hormone release

hormone release
hormone release

Effect of Intragastric or Intraduodenal Administration of a Polymeric Diet on Gallbladder Motility,Small-Bowel

Transit Time,and Hormone Release

Michiel Ledeboer,M.D.,Ph.D.,Ad A.M.Masclee,M.D.,Ph.D.,Iza ¨k Biemond,Ph.D.,and

Cornelis https://www.360docs.net/doc/0c9968575.html,mers,M.D.,Ph.D.

Department of Gastroenterology-Hepatology,Leiden University Medical Center,Leiden,The Netherlands

Objective:During postpyloric tube feeding,GI intol-erance is observed more frequently than during prepy-loric feeding,possibly by evoking a stronger GI re-sponse.Methods:We investigated the effect of intragastric and intraduodenal administration of a poly-meric diet (125kcal/h)on gallbladder motility (by ultra-sonography),duodeno-cecal transit time (by lactulose H 2breath test),and GI hormone release (including chole-cystokinin,pancreatic polypeptide,and gastrin).Six healthy subjects (two male,four female;mean age 22yr,range 18–27yr)were studied on two separate occasions in random order during 6h of continuous administra-tion of the diet through either the gastric or duodenal port of a two-lumen tube.Results:Intraduodenal feeding resulted in a more rapid contraction of the gallbladder,from 32?4to 23?4cm 3at 10min (p <0.05),reaching a minimum of 6?1cm 3,in contrast to intragastric feeding (31?4to 19?3cm 3at 60min,p <0.05;minimum 14?1cm 3).The gallbladder remained con-tracted during the 6-h study period during both in-traduodenal and intragastric feeding.Small-bowel tran-sit time was significantly accelerated during intraduodenal compared with intragastric feeding (51?12vs 81?9min;p ?0.003).Plasma cholecystokinin secretion was significantly (p <0.05)increased during intraduodenal compared with intragastric feeding (848?107vs 279?89pmol ?L ?1?360min).The same was true for pan-creatic polypeptide secretion.However,gastrin release was significantly (p <0.05)higher during intragastric feeding.Conclusions:Intraduodenal feeding elicited a stronger GI response than intragastric feeding,as dem-onstrated by accelerated small-bowel transit time,more rapid and stronger gallbladder contractions,and in-creased cholecystokinin and pancreatic polypeptide re-lease.Gastrin release,on the other hand,was stronger during intragastric feeding.(Am J Gastroenterol 1998;93:2089–2096.?1998by Am.Coll.of Gastroenterology)

INTRODUCTION

In patients who are unable to eat but who have a func-tioning GI tract,enteral tube feeding is the preferred method for nutritional support.Enteral nutrition is usually adminis-tered through nasogastric or nasoenteric feeding tubes.In patients with gastric retention,nasogastric feeding is con-traindicated and introduces the risk of regurgitation and pulmonary aspiration (1,2).On the other hand,bypassing the pylorus,as with nasoenteric feeding,interferes with normal gastric function because the control mechanisms of gastric emptying that regulate the caloric load to the duo-denum are eliminated.Abdominal symptoms such as cramps,distention,and diarrhea are more common during nasoenteric feeding than during nasogastric feeding (3,4).Diarrhea is the most common complication of enteral feeding and occurs in up to 30%of patients (3).Compared with intragastric feed-ing,intraduodenal feeding increases the colonic inflow of fluids from the small bowel (5).In a recent study,distur-bances in colonic absorptive function have been proposed as an etiological factor in enteral feeding–related diarrhea (6).GI motility and secretion are regulated by gut hormones,such as cholecystokinin (CCK)(7,8).It is not known whether during continuous feeding,the site of nutrient ad-ministration (intraduodenal or intragastric)affects the mag-nitude of gut-hormone secretion in response to nutrients.We hypothesized that intraduodenal feeding elicits a stronger GI response than intragastric feeding because we have previ-ously shown that endogenous CCK secretion after bolus infusion of fat to the duodenum was greater than after bolus infusion of fat to the stomach (9).To test this hypothesis,we compared:1)the secretion of the GI hormones CCK,gastrin,and pancreatic polypeptide (PP);2)gallbladder motility,which is regulated mainly by CCK;and 3)duodeno-cecal transit time in response to continuous intragastric and intraduodenal ad-ministration of a polymeric diet in healthy subjects.

MATERIALS AND METHODS

Subjects

Six healthy volunteers (two male,four female;mean age 22yr,range 18–27yr)participated in the study.None of the

Received Apr.6,1998;accepted June 5,1998.

T HE A MERICAN J OURNAL OF G ASTROENTEROLOGY

Vol.93,No.11,1998Copyright ?1998by Am.Coll.of Gastroenterology ISSN 0002-9270/98/$19.00Published by Elsevier Science Inc.PII S0002-9270(98)00480-8

2089

subjects had a history of GI disease,gallstones,or surgery,and none were taking any medication.The presence of gallstones or sludge was excluded by ultrasonography.In-formed consent was obtained from each subject,and the protocol was approved by the ethical committee of the Leiden University Medical Center.

Protocol

Each subject participated in two experiments performed on separate occasions in random order with an interval of ?7days.After an overnight fast,the subjects were intubated with a double-lumen polyurethane feeding tube.The prox-imal port was located in the antral part of the stomach,and the distal port was positioned in the horizontal part of the duodenum.Correct position of the ports was verified by fluoroscopy.An intravenous cannula was inserted into an antecubital vein of one arm for blood sampling.Basal gall-bladder images,breath samples,and blood samples were obtained 30,15,and 0min before the start of the experi-ment.The experiment was started by administration of 6g of lactulose (Legendal;Inpharzam,Amersfoort,The Neth-erlands)in 70ml of water (osmolality,280mOsm/kg)within 2min through the distal port into the duodenum to determine small-bowel transit time by hydrogen breath anal-ysis.Thereafter,continuous administration of a polymeric

diet was started (Nutrison;Nutricia,Zoetermeer,The Neth-erlands;100ml Nutrison contains 4.0g LCT fat,12.0g lactose-free carbohydrates,and 4.0g protein;100kcal ?420kJ,osmolality:260mOsm).The diet was given either through the gastric (proximal)or the duodenal (distal)port at a rate of 125ml/h for 6h.Gallbladder images,

breath

F I

G .1.Gallbladder volumes (cm 3,mean ?SEM)in six healthy subjects before and during intragastric (squares )or intraduodenal (triangles )administration of a polymeric diet (Nutrison;Nutricia,Zoetermeer,The Netherlands)at a rate of 125ml/h for 6h.*Significant (p ?0.05)differences between intragastric and intraduodenal feeding.

T ABLE 1

Small-Bowel Transit Time and Abdominal Symptoms During Intragastric

or Intraduodenal Administration of a Polymeric Diet

Subject Small-Bowel Transit Time

(min)

Abdominal Symptoms*

Intragastric Intraduodenal Intragastric Intraduodenal 1120100??27530??35025??47045??58030??6

9075?

?

Mean ?SEM

81?9

51?12?

The diet (Nutrison;Nutricia,Zoetermeer,The Netherlands)was given at a rate of 125ml/h for 6h.*Borborygmi and diarrhea.

?Significant (p ?0.003)difference in mean small-bowel transit time between intragastric and intraduodenal feedings.

2090LEDEBOER et al.AJG –Vol.93,No.11,1998

samples,and blood samples for determination of plasma CCK and PP and serum gastrin were drawn at regular intervals.

Measurement of gallbladder volume

Gallbladder volumes measured with real-time ultrasonog-raphy (Technicare;3.5-MHz transducer)were calculated by the sum of cylinders method using a computerized system (10,11).In this method,the longitudinal projection of the gallbladder is divided into a series of cylinders of equal height in which the diameters are perpendicular to the lon-gitudinal axis of the gallbladder image.The uncorrected volume is the sum of volumes of these separate cylinders.To correct for the displacement of the longitudinal image of the gallbladder from the central axis,a correction factor is calculated from the longitudinal and transverse scans of the gallbladder.Gallbladder volume is calculated by multipli-cation of the uncorrected volume by the square of the correction factor.The mean of the two measurements was used for further analysis.The assumptions and the mathe-matical formula used to calculate gallbladder volume have been described and validated previously (10,11).

Small-bowel transit time

Small-bowel transit time was determined by lactulose hydrogen breath analysis,as described by Bond and Levitt (12).Hydrogen gas is generated by bacterial flora from unabsorbed carbohydrates in the colon.Arrival of the non-absorbable carbohydrate lactulose into the colon can be detected by an increase in pulmonary hydrogen excretion.Samples of end-expiratory breath were taken under basal conditions and every 5min after intraduodenal lactulose administration until a sustained increase was observed.The samples were collected in 25-ml plastic syringes and were immediately analyzed in a hydrogen breath-test unit (Lac-toscreen,Hoekloos,The Netherlands).Small-bowel transit time was defined as the time between lactulose administra-tion and a sustained rise in breath hydrogen concentration of ?10parts per million (ppm)above the basal level.In our department,the mean coefficient of variation for duodeno-cecal transit time using the lactulose hydrogen breath test with 6g of lactulose is 12%?5%(13).

Assays of CCK,PP,and gastrin

Blood samples were collected in EDTA-containing tubes and were kept on ice during the experiment.Plasma CCK was measured by a sensitive and specific radioimmunoassay using antibody T 204(14,15).This antibody binds to all carboxy-terminal CCK peptides containing the sulfated ty-rosyl region.The detection limit of the assay is 0.3pmol/L plasma.The intra-assay variation ranged from 4.6%to 11.5%,and the interassay variation ranged from 11.3%to 26.1%(14).Plasma PP concentrations were measured by a sensitive and specific radioimmunoassay as described pre-viously (16).Serum gastrin concentrations were determined by a sensitive and specific radioimmunoassay using a rabbit antiserum with equal binding to sulfated and unsulfated forms of circulating gastrin (17).

Statistical analysis

Results are expressed as means ?SEM.The gallbladder volumes are expressed in cubic centimeters (cm 3),plasma CCK and PP levels in pmol/L,and serum gastrin levels in ng/L.Data were analyzed for statistical significance by analysis of variance.When this indicated a probability of ?0.05for the null hypothesis,Student-Newman-Keuls anal-yses were performed to determine which values between or within the experiments differed significantly.The signifi-cance levels were set at p ?0.05.

RESULTS

Gallbladder volumes

Basal gallbladder volume at t ?0min was not signifi-cantly different between the experiments:30.6?3.6cm 3before intragastric and 31.5?4.3cm 3before intraduodenal feeding.During intragastric feeding,a significant (p ?0.05)contraction was observed starting from 60min to a

volume

F I

G .2.Individual data and means of small-bowel transit time (min)in six healthy subjects during intragastric (IG)or intraduodenal (ID)admin-istration of a polymeric diet (Nutrison)at a rate of 125ml/h for 6h.*Significant (p ?0.003)difference in mean small-bowel transit time between intragastric and intraduodenal feeding.

AJG –November 1998INTRAGASTRIC OR INTRADUODENAL POLYMERIC DIET 2091

of 18.6?2.5cm 3(39%?8%reduction in gallbladder volume),reaching a minimum of 13.5?1.4cm 3(55%?4%reduction)at t ?90min (Fig.1).The gallbladder remained significantly contracted starting from 60min until the end of the study.Intraduodenal feeding resulted in a rapid and significant contraction of the gallbladder starting from 10min to a volume of 23.2?4.2cm 3(26%?13%reduction),reaching a minimum of 6.4?0.8cm 3(80%?3%reduction)at t ?135min.The gallbladder remained significantly (p ?0.05)smaller starting from 15min for all 6h of intraduodenal feeding compared with both the basal level and intragastric feeding.

Small-bowel transit time

Fasting hydrogen breath levels were ?10ppm in all subjects.A sustained increase in breath hydrogen excretion of ?10ppm was observed in all subjects after the admin-istration of lactulose.Mean small-bowel transit time during intragastric feeding was 81?9min.Small-bowel transit time was significantly (p ?0.003)accelerated during in-traduodenal feeding (51?12min).Individual data for transit times are presented in Table 1and Figure 2.Two subjects (Table 1,nos.2and 5)experienced symptoms of borborygmi and diarrhea during and after intraduodenal feeding,whereas no side effects were reported during or after intragastric feeding.

Plasma CCK concentrations

Basal plasma CCK concentrations were not significantly different between the intragastric and the intraduodenal ex-periments:2.4?0.2and 2.5?0.3pmol/L,respectively,at t ?0min (Fig.3).During intraduodenal feeding,a rapid and significant (p ?0.05)increase in plasma CCK concentra-tion was observed to 6.4?1.0pmol/L at 10min,reaching a peak level of 6.6?0.8pmol/L at 20min.Plasma CCK concentrations remained significantly elevated during all 6h of intraduodenal feeding compared with both basal levels (p ?0.05)and intragastric feeding (p ?0.01).During intragastric feeding,a smaller but still significant (p ?0.05)increase in plasma CCK was observed after 10min to 3.2?0.3pmol/L,reaching a peak level of 3.3?0.3pmol/L after 45min.Plasma CCK levels remained elevated over baseline during all 6h of intragastric feeding.

Plasma PP concentrations

Fasting plasma PP levels (time ?30to 0min)were not significantly different between the experiments.During in-traduodenal feeding,significant (p ?0.05)increases in plasma PP levels were observed over baseline starting from t ?10min and continuing throughout the rest of the experiment (Fig.4).During intragastric feeding,plasma PP levels increased significantly (p ?0.05)over baseline start-ing from t ?30min and continuing (p ?0.05)

throughout

F I

G .3.Plasma CCK concentrations (pmol/L,mean ?SEM)in six healthy subjects at basal levels and during intragastric (squares )or intraduodenal (triangles )administration of a polymeric diet (Nutrison)at a rate of 125ml/h for 6h.Significant (*p ?0.05,**p ?0.01)differences are seen between intragastric and intraduodenal feeding.

2092LEDEBOER et al.AJG –Vol.93,No.11,1998

the rest of the experiment.In addition,during intraduodenal feeding,plasma PP levels were significantly (p ?0.05)elevated compared with intragastric feeding from t ?20to t ?120min.After 120min,no significant differences were observed between intragastric and intraduodenal feeding.Serum gastrin concentrations

Fasting serum gastrin levels (time ?30to 0min)were not significantly different between the experiments.Both during intragastric and intraduodenal feeding,a significant (p ?0.05)increase in serum gastrin levels was observed compared with basal levels starting from t ?10min,and these remained significantly increased during the entire experiment (Fig.5).In addition,serum gastrin levels during intragastric feeding were significantly (p ?0.05)elevated compared with intraduodenal feeding from 120to 360min.The results of integrated hor-mone secretion are listed in Table 2.

DISCUSSION

Our results indicate that continuous enteral feeding by the duodenal route induces a stronger GI response as demonstrated by increased CCK and PP secretion,stronger gallbladder con-traction,and accelerated small intestinal transit time.

CCK release into the circulation from endocrine I cells in the duodenum and jejunum is stimulated by contact with intraluminal nutrients,especially fat and protein (18–20).CCK is involved in the regulation of gallbladder motility,exocrine pancreatic secretion,gastric emptying,and intes-tinal motility (7,8,21,22).Studies with CCK receptor antagonists have clearly demonstrated that CCK is the major hormonal regulator of postprandial gallbladder contraction (7,8).Infusion of CCK in physiological plasma concentra-tions stimulates gallbladder contraction in a dose-dependent manner (23).The increased gallbladder contraction ob-served during intraduodenal administration of the polymeric diet therefore resulted from an augmented CCK response.It is not known why intraduodenal administration of the diet resulted in a stronger CCK response than intragastric feeding,but several factors may be involved.First,intra-gastric administration of the diet may have resulted in de-livery of a smaller amount of nutrients to the duodenum.During the first hours after starting intragastric nutrient administration,gastric volume increases but then stabilizes after 90–180min,whereby gastric emptying is nearly equal to the rate of administration of nutrients to the stomach (24).We have not measured gastric volume,but it is unlikely that large amounts of the polymeric diet were retained in the stomach.All subjects were young and healthy volunteers;none had a history of delayed gastric emptying,and symp-toms of delayed gastric emptying such as epigastric

fullness

F I

G .4.Plasma PP concentrations (pmol/L,mean ?SEM)in six healthy subjects at basal levels and during intragastric (squares )or intraduodenal (triangles )administration of a polymeric diet (Nutrison)at a rate of 125ml/h for 6h.*Significant (p ?0.05)differences between intragastric and intraduodenal feeding.

AJG –November 1998INTRAGASTRIC OR INTRADUODENAL POLYMERIC DIET 2093

were not reported.In addition,plasma CCK secretion after 180min,when gastric emptying equals gastric nutrient delivery,remained significantly reduced compared with in-traduodenal feeding.A more likely explanation for the in-creased CCK response after intraduodenal administration of the diet is that nutrients were distributed over a larger area of CCK-releasing cells in the proximal small intestine.The release of upper-gut hormones and stimulation of gallblad-der contraction and pancreatic enzyme secretion depend on the length of small intestine exposed to nutrients (25,26).In a previous study,we demonstrated that bolus administration of fat to the duodenum elicited higher plasma CCK levels than intragastric bolus administration of an equal amount of fat (9).

Intraduodenal administration of the diet also significantly accelerated duodeno-cecal transit time as measured with the lactulose H 2breath https://www.360docs.net/doc/0c9968575.html,ctulose itself,as a nonabsorbable carbohydrate,may accelerate intestinal transit and induce al-terations in small intestinal motility when administered in larger doses,but not with doses ?10g,as we have used (27).CCK contributes to the transition from a fasting to a fed motility pattern in the small intestine after meal ingestion (8,28).Intestinal transit is more rapid during fed than during fasting https://www.360docs.net/doc/0c9968575.html,K accelerates small intestinal transit.Recently,we demonstrated that infusion of CCK to physiolog-ical postprandial plasma CCK levels induced a fed jejunal motor pattern and accelerated duodeno-cecal transit (21).The significantly shorter small intestinal transit time that we ob-served during intraduodenal administration of the diet most likely is related to an augmented CCK secretion.It remains to be determined whether small intestinal motor patterns are dif-ferent between intragastric and intraduodenal nutrient delivery.Apart from CCK,the secretion of PP was also significantly increased during intraduodenal feeding.It is well known that CCK regulates PP secretion during the intestinal phase of nutrient digestion,and the increased PP secretion during in-traduodenal feeding results from increased CCK secretion (29–31).PP secretion is also dependent on vagal cholinergic mechanisms.Vagal cholinergic blockade with atropine abol-ishes the PP response to intraduodenal nutrient perfusion (30).In a recent study comparing intraduodenal with intragastric nutrient delivery,PP levels were found to be more elevated after intragastric feeding (30).In that study,plasma CCK secretion was not significantly different between the routes of nutrient delivery.These results are in contrast to the findings of our study.However,it should be noted that the protocol of that study was different from ours because nutrients were delivered to the duodenum by continuous perfusion,whereas the intra-gastric meal was administered as a bolus.Gastric distention

is

F I

G .5.Serum gastrin concentrations (ng/L,mean ?SEM)in six healthy subjects at basal levels and during intragastric (squares )or intraduodenal (triangles )administration of a polymeric diet (Nutrison)at a rate of 125ml/h for 6h.*Significant (p ?0.05)differences between intragastric and intraduodenal feeding.

2094LEDEBOER et al.AJG –Vol.93,No.11,1998

known to evoke PP release,and this may have resulted in higher PP levels after the intragastric meal(32).

Serum gastrin levels were significantly increased during both intragastric and intraduodenal feeding.Because it is well known that the gastrin-producing cells(G-cells)are located in both the antrum and the duodenum,this finding is not surpris-ing.However,gastrin release in response to a meal originates predominantly from the gastric antrum,and therefore an aug-mented gastrin release during intragastric feeding is expected (33).In our study,serum gastrin levels during intragastric feeding were significantly elevated compared with intraduode-nal feeding starting from2h after the onset of feeding.The augmented gastrin release during intragastric feeding occurs as a physiological response to an increase in gastric pH,as intra-gastric administration of a diet increases intragastric pH(34). We have shown that continuous intraduodenal administra-tion of a polymeric diet induces a stronger GI response than delivery of the same diet by the intragastric route.Two of the healthy volunteers experienced abdominal symptoms(borbo-rygmi,diarrhea,and cramps)during intraduodenal feeding, whereas no symptoms were reported during intragastric feed-ing.We suggest that the stronger GI response evoked by intraduodenal feeding may have a role in the pathogenesis of enteral feeding–induced diarrhea.When diarrhea occurs during enteral feeding,one should consider altering the route of de-livery of nutrients from postpyloric to prepyloric.

ACKNOWLEDGMENTS

This study was supported by a grant from the Nutricia Research Foundation,Nutricia BV,Zoetermeer,The Neth-erlands.

Reprint requests and correspondence:Ad A.M.Masclee,Department of Gastroenterology-Hepatology,Leiden University Medical Center,Building 1,C4-P,P.O.Box9600,2300RC Leiden,The Netherlands.

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T ABLE2

Integrated Incremental Secretion of CCK,PP,and Gastrin in Six

Healthy Subjects During Intragastric or Intraduodenal

Administration of a Polymeric Diet

Hormone Intragastric Intraduodenal

CCK secretion(pmol?L?1?360min)279?89848?107*

PP secretion(pmol?L?1?360min)5860?7808540?1400*

Gastrin secretion(ng?L?1?360min)9570?4706030?1030*

The diet(Nutrison;Nutricia,Zoetermeer,The Netherlands)was given at

a rate of125ml/h for6h.

*Significant(p?0.05)differences between intragastric and intraduo-

denal feeding.

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2096LEDEBOER et al.AJG–Vol.93,No.11,1998

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Release_Notes_LS-DYNA-971_R4_2_1

LS-DYNA Software Version 971 (R4.2.1) Release Notes

CONTENTS Page 1.INTRODUCTION 1 2.ENHANCEMENTS AND MODIFICATIONS MADE TO VERSION 971 RELEASE 4.2.1 2 2.1AIRBAGS 2 2.2ALE 2 2.3CONSTRAINED OPTIONS 3 2.4CONTACT OPTIONS 3 2.5CONTROL OPTIONS 4 2.6DATABASE & OUTPUT 6 2.7DEFINE OPTIONS 7 2.8EFG 8 2.9ELEMENTS 8 2.10EOS 9 2.11IMPLICIT 10 2.12INCLUDE OPTIONS 11 2.13INITIAL CONDITIONS 11 2.14INTERFACE 12 2.15LOADS 12 2.16MATERIAL MODELS 13 2.17PERAMETER 17 2.18PERTURBATION 17 2.19RIDGEWALL 17 2.20SECTION OPTIONS 17 2.21SENSOR 18 2.22SET OPTIONS 19 2.23SPH 19 2.24TITLE 19 2.25RESTART_INPUT_DATA 19

1. INTRODUCTION LS-DYNA 971 release 4.2.1 is an enhanced and bug-fixed release built on LS-DYNA 971 release 3. This release is not being issued to clients on CD. The software can be downloaded from the Oasys Ltd website at: https://www.360docs.net/doc/0c9968575.html,/dyna. The version, revision (build) number and date of the LS-DYNA code are as follows: Version ls971 R4.2.1 Revision 53450 The revision number, precision and version type can be checked in the test box printed at the top of the .OTF and MESSAG files as per the example below. ___________________________________________________ | | | Livermore Software Technology Corporation | | | | 7374 Las Positas Road | | Livermore, CA 94551 | | Tel: (925) 449-2500 Fax: (925) 449-2507 | | https://www.360docs.net/doc/0c9968575.html, | |_________________________________________________| | | | LS-DYNA, A Program for Nonlinear Dynamic | | Analysis of Structures in Three Dimensions | | Version : ls971d R4.2.1 Date: 06/08/2009 | | Revision: 53450 Time: 07:09:25 | | | | Features enabled in this version: | | Shared Memory Parallel | | ANSYS Database format | | 32 Bit IEEE Binary File | | | | Licensed to: ATG OVE ARUP | | Issued by : arup | | | | Platform : PC WIN32 | | OS Level : Windows XP Pro SP3 B2600 | | Compiler : Intel Fortran Compiler 10.1 | | Hostname : MCCPC6CQHB4J | | Precision : Double precision (I8R8) | | Product ID : 53929 | | | | Unauthorized use infringes LSTC copyrights | |_________________________________________________|

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