Gastrointestinal and biliopancreatic response to continuous nasogastric feeding in man: effect of increasing nutrient infusion rate

Gastrointestinal and biliopancreatic response to continuous nasogastric feeding in man: effect of increasing nutrient infusion rate

CIinicol Nutnrion 0 Longman (1994) 13: 307-3 I3 Group Ltd 1994 Gastrointestinal and biliopancreatic response to continuous nasogastric feeding in m...

770KB Sizes 1 Downloads 10 Views

CIinicol Nutnrion 0 Longman

(1994) 13: 307-3 I3

Group Ltd 1994

Gastrointestinal and biliopancreatic response to continuous nasogastric feeding in man: effect of increasing nutrient infusion rate N. VIDON”,

P. SOGNP, S. CHAUSSADE+,

B. HUCHET*

and J. J. BEPINIER*

*lNSERM UZ90, hbpital Saint Lazare, 75010 Paris, France, %ervice d’ht+patogastroent&ologie, Cochin, 75013 Paris, France (Correspondence to: NV, Laboratoire de Pharmacie Gaknique, Pharmacie, 4 avenue de I’Observatoire, 75270 Paris cedex 06, France)

H6pitat FacuM de

ABSTRACT-Nasogastric feeding is a safe and inexpensive procedure used in various conditions to provide artificial nutritional support. However, the effects of increasing energy load of nutrients during continuous enteral nutrition on gastric physiology, biliopancreatic secretions and intestinal absorption of nutrients are unknown. A nutrient solution (1 kcaI/ml, 15% proteins, 30% lipids, 55% carbohydrates) was randomly infused at three rates, 1.5, 3.0 and 4.5 ml/min, into the gastric antrum in 6 volunteers over a 6 h period. Gastric emptying, gastric and biliopancreatic secretion, and intestinal absorption were studied using a perfusion technique. Gastric emptying rate reached the infusion rate during continuous enteral nutrition at 1.5 and 3.0 ml/min although a steady state was not reached at 4.5 ml/min. During feeding at 1.5, 3.0 and 4.5 ml/min, the median gastric pH values were 1.9, 2.3 and 3.0 respectively and the total gastric volumes at the sixth hour were 78 t- 13, 226 + 43 and 539 + 101 ml respectively. There was a significant increase in biliary and pancreatic secretion between 1.5 and 3.0 ml/min but not between 3.0 and 4.5 ml/min. Gastric emptying became the limiting factor in lipid and in carbohydrate absorption. Our study shows that, in healthy volunteers, the maximal infusion rate of a nutrient solution infused into the stomach should be approximately 3 mI/min to avoid complications such as nausea, vomiting, regurgitation and pulmonary inhalation.

feeding decreases bacterial translocation (8-12) and systemic infection. However, nasogastric feeding exposes patients, more particularly critically ill patients, to increased risk of nausea, vomiting, reflux of gastric contents and pulmonary inhalation (13-16). The risk factors in pulmonary inhalation are gastric pH (17, 18) and gastric volume (19-22) dependent. These two parameters could be modified by reducing the energy load of the infusion or by increasing the gastric emptying rate. It has been suggested that there is a progressive decrease in gastric emptying correlated with an increasing energy load, and that the highest emptying rate of a composite meal is about 4.5 kcal/min (23). In fact, little is known about the effects of continuous nasogastric feeding on parameters of gastric and intestinal functions (24). The aim of this study was to evaluate the effect of an increasing nutrient infusion rate during continuous

Introduction There has been an improvement in the clinical practice of enteral and parenteral nutritional support in recent years. The protocol by which this support is administered is of major importance. Enteral nutrition is a safe and inexpensive procedure (1, 2). Moreover, the rationale for enteral feeding, as opposed to parenteral feeding, is based on the physiological effects on digestion, absorption and hormoneregulation. Enterally administered nutrients appear to preserve (3) the structure and function of the intestine to a greater degree than when the same nutrients are administered parenterally. In patients with Crohn’s disease, enteral nutrition decreases the inflammatory process in the intestine and ameliorates nutritional status (4). In patients with major burns (5, 6), sepsis or major trauma (7) with multiple organ failures, it has been shown that early enteral 307

308

ENTERAL NUTRITION AND DIGESTIVE FUNCTION IN MAN

nasogastric feeding on gastric physiology, biliopancreatic secretions and intestinal absorption of nutrients. Materials and methods Subjects

Studies were performed in 6 healthy male volunteers (age 20.7 f 0.2 years, weight 70.2 f 3.3 kg, height 177 f 3 cm, mean * SE) without any history of gastric or bowel disease. All subjects gave written informed consent to the protocol which was approved by the Ethics Committee of the Femand Widal-LariboisiereSaint Lazare hospitals. General procedure

Gastric and salivary secretion, gastric emptying, gastric and jejunal pH, jejunal flow rates, pancreatic and biliary secretions, as well as nutrient absorption rates, were evaluated during continuous infusion of a nutrient solution into the antrum over a 6 h period each day. In each subject the study was performed during 3 consecutive days with 3 different infusion rates randomly assigned: 1.5, 3.0 and 4.5 ml/mm. Gastric and duodenal function was determined by dilution of two aqueous non-absorbable markers, one present in the nutrient solution ( [14C]-PEG) and the other (PEG 4000) simultaneously infused into the duodenum. Injksed solution

1. The nutrient solution (Sondalis iso, Laboratoires SOPHARGHA, 92080 Paris-La Defense, France) contained [r4C]-PEG (polyethylene glycol 4000) 10 lXi/L. Its consisted of 50% carbohydrates dextri-maltose (12.5 g/l00 ml); 15% proteins - lactic (casein, 1.87 g/100 ml) and soya (1.87 g/l00 ml) proteins; 35% lipids - corn (0.92g /lOO ml) and colza (0.84 g/l00 ml) oils, linoleic acid (0.31 g/ml) and mild chain triglycerides (1.83 g/l00 ml). The osmolality was adjusted to 300 mOsmol/kg with NaCl and the energy load was 1 kcal/ml. Thus the intragastric energy rates were 1.5, 3 and 4.5 kcal/ min for the infusion rates 1.5, 3 and 4.5 ml/mm respectively. The pH was 7. 2. The duodenal recovery marker solution contained unlabelled PEG 4000 (10 g/l) which was dissolved in normal saline solution. It was infused (1 ml/mm) into the second part of the duodenum. Experimental design

The technique has been previously described (25-27).

Briefly, subjects were intubated with a double-lumen tube. After an overnight fast, the tube was positioned under fluoroscopic control with the perfusion point for PEG 4000 set at the ampulla of Vater and the duodenal aspiration site was positioned 20 cm lower, near the duodenojejunal junction. A gastric sump tube was then positioned with its tip in the antrum. The volunteers adopted a semi-upright sitting position for the entire duration of the study. The residual gastric contents were completely aspirated. Then the duodenal infusion of PEG at 1 ml/mm was started immediately before initiating the gastric infusion of nutrients. Duodenal contents were aspirated continuously at a rate of 1 ml/min and were sampled every 15 min for 6 h. Gastric contents were sampled every hour. At the end of the experiment, the gastric contents were completely aspirated. The stomach was then rinsed with 200 ml of normal saline solution to recover the remainder of the test solution marker. Analytical methods

Unlabelled PEG 4000 was measured in each intestinal sample by the turbidimetric method of Hyden (28) and [14C]-PEG was counted in a scintillation counter. Lipase concentrations were determined by automatic titration (Radiometer, Copenhagen, Denmark) at the constant temperature of 37’C; emulsified olive oil served as substrate and sodium hydroxide (O.OlN) as titrant. Lipase activities were expressed in international units (microequivalents of hydrogen ion liberated from the substrat.min/mL). Bile salts were measured by a fluorimetric method (29, 30). Carbohydrate concentrations expressed as glucose values, after amyloglucosidase hydrolysis, were estimated with an enzymatic method (kit ref. 716251 from Boeringer Mannheim, Mannheim, FRG). Glucose was phosphorylated to glucose-6-phosphate, which was used to reduce NADP into NADPH; the method measured the production of NADPH. Lipids, after hydrolysis, were expressed as total fatty acids extracted using the Blankenhom and Arhens technique (31) and titrated by employing the Dole technique (32). pH was measured with a pHmeter (Radiometer, Copenhagen, Denmark). In each gastric sample, [14C]-PEG,pH, carbohydrate and total fatty acid concentrations were measured. Data treatment

Gastric emptying of the test solution, fluid flow rates, enzymes and bile salt outputs and carbohydrate absorption rates were determined utilizing the usual formulae (26). The main step in analysis was the

CLINICALNUTRITION

measurement of duodenal flow rate from the dilution of PEG 4000 between the ampulla and the ligament of Treitz. Duodenal [t4C]-PEG output was estimated from the duodenal [14C]-PEG concentration multiplied by duodenal flow rate. Pyloric flow rate was obtained by dividing duodenal [i4C]-PEG output by the concentration of [14C]-PEG in the stomach measured at the same time. Gastric volume was obtained by dividing gastric content in [14C]-PEG (amount infused minus amount delivered at the pylorus) by the concentration of [‘“Cl-PEG in the stomach measured at the same time. The volume of nutrients remaining in the stomach was calculated by dividing gastric content in [llC]-PEG by the concentration of [14C]-PEG measured in the nutrient solution infused into the stomach. Amounts of lipase and bile salts delivered to the ligament of Treitz were calculated from the duodenal flow rate and the concentration of lipase and bile salts in duodenal samples. Carbohydrate absorption was estimated as the amount of carbohydrate passing through the pylorus minus the amount delivered at the ligament of Treitz over the same time interval. Lipid absorption rates were also determined as Cortot et al (33) who have shown that the aqueous and lipid phases of a meal, when taken in homogenized form, empty together. Statistical analysis The gastroduodenal and biliopancreatic outputs as well as the gastric volumes in each gastric infusion load were measured as area under curves (AUC) (34). The AUC values were compared with ANOVA. pH were expressed as median (extremes values) and compared with non-parametric Kruskal-Wallis test. Regression analysis was used to correlate gastric emptying and intestinal absorption of lipids and glucose. Values were expressed as mean f SE. p < 0.05 was considered statistically significant.

Table

AUC values for gastroduodenal

Nasogastric AUCof AUC of AUC of AUC of AUC of AUC of AUC of

and biliopancreatic

feeding

gastric emptying of nutrients (ml.h.min’) gastric and salivary secretions (m1.h) duodenal flow rate (ml.h.min-‘) lipase output (IU.h.min’) bile salts output (pmol.h.min-‘) absorption of glucose (mg.h.min-I) absorption of lipids (pmol.h.mn-‘)

Results are expressed as m zkSE. ’ different from 1.5ml/min (p < 0.05) h different from 3.0 ml/mm (p < 0.05)

309

Gastric emptying of nutrients

5 4 3 2 1 0 0

1

2

3 4 Time (h)

5

6

Fig. 1. Gastric emptying rates of nutrients during a 6 h period of naso-gastric feeding at I.5 (0),3.0 (0) and 4.5 (A) ml/min in 6 healthy volunteers.

Results The study was well tolerated for all subjects. The total recovery of the test solution marker ([14C]-PEG) was calculated by adding the quantity of [i4C]-PEG contained in the gastric samples, in the final aspiration, and in the gastric lavage to that of [ 14C]-PEG passing the ligament of Treitz. The values were 98.5 + 3.6%. 94.6 It 1.1% and 89.3 + 2.4% for 1.5, 3 and 4.5 ml/min respectively (not different). Gastric functions During infusion at 1.5 ml/min and 3.0 ml/min, a steady state began between the first and the third hour after the onset of the infusion (Figs 1 & 2, Table). In the steady state, the gastric emptying was equal to the total of the outputs of the nutrient solution and the gastric and salivary secretions. During infusion at 4.5 ml/min, the steady state was not reached at the end of the 6 hour period in 4 out of 6 patients. For

functions during nasogastric I.5 ml/min 1.5 * 0.3 387+ 116 22.7 + 2.7 11991f3302 127* 10 518k76 743 rt 57

feeding in 6 healthy volunteers over a 6 h period. 3.0 mI/min 14.9 f 1.1a 745 * 190 36.2 + 2.9a 15404 f 3630 192f21” 769 k 127” 1323 + 103”

4.5 mllmin 18.5 f 1.2a,b 900 f 135a 37.0 rt 2.9a 16748 f49313 187f24a 1044 f 101a.s 1687 k 137a,b

3IO ENTERALNUTRITIONAND DlGESTIVE FUNCTION IN MAN

1

4

600

1.5

mL/min

2 5 500

3

Q)400 ;300 * 200 0 ._

*

:1OO 0

u”

0

1

2

3

4

5

6

1

1

I

3

I

1

0

600

l

I

1

1

2

I

I

3 4 Time (h)

*0

I

1

5

6

Fig. 3.

Gastric pH during a 6 h period of naso-gastric feeding at 1.5 (0) 3.0 (0) and 4.5 (A) ml/min in 6 healthy volunteers. 4.5 vs 1.5: * = p < 0.05 and ** = p < 0.01; 4.5 vs 3.0: ’ = p < 0.05.

z E5W E 4oo 5 300 > 0 200 ‘C pO

1.6 and 3.0) and 3.0 (extreme values 1.8 and 4.1) for 1.5, 3.0 and 4.5 mYmin respectively (Fig. 3). The gastric pH was higher for 4.5 ml/min than for 3.0 or 1.5 ml/min.

0

(3

Gastric pH (median values)

0

600 ”

pJ

14.5

1

2

3

4

5

6

Duodenal functions The duodenal flow rate (Fig. 4) was similar with 3.0 and 4.5 ml/min, but higher than with 1.5 ml/min. Lipase (Fig. 5) outputs increased when energy loads increased but the difference was only statistically significant (Table) between 1.5 and 4.5 mlfmin. Bile salt (Fig. 6) outputs were statistically higher with 3 and 4.5 ml/min than with 1.5 ml/min but no difference could be detected between the two highest infusion rates (Table).

mL/min

a400 E = 300 g 0200 ._ g 100 g

0 -0

Duodenal flow rate 81

2

3

4

5

6

Fig. 2.

Volumes of nutrients and volumes of salivary and gastric secretions present in the stomach during a 6 h period of nasogastric feeding at 1S, 3.0 and 4.5 mumin in 6 healthy volunteers.

64-

these 4 volunteers, the rate of gastric infusion remained smaller than the pylorus nutrient output. Gastric and salivary secretions may be evaluated if we consider that these secretions left the stomach at the same ratio as the nutrients (Fig. 2, Table). The volume of these secretions was higher for 4.5 ml/min than for 1.5 ml/min. However, it was not different between 1.5 and 3.0 and between 3.0 and 4.5 ml/min. The median of pH values at the sixth hour was 1.9 (extreme values 1.5 and 2.3), 2.3 (extreme values

-,

2

T

T

mL’mu

i

1

O! 0

I

I

1

2

I

I

1

I

4

5

6

Tim: (h) Fig. 4. Duodenal flow rates during a 6 h period of naso-gastric feeding at 1.5(U), 3.0 (0) and 4.5 (A) mumin in 6 healthy volunteers.

~~IC.~~_NUTRITI~N

5ooo 4ooo

Bile salts output

Lipase output

1

311

50 1 [email protected]

lU/mi

3000 2000 1000

1

O-l

0

,

,

1

2

10 I

I

3 (h; Time

I

5

1

6

0-l

0

Fig. 5.

Lipase outputs during a 6 h period of naso-gastric feeding at 1.5 IO). 3.0 (0) and 4.5 (A) ml/nun in 6 healthy volunteers.

,

I

1

2

3

4

I

I

5

6

Time (h)

Fig.6.

Bile salts outputs during a 6 h period of naso-gastric feeding at 1.5 (0). 3.0 (0) and 4.5 (A) ml/nun in 6 healthy volunteers.

The absorption of carbohydrates and lipids increased with the infusion rate (Table). Moreover, the rate of absorption of carbohydrates and lipids was well correlated with the gastric emptying rate of nutrients

steady state was obtained during infusion of 1.5 and 3.0 ml/min. However, at the rate of 4.5 ml/min, the steady state was not reached at the end of the study period. The total intragastric volume increased during the same period presumably indicating an increased risk of nausea and vomiting. It should therefore be recommended not to exceed a continuous infusion rate of 3.0 ml/min. However, in patients receiving enteral nutritional support (i.e. critically ill patients or patients with burns) gastric emptying may be

(Fig. 7).

Discussion Our study demonstrated that, during nasogastric feeding with a same standard diet formulation, the variations of infusion rate were clearly responsible for large modifications in pH and in gastric volume. A Absorption

0 Gastric

of

1 emptying

delayed. In these patients, the maximum energy load should be lower. During enteral nutrition given at a rate of less than

lipids

2 of

(FmoVmin)

3 nutrients

4 (ml/min)

Fig.7. Absorption of nutrients during a 6 h period of naso-gastric feeding at 1S. 3.0 and 4.5 m&in in 6 healthy volunteers. The correlations between gastric emptying and absorption of glucose or lipids are represented. Mean values at 0. 1,2, 3, 4, 5 and 6 h during nasogastric feeding are used for statistical analysis for the 3 infusion rates (n = 2 I for glucose and n = 2 1 for lipids).

312

ENTERAL NUTRITION AND DIGESTIVE FUNCTION IN MAN

3 ml/min, the occurence of vomiting and oesophageal reflux is estimated to be 5% and 8% respectively (2, 14). The risk of inhalation and pneumonia during continuous enteral nutrition is great (54%) in ventilated intensive care unit patients (15). Reflux of gastric contents and pulmonary inhalation are related to the gastric volume (19-22) and gastric pH (17, 18). This study showed that the higher the energy load, the greater was the risk of regurgitation. The respective rate of energy content and volume of the nutrient solution in the regulation of gastric emptying should be discussed. However the energy content is probably the main factor of regulation as previously demonstrated for tested meals (35, 36). The risk of regurgitation is more critical when the pH is lower than 3 (18, 37). The intragastric median pH values were significantly higher in patients receiving enteral feeding at 4.5 ml/min. However, this value was found to be approximately 3. These results demonstrated that the risk of acid regurgitation and Mendelson’s syndrome was substantial at 4.5 ml/mm but may be present at all outputs. Our results are in agreement with those found by Armstrong et al (38) who showed that gastric pH values remain low during gastric enteral nutrition but are higher during duodenal enteral nutrition or parenteral nutrition. At 4.5 mllmin, the highest intragastric pH value was probably related to the fact that the gastric secretions were proportionally lower than during infusion at 1.5 and 3.0 ml/mm and more buffered by the nutrient solution. The use of prokinetic and antisecretory medications merits further investigation to evaluate their efficacy in order to prevent regurgitation during enteral feeding. The biliopancreatic secretions were similar at 3.0 and 4.5 ml/min but higher than those measured at 1.5 ml/mm. These results suggested that biliopancreatic secretions are related to the nutrient output delivered into the duodenum during an enteral feeding. The duodenal energy output, which is responsible for maximum biliopancreatic secretions, may be approximately 3.0 kcallmin. Above this level, the biliopancreatic secretions could not be increased in relation with either a saturable phenomenon or regulation mechanisms. However despite this brake, pancreatic secretions were probably in excess for luminal digestion. These mechanisms could originate at the duodenal, jejunal or ileal level. Under these physiological conditions in heaIthy patients, it is unlikely that the inhibition of biliopancreatic secretions could be result of an ileal brake. In contrast, it has been demonstrated that intrajejunal feeding at a energy load higher than 2.0 kcal/min was able to cause an inhibition of biliopancreatic secretions (39,40) and gastric emptying (41). This jejunal brake

was related to the energy load and not to the type of nutrients (42). In this study, the total energy load which reached the angle of Treitz could be estimated at 0.7, 1.8 and 2.2 kcal/min for 1.5, 3.0 and 4.5 ml/ min respectively. So for 4.5 ml/mm, it reached the value inducing the jejunal brake. The inhibition of biliopancreatic secretion may be the result of a jejunal brake. In this study, the duodenal absorption rate of carbohydrates and lipids were linearly correlated to the duodenal nutrient load. In fact, the glucose absoption rate is a saturable phenomenon according to the Michaelis-Menten equation. However this phenomenon occurs for higher duodenal outputs than those obtained here (43-46). In conclusion these results clearly show that in patients with normal digestive functions the maximal infusion rate of a standard diet solution containing 1 kcal/ml infused into the stomach should not be more than approximately 3 ml/min to avoid complications such as reflux, regurgitation, vomiting and pulmonary inhalation. These results could be of importance for patients treated by nocturnal cyclic enteral nutrition.

Acknowledgments The authors wish to thank Mr Richard Medeiros for his advice in editing the manuscript.

References 1. Heymsfield S B, Bethel R A, Ansley J D et al. Enteral hyperalimentation: an alternative to central venous hyperalimentation. Ann Int Med 1979; 90: 63-7 1. 2. Cataldi-Betcher E L, Seltzer M H, Slocum B A et al. Complications occuring during enteral nutrition support: a prospective study. JPEN 1983; 7: 546-552. 3. Wilmore D, Smith R, O’Dwyer S. The gut: a central organ after sepsis. Surgery 1988; 104: 917-923. 4. Fisher R L. Nutrition and gastrointestinal diseases, Current Opinion in Gastroenterology 1990; 6: 821-825. 5. Mochizucki H, Trocki 0, Dominioni L et al. Mechanism of prevention of postbum hypermetabolism and catabolism by early enteral feeding. Ann Surg 1984; 200: 297-310. 6. Chiarelli A, Enzi G, Casadei A, Baggio B, Valerio A, Mazzoleni F. Very early nutrition supplementation in burned uatients. Am J Clin Nutr 1990: 51: 1035-1039. I. Moore F A, Moore E E, Todd J. TEN versus TPN following major abdominal trauma reduced septic morbidity. J Trauma 1989; 29: 916-923. 8. Alverdy J C, Aoys E, Moss G S. Total parenteral nutrition promotes bacterial translocation from the gut. Surgery 1988; 104: 185-190. 9. Spaeth G, Specian R D, Berg R D et al. Bulk prevents bacterial translocation induced by the oral administration of total parenteral nutrition solution. JPEN 1990; 14: 442-447. 10. Alverdy J C, Aoys E, Moss G S. Effect of commercially

CLINICAL NUTRITION

11.

12.

13. 14.

15.

16. 17.

18.

19.

20.

21. 22.

23. 24.

25.

26.

27.

28.

29.

available chemically defined liquid diets on the intestinal microflora and bacterial translocation from the gut. JPEN 1990; 14: l-6. Deitch E A. The role of intestinal barrier failure and bacterial translocation in the development of systemic infection and multiple organ failure. Arch Surg 1990; 125: 403-404. Mainous M, Xu D. Lu Q et al. Oral-TPN-induced bacterial translocation and impaired immune defense are reversed by feeding. Surgery 1991; 110: 277-284. Jones B J M, Payne S, Silk D B A. Indications for pump-assisted enteral feeding. Lancet 1980; i: 1057-1058. Payne%James J, de Gara C. Grimble G et al. Nutritional support in hospitals in the United Kingdom: national survey 1988. Health Trends 1990; 22: 9-13. Jacobs S, Chang R W S, Lee B, Bartlett F W. Continuous enteral feeding: a major cause of pneumonia among ventilated intensive care unit patients. JPEN 1990; 14: 353-356. Lowe D K, Puyana J C. Nutritional support in the intensive care unit. Nutrition 1991; 7: 290-298. Mendelson C L. Aspiration of stomach contents into lungs during obstetric anesthesia. Am J Obstet Gynec 1946; 52: 191-205. Christensen V, Skovsted P. Effects of general anaesthetics on the pH of gastric contents in man during surgery: a survey of halothane, fluroxene and cyclopropane anaesthesia. Acta Anaesth Stand 1975; 19: 49-54. Bonnister W K, Sattilaro A J. Vomiting and aspiration during anesthesia. Review. Anaesthesiology (Philadelphie) 1962; 23: 25 l-264. Ong B Y, Palahniuk R J, Cumming M. Gastric volume and pH in out-patients. Canad Anaesth Sot J 1978; 25: 36-39. Nimmo S. Effect of anaesthesia on gastric motility and emptying. Br J Anaesth 1984; 56: 29-35. Kleibeuker J H, Van Ek W B. Acute effects of continuous nasogastic tube feeding on gastric function: comparison of a polymeric and a non polymeric formula. JPEN 1991; 15: 8&84. Bemier J J. Adrian J, Vidon N. Les aliments dans le tube digestif. Doin Cd, Paris 1988,468. Etienne A, Rigaud D, Accary J P, Mignon M. Comportement secrktoire, moteur et hormonal de l’estomac pendant une alimentation 6ltmentaire continue, instill&e en site gastrique ?i diffkrents dkbits chez le sujet normal. Gastroent&ol Clin Biol 1982; 6: 628-637. Bernier J J, Lebert A. Vitesse de 1’8vacuation de l’estomac et du duodenum au tours de I’hyperglycCmie provoquCe per OS. Biol GastroentCrol (Paris) 197 1; 4: 35 l-352. Malagelada J R, Longstreth G F, Summerskill W H J. Go V L W. Measurement of gastric functions during digestion of ordinary solid meals in man. Gastroenterology 1976; 70: 203-210. Vidon N, Muschart J M, Cosnes J et al. Etude critique de l’estimation de la vidange gastrique par la m&ode de perfusion duodinale d’une substance non absorbable g faible dtbit. Gastroentdrol Clin Biol 1979; 3: 549-552. Hyden S. A turbidimetric method for the determination of high polyethylene glycols in biological material. Ann R Co11 Swed 1955; 22: 139-145. Iwata T. Yamasaki K. Enzymatic determination and thin-layer

Submission date: 8 February

30.

31.

32.

33.

34.

35.

36.

37. 38.

39.

40.

41.

42.

43.

44.

45.

46.

1994; Accepted after revision 19 April 1994

3 13

chromatography of bile acids in blood. J Biochem 1969; 56: 424-431. Murphy G M, Billing B H, Baron D N. A fluorometric and enzymatic method for the estimation of serum total bile acids. J Clin Path01 1970; 23: 594-598. Blankenhom D H, Arhens E H. Extraction, isolation and identification of hydrolytic products of triglyceride digestion in man. J Biol Chem 1955; 212: 69-81. Dole V P. A relation between nonesterified fatty acids in plasma and the metabolism of glucose. J Clin Invest 1956: 35: 150-154. Cortot A, Phillips S F, Malagelada J R. Gastric emptying of lipids after ingestion of an homogenized meal. Gastroenterology 1979; 76: 939-944. Matthews J N S, Altman D G, Cambell M J, Royston P. Analysis of serial measurements in medical research. BMJ 1990; 300: 230-235. Ruskone A, Cosnes J, Vidon N, Couzigou P, Bemier J J. S&rition et vidange gastriques apr& differents repas homog6ntisCs chez l’homme. Gastroenterol Clin Biol 1980; 4: 777-785. Jian R, Ruskone A, Filali A, Ducrot F, Rain J D, Bernier J J. Effet de l’augmentation de la charge calorique d’un repas sur la vidange gastrique de ses phases solide et liquide. Gastroenterol Clin Biol 1986; 10: 831-836. Teabeaut J R. Aspiration of gastric contents. Experimental study. Am J Path 1952: 28: 51-68. Armstrong D, Castiglione F, Emde C et al. The effect of continuous enteral nutrition on gastric acidity in humans. Gastroenterology 1992; 102: 1506-1515. Vidon N. Pfeiffer A, Franchisseur C, Bovet M, Rongier M, Bemier J J. Effect of different caloric loads in human jejunum on meal-stimulated and non-stimulated biliopancreatic secretion. Am J Clin Nutr 1988: 47: 400-405. Vidon N, Chaussade S, Merite F, Huchet B, Franchisseur C, Bemier J J. Inhibitory effect of high caloric load of carbohydrates or lipids on human pancreatic secretions: a jejunal brake. Am J Clin Nutr 1989; 50: 231-236. Vidon N, Pfeiffer A, Chayvialle J A et al. Effect of jejunal infusion of nutrients on gastrointestinal transit and hormonal response in man. Gastroent&ol Clin Biol 1989; 13: 1042-1049. Sogni P, Vidon N, Chaussade S, Huchet B. Inhibitory effect of jejunal high caloric nutrient load on human biliopancreatic secretion. The role of atropine, naloxone and composition of nutrient solutions. Clin Nutr 1993; 12: 24-28. Modigliani R, Bemier J J. Absorption of glucose, sodium and water by the human jejunum studied by intestinal perfusion with a proximal occluding balloon and at a variable flow rate. Gut 1971: 12: 184-193. Ferraris R P, Yasharpour S, Kent Lloyd K C, Mirzayan R. Diamond J M Luminal glucose concentrations in the gut under normal conditions. Am J Physiol 1990; 259: G822-G837. Fine K D, Santa Ana C A, Porter J L. Fordtran J S. Effect of D-glucose on intestinal permeability and its passive absorption in human small intestine in vivo. Gastroenterology 1993; 105: 1117-1125. Ferraris D P, Lee P P, Diamond J M. Origin of regional and species differences in intestinal glucose uptake. Am J Physiol 1989: 257: G689-G697.