattern of activity, slow-wave frequency, or the caudal migration of the interdigestive myoelectric complex. The present study indicates that the nuerohumoral mechanisms responsible for initiation of the interdigestive myoelectric complex may be different from those responsible for its caudal migration.

Animals↗
PubMed1975

Depression of antral and serum gastrin concentration by food deprivation in the rat.

In rats fasted 4 days, immunoreactive gastrin concentrations decreased to one-third of the fed levels in antral tissue and to one-eight of the fed levels in serum. The number of antral cells that reacted with fluorescent antigastrin antiserum was also correspondingly decreased. After refeeding, serum gastrin returned to normal levels in 6 days, whereas antral gastrin concentration recovered after 9 days. Normal gastrin levels were maintained in rats fed a nutritious liquid diet over a 6-day period, whereas tissue and serum hormone concentrations decreased to low levels in rats placed on a high bulk non-nutritive diet over the same period. These results suggest that food in the gastrointestinal tract is necessary for the maintenance of normal serum and antral gastrin concentration in rats. The effect of food is most likely attributable to chemical constituents and not distention by bulk.

Animals↗
PubMed1975

Structural and hormonal alterations in the gastrointestinal tract of parenterally fed rats.

This study examines the effect of prolonged absence of oral food intake on structural parameters of the gastrointestinal tract in rats maintained nutritionally by intravenous feeding for up to 3 weeks. During this time, their body weights increased by 22%. Controls fed a nearly isocaloric oral diet were sham operated and harnessed in the same manner as their parenterally fed counterparts. Parenteral feeding resulted in a significant decrease in the weights (per 100 g body weight) of the oxyntic gland area of the stomach, small intestine, and pancreas. The weights of the spleen, testes, kidneys, and antral region of the stomach were unaltered. In the small intestine there was a significant loss of DNA and a near doubling of the RNA:DNA ratio in the parenterally fed animals. In the absence of an oral diet antral gastrin levels decreased to one-thirtieth of the control level. The following conclusions are suggested by these results. First, the oral intake and/or physical presence of food within the gastrointestinal tract are necessary for structural maintenance of some tissues of that tract. Second, the disproportionate decrease in weight that occurs in certain tissues is apparently unrelated to the absence of nutrients which might normally be utilized directly from the lumen. Third, maintenance of normal tissue stores of the hormone, gastrin, is dependent on stimuli provided by oral ingestion and the presence of food in the gastrointestinal tract.

Animals↗