Study of the effect of jejuno-ileal distension on the motor activity of the stomach with evidence of "entero-gastric inhibitory reflex"

BACKGROUND/AIMS: In chronic constipation due to delayed colonic transit, stasis of the ileal contents with resulting ileal distension may occur. The current study investigated the effect of ileal and jejunal distension on the gastric motility, aiming at elucidating the possible existence of a relationship and its role in the flow through the gut. METHODOLOGY: The response of the gastric pressure to ileal and jejunal balloon distension in increments of 2 mL of saline was recorded in 12 mongrel dogs. The test was repeated after separate local anesthetization of the ileum, jejunum and stomach. RESULTS: 2- and 4-mL ileal balloon distension produced no significant gastric pressure response, while 6- and up to 10-mL distension effected decrease of the antral and corporeal pressures (p < 0.05, p < 0.05, respectively). Jejunal distension produced a gastric pressure decline (p < 0.05) with 4 and up to 10 mL of saline. The gastric pressure decrease did not show significant changes with the various distending volumes. It was maintained as long as ileal or jejunal distension was continued. Distension of the anesthetized ileum or jejunum caused no gastric pressure changes, nor did ileal or jejunal distension produce pressure changes in the anesthetized stomach. CONCLUSIONS: The gastric pressure decline and presumably hypotonia upon ileal or jejunal distension with big volumes postulate a reflex relationship which we call "entero-gastric inhibitory reflex". The small intestine is suggested to slow down gastric emptying through this reflex. A balance is thus created between chyme delivery from the stomach and chyme processing by the small intestine. Reflex derangement in neurogenic and myogenic diseases may result in gastrointestinal disorders, a point that needs to be investigated.     

Study of the motile activity of the small intestine in constipated subjects

BACKGROUND/AIMS: A recent study has demonstrated that rectal balloon distension effected inhibition of jejunal and ileal motility (Shafik, Hepatogastroenterology, 2000). It was hypothesized that rectal distension occurring in rectal inertia constipation might cause enteric hypotonia. This hypothesis was investigated. METHODOLOGY: Twenty-three patients with rectal inertia constipation (18 women, 5 men mean age 38.8 +/- 10.6 SD years) and 10 healthy volunteers (7 women, 3 men, mean age 37.2 +/- 9.8 SD years) were studied. The rectal, jejunal and ileal pressures were measured by means of saline-perfused tubes. The pressure response of rectum, jejunum and ileum to rectal balloon distension in increments of 50 mL of saline was recorded. RESULTS: The mean basal rectal, jejunal and ileal pressures measured in the patients with rectal inertia were significantly (P < 0.05) lower than those of the volunteers. Fifty-milliliter rectal balloon distension caused no rectal, jejunal or ileal pressure response in either the volunteers or patients. One hundred-milliliter distension effected in volunteers a rectal pressure elevation (P < 0.001) and a decline of jejunal (P < 0.05) and ileal (P < 0.05) pressures which were maintained as long as rectal distension was continued. In patients, no significant (P > 0.05) pressure changes were registered from the rectum, jejunum or ileum. Rectal distension with 150 and 200 mL caused balloon expulsion in the volunteers and in patients no significant rectal, jejunal or ileal pressure changes (P > 0.05). CONCLUSIONS: Rectal inertia was associated with reduced jejunal and ileal pressures, presumably indicating the presence of enteric hypotonia. The inertia-hypotonia relationship is proposed to be mediated through the recto-enteric reflex and transmitted by the enteric nervous plexus. The enteric hypotonia is suggested to prolong the intestinal transit, act as a contributing factor in the genesis of constipation and may explain some of its clinical manifestations.     

Effect of rectal distension on the small intestine with evidence of a recto-enteric reflex

BACKGROUND/AIMS: To study the effect of rectal distension on jejunal and ileal motility aiming at the assessment of the possible role of rectal distension induced by constipation on the transport of the material in the gut. METHODOLOGY: The rectum of 16 healthy volunteers (mean age: 38.6 +/- 11.7 years, 10 men, and 6 women) was distended by a balloon filled with water in increments of 50 mL up to 200 mL and the response of the jejunal and ileal pressures was recorded. The test was repeated distending the anesthetized rectum 20 min and 3 hours after anesthetization. RESULTS: Rectal distension with 50 mL of water effected no jejunal or ileal pressure changes (P > 0.05). One hundred-mililitre (100-mL) rectal distension produced decrease of jejunal and ileal pressures (P < 0.05) which lasted as long as distension was maintained. Rectal distension with 150 and 200 mL caused jejunal and ileal pressure response similar to that of the 100 mL distension (P > 0.05). Distension of the anesthetized rectum effected no significant jejunal or ileal pressure changes. CONCLUSIONS: The results were reproducible in the individual subject. The decline of the intestinal pressure upon rectal distension postulates a reflex relationship between the 2 conditions. This reflex nature is evidenced by reproducibility and by its absence on distension of the anesthetized rectum. We termed this reflex relation: "recto-enteric reflex". It is suggested that under normal physiologic conditions the reflex inhibits the intestinal transit, thus giving the rectum time to evacuate itself. Continuous rectal distension, as occurs in inertia constipation, appears to effect enteric hypotonia, a hypothesis which requires further studies.     

Role of the longitudinal smooth muscle coat in the ileal motile activity: evidence of ileo-ileal inhibitory reflex

BACKGROUND: All gut movements are claimed to be activated essentially by the concentric contraction of the circular muscle, moving the chyme aborally. The role of the longitudinal smooth muscle of the small intestine in gut motility is poorly understood; this point was investigated in the current study. METHODS: The abdomens of 14 crossbreed dogs (eight dogs, six bitches) were opened. A segment of the small intestine was distended by a balloon in increments of 2 mL of saline, and the pressure and electrical activity were recorded proximally and distally to the balloon. The gut wall around the balloon was anesthetized and the test was repeated. The longitudinal muscle coat of the small intestine segment was then excised, and the pressure response and electrical activity were recorded on ileal distension. RESULTS: Two milliliter ileal distension produced pressure decrease (P < 0.05) proximally and distally to the balloon and caused balloon movement. Four, 6 and 8 mL distension effected similar pressure response, while 10 mL showed no response. Electrical waves were recorded from the three electrodes applied to the ileal segment. Upon ileal distension, electrical activity increased over the distended area, with no activity proximally and distally to it. Balloon distension of the anesthetized ileal segment produced no pressure response or electrical activity. After longitudinal myectomy, no electrical activity was recorded at rest or upon ileal distension, and the balloon did not move. CONCLUSION: Ileal distension initiated circular muscle contraction only in the presence of the overlying longitudinal muscle, which appears to transmit the electrical activity to the circular muscle upon ileal distension. Ileal contraction is suggested to initiate ileal hypotonia in the proximal and distal ileal segments mediated through an 'ileo-ileal inhibitory reflex' that leads to aboral progress of the proximally and distally located chyme.     

Duodeno-jejunal junction dyssynergia： Description of a novel syndrome

AIM： To investigate the hypothesis that duodeno-jejunal dyssynergia existed at the duodeno-jejunal junction.
METHODS： Of 112 patients who complained of epigastric distension and discomfort after meals, we encountered nine patients in whom the duodeno-jejunal junction did not open on duodenal contraction. Seven healthy volunteers were included in the study. A condom which was inserted into the ist duodenum was filled up to 10 mL with saline in increments of 2 mL and pressure response to duodenal distension was recorded from the duodenum, duodeno-jejunal junction and the jejunum.
RESULTS： In healthy volunteers, duodenal distension with 2 and 4 mL did not produce pressure changes, while 6 and up to 10 mL distension effected significant duodenal pressure increase, duodeno-jejunal junction pressure decrease but no jejunal pressure change. In patients, resting pressure and duodeno-jejunal junction and jejunal pressure response to 2 and 4 mL duodenal distension were similar to those of healthy volunteers. Six and up to 10 mL 1^st duodenal distension produced significant duodenal and duodeno-jejunal junction pressure increase and no jejunal pressure change.
CONCLUSION： Duodeno-jejunal junction failed to open on duodenal contraction, a condition we call ＇duodenojejunal junction dyssynergia syndrome＇ which probably leads to stagnation of chyme in the duodenum and explains patients＇ manifestations.     

Duodenal infusion of different nutrients and the site of gaseous stimulation influence intestinal gas dynamics

OBJECTIVE: Excessive intestinal gas can be involved in postprandial abdominal symptom generation, but whether the small bowel influences intestinal gas dynamics, depending on the ingested meal, remains to be demonstrated. We compare the intestinal response to a proximal and distal small intestinal gas challenge during different duodenal nutrient components. MATERIAL AND METHODS: We randomly studied 32 healthy subjects, twice, on different days with a gas mixture infused at 12 ml/min either directly into the proximal jejunum or into the ileum; during duodenal lipids, amino acids, glucose, at 1 kcal/min each, or saline (n=8 for each group). Gas evacuation was monitored continuously and abdominal perception and girth changes were assessed. RESULTS: In response to the jejunal gas challenge, duodenal lipids delayed intestinal gas clearance more potently than amino acids (733+/-26 ml and 541+/-108 ml final gas retention; p<0.001), but when gas was directly infused into the ileum the retained volumes were much smaller (271+/-78 ml and 96+/-51 ml; p<0.001). During duodenal glucose, intestinal gas clearance following jejunal or ileal gas infusion was not significantly influenced. Abdominal perception in response to the jejunal and ileal gas challenge only increased slightly during duodenal lipids (2.0+/-0.3 score and 2.3+/-0.6 score; p<0.05 versus control). CONCLUSION: Postprandial intestinal gas clearance is hampered by duodenal lipids and amino acids but not by glucose. Specific inhibitory effects are more pronounced when gas is infused into the jejunum, which underlines the importance of the small intestine in postprandial gas retention.     

Sites of symptomatic gas retention during intestinal lipid perfusion in healthy subjects

BACKGROUND: Gas pooling within the gut may produce abdominal symptoms but the segment of the intestine responsible for gas retention is unknown. Our aim was to determine the role of the proximal and distal bowel in symptomatic gas accumulation using an experimental model of gas retention triggered by intraluminal lipids. SUBJECTS: Sixteen healthy subjects. METHODS: A gas mixture (N2, O2, and CO2 in venous proportions) was infused into the intestine at12 ml/min for three hours and gas evacuation was continuously measured via an anal cannula connected to a barostat. Abdominal perception and girth changes were measured at 10 minute intervals. Lipids (1 kcal/min) were simultaneously perfused either into the duodenum (n = 8) or into the ileum (n = 8). Each subject was studied twice on separate days, with gas infused into the jejunum or ileum. RESULTS: Duodenal lipids produced retention of gas infused into the jejunum (646 (62) ml) but the volume retained was much smaller when gas was infused directly into the ileum (262 (90) ml; p<0.05). The effects on gas retention were even more pronounced during ileal perfusion of lipids (1546 (184) ml during jejunal gas infusion and 847 (142) ml during ileal gas infusion; p<0.05). Abdominal distension correlated with the volume of gas retained (r = 0.87; p<0.001). Healthy subjects tolerated gas retention, and significant symptoms (score 3.7 (0.8)) developed only during jejunal gas infusion plus ileal lipid perfusion when gas retention was very large. CONCLUSION: Intraluminal lipids induce intestinal gas retention, predominantly acting on the proximal small bowel.     

Impaired small bowel gas propulsion in patients with bloating during intestinal lipid infusion

OBJECTIVE: In healthy individuals, intraluminal lipids delay intestinal gas clearance, and this reflex is exaggerated in patients with irritable bowel syndrome (IBS). Our aim was to determine the site of action of abnormal lipid-induced reflexes in IBS. METHODS: In six patients with (IBS) predominantly complaining of bloating and in six healthy subjects, a mixture of gas (N2, O2, and CO2 in venous proportions to minimize diffusion) was infused (12 mL/min) either into the jejunum or into the ileum for 2 h, with simultaneous perfusion of lipids (0.5 kcal/min) into the proximal duodenum. Rectal gas evacuation was measured by a barostat. Abdominal perception (by a 0-6 scale) and girth changes were measured at 15-min intervals. The effects of jejunal versus ileal gas infusion were compared by paired tests in random order on separate days. RESULTS: IBS patients exhibited significant gas retention during infusion of gas into the jejunum (398 +/- 90 mL vs-210 +/- 105 mL in health, p < 0.05) but not during ileal infusion (-79 +/- 87 mL vs-79 +/- 78 mL in health, NS; p < 0.05 vs jejunal infusion). Gas retention during jejunal gas infusion in IBS patients was associated with significant abdominal distension (11 +/- 3 mm girth increment vs 0 +/- 1 mm during ileal gas infusion and 1 +/- 1 mm in health, p < 0.05 for both) and abdominal symptoms (3.6 +/- 0.6 score vs 2.6 +/- 0.7 score during ileal gas infusion and 1.6 +/- 0.5 score in health, p < 0.05 for both). CONCLUSIONS: In IBS patients intraluminal lipids impair intestinal gas clearance because of upregulated reflex inhibition of small bowel transit, without appreciable colonic effects.     

Further characterisation of the 'ileal brake' reflex in man--effect of ileal infusion of partial digests of fat, protein, and starch on jejunal motility and release of neurotensin, enteroglucagon, and peptide YY.

Previous studies have shown that ileal infusion of partially digested triglyceride inhibits jejunal motility. The partial digest used in those studies contained a mixture of glycerol, free fatty acid, mono-, di-, and triglycerides. In Part I of the present study we have separately infused emulsions containing either glycerol 3.1 g (n = 6), oleic acid 9.6 g (n = 6), triolein 10 g (n = 12), or medium chain triglycerides 10 g (n = 6) into the ileum and have recorded the effect this has on jejunal motility. Five further subjects received infusions of partial hydrolysates of corn starch 10 g and lactalbumin 7 g. Marked inhibition of jejunal pressure wave activity was seen after all three lipid infusions, per cent activity falling from a control of 37.7 (7.7) to 6.2 (2.1) and 22.4 (8.2)% 30 min after completing the oleic acid and triolein infusions respectively, and from a control value of 39.5 (4.1) to 17.7 (4.7) after MCTs (all p less than 0.05). No significant fall occurred after infusion of glycerol, protein or carbohydrate. All three lipid infusions raised plasma concentrations of neurotensin, enteroglucagon and peptide YY equally effectively, although only the rise in peptide YY correlated significantly with the inhibition of jejunal pressure wave activity (r = 0.80, n = 6, p less than 0.05). In Part II of this study six subjects received a 3 ml/min jejunal infusion of an isotonic carbohydrate saline solution followed after three hours by a similar infusion of a partial digest of lipid. During each infusion flow and transit time was measured by marker and dye dilution. Jejunal infusion of the carbohydrate-saline solution was associated with low jejunal flow, 4.7 (1.0) ml/min and a mean transit time through the 50 cm study segment of 36.5 (7.1) min. By contrast jejunal infusion of partially digested triglyceride was associated with a markedly increased flow, 9.0 (1.2) ml/min, a fall in mean transit time to 20.3 (2.6) min and significant rises in pancreaticobiliary secretions. Jejunal triglyceride also increased the incidence of prolonged high amplitude jejunal pressure waves in four of six subjects. These studies suggest that there are important differences in the jejunal response to ileal versus jejunal lipid. While long and median chain free fatty acids infused into the ileum exert an inhibitory effect on jejunal motility, when infused directly into the jejunum partially digested triglyceride accelerates transit, increases jejunal flow and subtly alters the pattern of jejunal contractions.     

Comparisons of the effects on satiety and eating behaviour of infusion of lipid into the different regions of the small intestine.

Food intake and feelings of hunger and fullness were monitored in paired studies carried out in two groups of six healthy non-obese male volunteers during infusion of isotonic solutions of either a 50% corn oil emulsion or saline into the jejunum or into the ileum. Infusion of the lipid emulsion at a rate of 1.2 ml/min (4.9 kcal/min) into either the ileum or the jejunum significantly reduced the period of eating (p less than 0.01) and the quantity of food consumed (p less than 0.01), but neither affected the rates of drinking or the amount of fluid consumed. Infusion of the lipid emulsion into the jejunum also significantly reduced the sensations of hunger before the meal (p less than 0.05), and the rate of ingestion (p less than 0.01). Ileal infusion did not influence these indices. The results suggest that jejunal and ileal infusion of lipid reduces the size of the meal that could be consumed possibly by inhibiting gastric emptying. The alleviation of hunger before ingestion and the slower rate of eating, however, suggests that jejunal lipid activates an additional mechanism that influences the appetite centre in the hypothalamus directly.     

Effect of neurotensin on gut mucosal growth in rats with jejunal and ileal Thiry-Vella fistulas.

Neurotensin (NT) stimulates growth of normal and atrophic small bowel mucosa; the mechanisms for this trophic effect of NT are not completely known. The purpose of this study was to (a) determine whether the trophic effect of NT is mediated by mechanisms involving luminal or nonluminal factors and (b) determine whether NT exerts a differential trophic effect on either jejunal or ileal mucosa. Twenty-eight male Sprague-Dawley rats underwent construction of either a jejunal or ileal Thiry-Vella fistula (TVF). After a 1-week recovery period, rats were further subdivided into groups to receive either saline (control) or NT (300 micrograms/kg). Rats were killed on day 6, and TVF as well as corresponding segments of intact jejunum or ileum were removed. Mucosa was scraped, weighed, and analyzed for DNA and protein content. In addition, representative sections of full-thickness bowel from each group were examined histologically. In the jejunal TVF group, NT increased mucosal growth measurements in both the TVF and the intact jejunum. However, in the ileal TVF group, NT stimulated proliferation of intact ileal mucosa only; it had no effect on ileal mucosa in the TVF. These results suggest that NT exerts a systemic effect independent of luminal factors on the proliferation of proximal gut mucosa in addition to an indirect effect produced by stimulation of endogenous luminal secretions. In contrast, an indirect mechanism appears to be the predominant action of NT on growth of distal gut mucosa.     

The localization of the site(s) of neurotensin release in man and dog

The major source of neurotensin in the gut is the ‘N’ cell and this is found in the highest density in the ileum. The ingestion of food, particularly fat, causes the biphasic release of neurotensin-like immunoreactivity (NTLI) into the circulation. The early peak occurs sooner than expected if it is due to the presence of chyme in the ileum, suggesting that the early release of neurotensin is due to a more proximal concentration of N cells or that neurotensin is released from the ileum by a more proximal stimulus. This paper investigates the site(s) of neurotensin release by studying: three groups of patients with various resections of the small intestine and the fashioning of duodenostomies, jejunostomies and ileostomies; and the dog with chronic gastric, duodenal and ileal fistulae, and following ileal resection. The results indicate that the jejunum and ileum are critical in the release of neurotensin following fat stimulation and that the stomach and duodenum have no direct role. The stimulation of the jejunum by fat causes the early rise of plasma NTLI by releasing neurotensin from the ileum. If chyme is prevented from passing to the distal jejunum the magnitude of the early peak is diminished and the second, later, peak is abolished. The second peak of plasma NTLI is due to the direct luminal stimulation of the distal jejunum and ileum by the products of fat digestion. Ileal resection completely abolishes any release of plasma NTLI in response to fat. It was concluded that the source of neurotensin released by the ingestion of food is the ileum. The release of neurotensin from the distal gut is dependent upon a signal from the proximal to the distal gut. The identity of the signal is unknown, but it is either neural or humoral and previous studies suggest a cholinergic-dependent reflex.     

Human intestinal motor activity and transport: effects of a synthetic opiate

Effects of opiates on intestinal motor activity and transport of water and electrolytes have been studied separately in previous investigations. The aim of these experiments was to evaluate simultaneously the effects of a synthetic opiate, loperamide, on motor activity and transport in the human intestine. Jejunal, ileal, and colonic perfusions were performed in 9 healthy volunteers. After application of loperamide (12 mg), cyclically recurring migrating motor complexes in the small intestine occurred at a significantly higher frequency than after application of placebo. This was primarily due to a decrease in the duration of irregular motor activity (phase II). Loperamide increased the transit time in the jejunum but not in the ileum or in the colon. Transport rates of water and electrolytes and transmural electrical potential differences were not significantly affected by the drug. These results suggest that opiates exert their constipating effect by inhibiting phase II-related irregular motor activity.     

Study of the duodenal contractile activity during antral contractions

AIM: To investigate the hypothesis that duodenal bulb (DB) inhibition on pyloric antrum (PA) contraction is reflex. METHODS: Balloon (condom)-tipped tube was introduced into 1st duodenum (DD) and a manometric tube into each of PA and DD. Duodenal and antral pressure response to duodenal and then PA balloon distension with saline was recorded. These tests were repeated after separate anesthetization of DD and PA. RESULTS: Two and 4 mL of 1st DD balloon distension produced no pressure changes in DD or PA (10.7 ± 1.2 vs 9.8 ± 1.2, 11.2 ± 1.2 vs 11.3 ± 1.2 on H2O respectively, P > 0.05). Six mL distension effected 1st DD pressure rise (30.6 ± 3.4 cm H2O, P < 0.01) and PA pressure decrease (6.2 ± 1.4 cm H2O, P < 0.05); no response in 2nd, 3rd and 4th DD. There was no difference between 6, 8, and 10 mL distensions. Ten mL PA distension produced no PA or 1st DD pressure changes (P > 0.05). Twenty mL distension increased PA pressure (92.4 ± 10.7 cm H2O, P < 0.01) and decreased 1st DD pressure (1.6 ± 0.3 cm H2O, P < 0.01); 30, 40, and 50 mL distension produced the same effect as the 20 mL distension (P > 0.05). PA or DD distension after separate anesthetization produced no significant pressure changes in PA or DD. CONCLUSION: Large volume DD distension produced DD pressure rise denoting DD contraction and PA pressure decline denoting PA relaxation. PA relaxation upon DD contraction is postulated to be mediated through a reflex which we call duodeno-antral reflex. Meanwhile, PA distension effected DD relaxation which we suggest to be reflex and termed antro-duodenal reflex. It is suggested that these 2 reflexes, could act as investigative tools indiagnosis of gastroduodenal motility disorders.     

Effects of intravenous calcitonin on water, electrolyte, and calcium movement across in vivo rabbit jejunum and ileum.

The influence of intravenously administered synthetic salmon calcitonin on water, electrolyte and calcium fluxes in in vivo rabbit jejunum and ileum was examined. Rabbits were divided into four groups: those receiving (1) saline intravenously while a glucose-free isotonic saline solution perfused the jejunum and ileum; (2) calcitonin intravenously while the same intestinal perfusate was used as in group 1; (3) intravenous saline while 10 mM glucose-isotonic saline solution perfused jejunum and ileum; and (4) intravenous calcitonin while the intestinal perfusate was of the same composition as in group 3. Calcitonin provoked a significant increase in jejunal and ileal water, sodium, and bicarbonate secretion in both the glucose-free and glucose-containing perfusate groups. No influence on calcium movement was noted. These results, similar to findings of Gray et al. (J Clin Invest 52:3084-3088, 1975) in human jejunum, suggest that calcitonin may play a role in the pathogenesis of the watery diarrhea noted in about one-third of patients with medullary carcinoma of the thyroid. In addition, these studies demonstrate the usefulness of the rabbit as an animal model with which to investigate further the effects of calcitonin upon intestinal fluid and electrolyte transport.     

Murine schistosomiasis mansoni: estimation on some immunohistological parameters of small bowel granulomas and renal parenchyma

One hundred and twenty five mice were divided into three groups: uninfected (I), and infected with 30 (II) and 60 (III) cercariae. Jejunal, ileal and renal sections were analyzed by direct immunofluorescence technique, aiming the detection of gamma globulins and complement C3. Intestinal sections were also stained by hematoxylin-eosin, during some periods of disease. The cellular composition of the jejunal and ileal granulomas seemed very similar, with many eosinophils and an increased number of mononuclear cells later on. The histological evaluation of these sections showed that the ileum may hold greater number of eggs, possibly being more affected than the jejunum. The results also suggest a mixed mechanism to the formation of intestinal granulomas, both cell and antibody mediated.     

Rectal distension inhibits postprandial small intestinal motor activity partially via the adrenergic pathway in dogs

Objective. Rectal distension is known to induce numerous upper gastrointestinal symptoms. The aim of this study was to investigate the effects and mechanisms of rectal distension on small intestinal myoelectrical and motor activities in 8 dogs using a pair of intestinal electrodes and an intestinal fistula. Material and methods. Experiment 1 entailed a 30-min baseline recording and a 30-min recording during rectal balloon distension at various volumes (60, 80, 100 and 120 ml) randomly. Experiment 2 comprised three sessions, each including a 30-min baseline recording, a 20-min recording after intravenous infusion of saline, phentolamine (3 mg/kg) or propranolol (3 mg/kg), respectively, and another 30-min recording during rectal balloon distending. Results. 1) Rectal distension resulted in reduced intestinal motility in a dose-dependent manner (r=0.68, p<0.001). 2) The reduction in intestinal motility was significantly diminished when infusions of phentolamine (2.7±1.0 versus 8.4±1.5, p<0.01) or propranolol (3.7±1.4 versus 8.4±1.5, p<0.05) were given, suggesting partial involvement of the alpha- and beta-adrenergic pathways. 3) Rectal distension did not affect the percentage of normal 17–22 cycles/min intestinal slow waves (97.5±2.5 versus 93.0±5.3, p>0.05), or their dominant frequency (17.2±1.2 counts per minute (cpm) versus 17.7±1.0 cpm, p>0.05), or dominant power (?4.8±2.5 versus ?8.2±2.9 dB, p>0.05). Conclusions. Rectal distension inhibits postprandial small intestinal motor activity in a distension volume-dependent manner in dogs, and this inhibitory effect is at least partially mediated via the alpha and beta adrenergic pathways and does not involve any alterations in intestinal slow waves.     

Functional and structural characteristics of the rat intestinal mucosa following ileo-jejunal transposition

The transformation of the rat ileal mucosa following interposition into the jejunum has been examined with respect to its functional and structural characteristics. Morphometric studies show that there is an increase in the size of the villi and crypts in the same proportions, such that the structures become longer than those of normal jejunal mucosa. There is no change in villus width or epithelial cell height and no evidence of mucosal damage. In agreement with these observations, there is an increase in the amount of DNA per unit weight mucosa in the transposed ileum. L-phenylalanine accumulation in vitro by transposed loops is reduced to the level of the control jejunum, whereas beta-methyl-D-glucose uptake is unchanged. Biochemical and histochemical determinations of various enzyme activities reveal that the levels in the transposed mucosa are much lower than in the controls. The results show that although certain features of the transposed ileum resemble those of the normal jejunum, this does not apply to all characteristics. It is argued that the ileal mucosa retains its normal functional properties, but undergoes hyperplastic changes, possibly as a result of contact with chyme that is richer in nutritive material, resulting in the establishment of a more immature cell population with a global reduction in enzyme levels and transport capacities.     

Effect of a model of canine jejunoileal orthotopic autotransplantation on jejunal and ileal transport of water and electrolytes

Canine jejunoileal transplantation induces an early profuse watery diarrhea of uncertain etiology. Our aim was to determine the temporal effects of a canine model of jejunoileal autotransplantation (a model devoid of confounding effects of ischemia-reperfusion or immune rejection) on basal jejunal and ileal absorption of water and electrolytes to determine if impaired absorption is responsible for the diarrhea. Our hypothesis was that net absorption of water and electrolytes in an enterically isolated loop would decrease after jejunoileal transplantation. Four groups of dogs (N 6) were prepared with 80-cm modified Thiry-Vella loops: group I, neurally intact jejunum; group II, autotransplanted jejunum; group III, neurally intact ileum; and group IV, autotransplanted ileum. The loops were perfused for 3 hr with 150 mM NaCl at 3 ml/min under fasted conditions; transit time through the loop was determined by bolus of a nonabsorbable marker. Dogs were studied on three separate days at one, two, eight, and nine weeks postoperatively. Net absorptive fluxes of water and electrolytes and transit times were similar (P>0.05) between neurally intact and autotransplant groups (group I vs II and group III vs IV) at each time point. Ileal loops absorbed more than jejunal loops, and transit was slower in ileal loops (eachP<0.05). Our findings suggest that, despite the obligate disruption of extrinsic innervation, enteric (intrinsic) neural continuity, and lymphatic drainage that accompanies this canine model of jejunoileal autotransplantation, net basal absorptive function of water and electrolytes during the fasted state was not decreased nor was transit altered either in jejunum or ileum. These findings have important implications for clinical small intestinal transplantation in man.Supported by NIH RO1 DK39337 (M.G.S.), Ethicon Corporation, and Mayo Foundation.     

Intestinal regrowth is amplified after jejunal but not ileal resection during tapeworm infection in the rat

The ileum possesses functions required by a healthy individual that are not fully supplanted by the duodenum or jejunum. Evidence suggests that the ileum may also be necessary to maintain an enteric parasite–host interaction. We hypothesized that the ileum is essential to the survival of the lumen-dwelling, rat tapeworm, H. diminuta. Male rats were divided into three groups: those with ileal or jejunal resections and nonresected controls. Half of each rat group was infected with the tapeworm. After jejunal resection, the weight but not length of intestinal remnant (duodenum + ileum) in infected rats returned to that of control, nonresected intestine 29 days after surgery and tapeworm numbers were fully maintained. In contrast, after ileal removal intestinal length and weight of the remaining duodenum and jejunum in infected rats were significantly decreased and tapeworm survival diminished. Data indicates that intestinal growth following resection is amplified by tapeworm infection when the ileum remains but diminished when the ileum is removed. Furthermore, loss of the ileum results in decreased infection intensity and dry weight of the tapeworm.