Presystemic influences on thirst, salt appetite, and vasopressin secretion in the hypovolemic rat

2007 ◽  
Vol 292 (5) ◽  
pp. R2089-R2099 ◽  
Author(s):  
Carrie A. Smith ◽  
Kathleen S. Curtis ◽  
James C. Smith ◽  
Edward M. Stricker

The present studies investigated the influence of presystemic signals on the control of thirst, salt appetite, and vasopressin (VP) secretion in rats during nonhypotensive hypovolemia. Rats were injected with 30% polyethylene glycol (PEG) solution, deprived of food and water overnight, and then allowed to drink water, 0.15 M NaCl, or 0.30 M NaCl. The PEG treatment, which produced 30–40% plasma volume deficits, elicited rapid intakes in an initial bout of drinking, but rats consumed much more 0.15 M NaCl than water or 0.30 M NaCl. In considering why drinking stopped sooner when water or concentrated saline was ingested, it seemed relevant that little or no change in systemic plasma Na+ concentration was observed during the initial bouts and that the partial repair of hypovolemia was comparable, regardless of which fluid was consumed. In rats that drank 0.15 M NaCl, gastric emptying was fastest and the combined volume of ingested fluid in the stomach and small intestine was largest. These and other observations are consistent with the hypothesis that fluid ingestion by hypovolemic rats is inhibited by distension of the stomach and proximal small intestine and that movement of dilute or concentrated fluid into the small intestine provides another presystemic signal that inhibits thirst or salt appetite, respectively. On the other hand, an early effect of water or saline consumption on VP secretion in PEG-treated rats was not observed, in contrast to recent findings in dehydrated rats. Thus the controls of fluid ingestion and VP secretion are similar but not identical during hypovolemia.

1990 ◽  
Vol 259 (1) ◽  
pp. G78-G85 ◽  
Author(s):  
M. L. Siegle ◽  
H. R. Schmid ◽  
H. J. Ehrlein

In the present study, effects of ileal infusions of nutrients on motor patterns of the proximal small intestine and on gastric emptying were investigated in dogs. An acaloric meal was administered orally, and equicaloric loads of amino acids, oleate, and glucose were infused into the ileum at different doses (0.3, 0.6, and 0.9 kJ/min). The computerized analysis of motor patterns was focused on the differentiation between stationary and propagated contractions recorded by closely spaced extraluminal strain gauges. All three nutrients exerted inhibitory effects on gastric emptying and on contraction force and frequency of the proximal small intestine. Additionally, the propulsive motor pattern induced by the acaloric meal was modulated by reducing the number of contraction waves and their length of spread. All the effects were dose dependent. Among the three nutrients, glucose significantly changed motility at lower doses compared with amino acids and oleate. We conclude that in dogs the ileal brake mechanism is induced by all three nutrients and that it influences not only contraction force and frequency but also the motor patterns of the proximal small intestine.


2000 ◽  
Vol 14 (suppl d) ◽  
pp. 141D-144D
Author(s):  
Georg Stacher

Epigastric fullness may be caused by a disordered gastric motor function, resulting in delayed gastric emptying, but may also be caused by rapid emptying, leading to a distention of the proximal small intestine. A rational diagnostic approach to a patient complaining of epigastric fullness is needed to reveal the underlying disorder or disease and to enable an adequate, targeted therapy. The clinical impression based on symptoms is unreliable and cannot distinguish function disorders and benign disease from severe conditions.


1994 ◽  
Vol 72 (2) ◽  
pp. 299-313 ◽  
Author(s):  
Helle N. Johansen ◽  
K. E. Bach Knudsen

The effect of cereal-based diets varying in dietary fibre (DF) on gastric emptying and glucose absorption over an isolated loop of jejunum was studied in four pigs fitted with two sets of re-entrant cannulas. The pigs were fed on either a wheat-flour diet or three diets based on oat flour (endosperm), rolled oats or oat bran containing different amounts of soluble DF. Mean transit time (MTT) of liquid estimated from the output from the first jejunal cannula was significantly higher with the two diets having the highest DF content, but MTT of dry matter (DM), starch, xylose and neutral non-starch polysaccharides (nNSP) was not correlated directly to the DF content of the diet. DF had a stimulatory effect on secretion of gastrointestinal juices, but the effect was not linearly correlated with the DF content of the diet. Starch was significantly degraded in digesta collected within 30 min after feeding with malto-oligosaccharides accounting for 140–147 g/kg total starch. The degradation was more extensive with higher DF and lower starch content of the diet. However, taking into account the differences in jejunal flow, the amount of malto-oligosaccharides available for absorption in the first 0.5 h decreased with higher levels of DF in the oat-based diets. The absorption of glucose from the isolated loop was 18–34 g/m intestine over an 8 h period with no significant differences between diets. This corresponded to a non-significant decrease in recovery of starch from 0.91 to 0.82 with increasing levels of DF and decreasing levels of starch in the diet. This suggests that the capacity for absorption of large doses of starch entering the proximal small intestine after ingestion of a carbohydrate-rich cereal-based diet has a major influence on the absorption at this site. Consequently any effect of DF on glucose absorption may be exerted either through the rate of gastric emptying or by impaired rate of absorption more distal in the small intestine and not by displacement of the site for starch absorption.


1983 ◽  
Vol 31 (6) ◽  
pp. 811-817 ◽  
Author(s):  
K Sjölund ◽  
M Ekelund ◽  
R Håkanson ◽  
A J Moody ◽  
F Sundler

Although gastric inhibitory peptide (GIP) has never been detected outside the upper small intestine by immunochemical methods, GIP-like immunoreactivity has been demonstrated by immunocytochemistry in the glucagon/glicentin cells of pancreas, and gut. In the present study several GIP antisera (five polyclonal and one monoclonal) were tested on specimens from pancreas and intestines of several mammalian species, including man. Two of the polyclonal antisera and the monoclonal one stained cells in the upper small intestine only, while the other three also stained cells in the pancreas, ileum, and colon. Monoclonal anti-GIP did not stain GIP cells in man. The immunostaining produced could not be abolished by pretreatment of the antisera with glucagon or glicentin in excess, whereas small amounts of synthetic or natural porcine GIP prevented the immunostaining. Thus, three of the antisera are specific for GIP, while the other three recognize not only GIP but also GIP-like peptides. The results suggest that the glucagon/glicentin cells contain peptides distinct from GIP but sharing an immunodeterminant with GIP. The GIP-like immunoreactivity in the glucagon cells of the rat pancreas was not altered by infusion of GIP or by elimination of the bulk of endogenous GIP by resection of the upper small intestine, indicating that the GIP-like peptide is produced in the glucagon cells rather than accumulated from the circulation. The nature of this GIP-like peptide is unknown. Conceivably, it represents the cryptic portion of the glucagon precursor molecule. In some species a proportion of the GIP cells in the proximal small intestine displayed glicentin-like immunoreactivity as well, emphasizing the relationship between GIP cells on the one hand and glucagon/glicentin cells on the other.


1960 ◽  
Vol 13 (2) ◽  
pp. 180 ◽  
Author(s):  
LEA Symons

The rate of absorption of D-glucose and L-histidine from the entire small intestine of the rat when measured by an intubation technique was not affected by infestation with the nematode Nippostrongylu8 muris. On the other hand, absorption of D-glucose from the infested jejunum when measured in vivo by a perfusion technique was severely reduced. The rate of gastric emptying was not affected by the infestation. There was a direct relationship between gastric emptying and the rate of absorption of glucose.


1981 ◽  
Vol 241 (1) ◽  
pp. R25-R30 ◽  
Author(s):  
T. H. Moran ◽  
P. R. McHugh

We have studied in Macaca mulatta both the gastric emptying of glucose, D-xylose, and fructose and the effects of these sugars on feeding. Glucose and D-xylose empty in the same fashion, i.e., linearly and more slowly with increasing concentration so that the delivery of solute to the small intestine is constant at 0.1 g/min over time and across concentrations. Fructose empties exponentially and more rapidly than the other sugars. When solutions of each of these sugars (37.5 g in 150 ml) preceded the monkey's daily 4-h feeding period there was a similar total reduction in food intake for each. However, fructose inhibited food intake in the first 2 h of feeding less than did the other sugars just as it inhibited gastric emptying less. D-Xylose, although mimicking glucose in both gastric emptying and feeding on the experimental day, produced, as it is poorly metabolized, a caloric deficit replaced by overeating on the subsequent control day. We conclude from the similarities between glucose and xylose that the stomach, while emptying nutrients, influences feeding and can be at least one source of signals for preabsorptive satiety and caloric homeostasis. The results with fructose require that other sites must be active to permit a similar regulation of feeding to occur despite differing gastric emptying characteristics.


1964 ◽  
Vol 47 (3) ◽  
pp. 258-268 ◽  
Author(s):  
Gerald Friedman ◽  
Jerome D. Waye ◽  
Leonard A. Weingarten ◽  
Henry D. Janowitz

1989 ◽  
Vol 61 (2) ◽  
pp. 285-290 ◽  
Author(s):  
K. M. Cunningham ◽  
N. W. Read

1. Three studies were carried out in each of six normal volunteers to investigate how lipid, when given at different stages during the course of a meal, affects gastric emptying and postprandial blood glucose and insulin concentrations.2. The control meal consisted of 300 ml beef consommé (50 kJ, 12 kcal), followed 20 min later by 300 g mashed potato (908 kJ, 217 kcal). In the two test meals, 60 g margarine were incorporated into either the soup or the mashed potato.3. The addition of margarine to either component of the meal delayed gastric emptying of the mashed potato (P< 0.05), but the pattern varied according to the component to which the fat was added.4. Incorporation of fat into the soup increased the lag phase (P< 0.05) but did not influence the slope of emptying of the mashed potato, while incorporation of fat into the mashed potato reduced the slope of emptying of the mashed potato (P< 0.05) but did not influence the lag phase.5. Addition of fat to either component of the meal reduced postprandial blood glucose (P< 0.05) and insulin responses, but when the fat was incorporated in the soup, peak glucose and insulin responses were delayed as well (P< 0.05).6. The results show that the effect of fat on gastric emptying and absorption of nutrients depends on when, in relation to the other components of the meal, the fat is consumed.


2011 ◽  
Vol 300 (5) ◽  
pp. R1091-R1099 ◽  
Author(s):  
S. Dayawansa ◽  
S. Peckins ◽  
S. Ruch ◽  
R. Norgren

Rats with bilateral lesions of the lateral hypothalamus (LH) fail to exhibit sodium appetite. Lesions of the parabrachial nuclei (PBN) also block salt appetite. The PBN projection to the LH is largely ipsilateral. If these deficits are functionally dependent, damaging the PBN on one side and the LH on the other should also block Na appetite. First, bilateral ibotenic acid lesions of the LH were needed because the electrolytic damage used previously destroyed both cells and axons. The ibotenic LH lesions produced substantial weight loss and eliminated Na appetite. Controls with ipsilateral PBN and LH lesions gained weight and displayed robust sodium appetite. The rats with asymmetric PBN-LH lesions also gained weight, but after sodium depletion consistently failed to increase intake of 0.5 M NaCl. These results dissociate loss of sodium appetite from the classic weight loss after LH damage and prove that Na appetite requires communication between neurons in the LH and the PBN.


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