Effects of enteral arginine supplementation on the structural intestinal adaptation in a rat model of short bowel syndrome

The nitric oxide precursor L-arginine (ARG) has been shown to influence intestinal morphology and intestinal absorptive function. The purpose of the present study was to determine the effect of enteral ARG supplementation on structural intestinal adaptation, cell proliferation, and apoptosis in a rat model of short bowel syndrome (SBS). Thirty male Sprague-Dawley rats were divided into three experimental groups: Sham rats underwent bowel transection, SBS rats underwent 75% small bowel resection, and SBS-ARG rats underwent bowel resection and were treated with ARG given in the drinking water (2%). Parameters of intestinal adaptation, enterocyte proliferation and enterocyte apoptosis were determined on day 14 following operation. We have demonstrated that SBS-ARG animals had a lower jejunal and ileal mucosal weight, jejunal mucosal DNA and protein, ileal mucosal protein, jejunal villus height, jejunal and ileal crypt depth, and enterocyte proliferation index and a greater enterocyte apoptosis compared to SBS untreated animals. We conclude that in a rat model of SBS enteral L-arginine inhibits structural intestinal adaptation. Possible mechanism for this effect may be decreased cell proliferation and increased cell apoptosis.     

Sandostatin impairs postresection intestinal adaptation in a rat model of short bowel syndrome

Because of its antisecretory properties, sandostatin has been advocated for the treatment of patients with short bowel syndrome (SBS). This study was conducted to determine the effect of sandostatin on structural intestinal adaptation, cell proliferation and apoptosis in a rat model of SBS. Sprague-Dawley rats were divided into three experimental groups: Sham rats underwent bowel transection, SBS rats underwent 75% small bowel resection, and SBS-sandostatin rats underwent bowel resection and were treated with sandostatin (SBS-SND). Parameters of intestinal adaptation, enterocyte proliferation, and enterocyte apoptosis were determined on day 14 following operation. We have demonstrated that SBS-SND animals demonstrated lower (vs SBS rats) duodenal and jejunal bowel weights, jejunal and ileal mucosal weight, jejunal and ileal mucosal DNA and protein, jejunal and ileal villus height, cell proliferation index in the ileum, and enterocyte apoptosis in jejunum and ileum. We conclude that in a rat model of SBS sandostatin decreases cell proliferation and inhibits structural intestinal adaptation.     

Effect of different total parenteral nutrition fuel mixes on small intestinal growth and differentiation in the infant miniature pig

Insulin has been proposed as an important factor in the regulation of growth and differentiation of the small intestine. In the newborn miniature pig, we induced significant physiologic increases in serum insulin and the insulin/glucagon ratio without altering serum glucose, beta-hydroxybutyrate, glucagon, cortisol, T3, and T4 using glucose-based total parenteral nutrition (TPN) in one group (group G) compared with a combination of glucose and fat in another group (group G/F). Control animals were sham-operated and fed a pelleted diet (group OC). Duodenal villus surface area and mucosal height were significantly greater in group G/F compared with group G. No other differences between the TPN groups were found in small intestinal growth, mucosal protein, deoxyribonucleic acid and ribonucleic acid content, and disaccharidase activities. As anticipated, group OC demonstrated increased intestinal length, weight, and villous surface area compared with the TPN groups. Ileal sucrase and jejunal and ileal maltase activities were greater in the TPN groups compared with those in group OC. Physiologic changes in serum insulin and the insulin/glucagon ratio induced by the TPN fuel mix do not appear to have altered small intestinal growth, composition, and differentiation in the healthy small intestine.     

Oral Insulin Enhances Intestinal Regrowth Following Massive Small Bowel Resection in Rat

Experimental studies have suggested that insulin (INS) plays an important role in small intestinal growth and development. In the present study we investigated the effect of oral INS on structural intestinal adaptation and enterocyte proliferation and loss via apoptosis in a rat model of short bowel syndrome (SBS). Male Sprague–Dawley rats were divided into three experimental groups: sham rats underwent bowel transection, SBS rats underwent 75% small bowel resection, and SBS-INS rats underwent bowel resection and were treated with oral INS given in the drinking water from the 3rd to the 15th postoperative day. Parameters of intestinal adaptation (bowel and mucosal weight, mucosal DNA and protein, villous height, and crypt depth), enterocyte proliferation, and apoptosis were determined on day 15. SBS-INS rats demonstrated a significant increase (vs SBS rats) in jejunal and ileal overall bowel and mucosal weight, ileal mucosal DNA and protein, ileal villous height, and crypt depth. SBS-INS rats also showed an increased cell proliferation index in jejunum and ileum and decreased apoptotic index in jejunum compared to SBS animals. In conclusion, in a rat model of SBS, oral INS strongly enhances intestinal adaptation.Possible mechanisms may include increased cell proliferation and decreased enterocyte loss via apoptosis. Contributed equally to the preparation of this article.     

Effects of octapeptide-cholecystokinin,secretin, and glucagon on intestinal mucosal growth in parenterally nourished rats

Nutrients in the lumen of the small intestine may cause the release of enteric hormones which directly or indirectly stimulate intestinal mucosal growth. Male Sprague-Dawley rats with either an intact small bowel or following jejunal resection were maintained on total parenteral nutrition (TPN). C-terminal octapeptide-cholecystokinin alone or combined with secretin, or glucagon alone were added to the intravenous nutrient solution and continuously infused. Control rats received only TPN or gastric infusion of isocaloric amounts of TPN solution. After 7 days, intestinal hypoplasia was noted in rats with an intact bowel maintained on TPN alone compared with the gastrically infused group. TPN did not maintain the proximal-distal gradient of mucosal mass. Continuous intravenous infusion of octapeptide-cholecystokinin alone and together with secretin in rats maintained on TPN significantly stimulated small bowel mucosal growth, partially restoring the proximal-distal gradient. Glucagon infusion did not stimulate mucosal growth. Rats with a jejunal resection and maintained on TPN for 7 or 14 days failed to develop mucosal hyperplasia of the ileum in contrast to rats given the TPN solution intragastrically. Continuous intravenous infusion of octapeptide-cholecystokinin in rats maintained on TPN after jejunal resection caused significant mucosal growth in the ileum compared with the rats maintained on TPN alone, but not to the extent seen in gastrically fed animals. Intravenous infusion of octapeptide-cholecystokinin stimulates small-bowel mucosal growth. Secretin appears to have an additional effect when given together with octapeptide-CCK. Although a direct trophic action by these hormones on the intestinal mucosa is possible, this effect is more likely mediated via stimulation of pancreaticobiliary secretions.This work was supported by the Morrison Trust of San Antonio. SQ 19,844 was generously provided by Dr. Miguel Ondetti of the Squibb Institute for Medical Research.     

The effect of resection of the jejunum and ileum on intestinal mucosal trophism. An experimental study on the rat]

Intestinal resection leads to anatomo-physiological adaptive changes in the small bowel depending on its localization and extension. Two 50% resection models were done, jejunal resection (55 cm.) and ileal resection (55 cm.), in the attempt to determine the trophic response of the remnant bowel from jejunal and ileal samples. Significant increases were seen in mucosal villous length, jejunal values were greater than ileal and the greatest values were when the whole ileum was conserved. No significant changes were observed in DNA contents. These data suggest the importance of the ileal segment in the intestinal adaptive process, especially on the jejunal segment, as well as the apparent end of this response two weeks after resection.     

Glucagon-like Peptide-2 Induces a Specific Pattern of Adaptation in Remnant Jejunum

Glucagon-like peptide-2 (GLP-2) is an enteroendocrine hormone which is uniquely trophic for the intestine; a physiological role in regulating nutrient absorptive capacity is becoming apparent. GLP-2, independent of enteral feeding, stimulates a classical pattern of intestinal adaptation in terminal ileum following resection. Herein we investigate the effects of GLP-2 on the jejunal remant using a rat model of short bowel syndrome (SBS). Juvenile 250- to 275-g SD rats underwent 80% distal small bowel resection, leaving 20 cm of proximal jejunum and venous catheterization. Animals were maintained with total parenteral nutrition (TPN) or TPN+10 μg/kg/hr GLP-2 (n=8 per group). After 7 days, intestinal permeability was assessed by urinary recovery of gavaged carbohydrate probes. Animals were euthanized, and the intestines taken for analysis of morphology, crypt cell proliferation, apoptosis, and expression of SGLT-1 and GLUT-5 transport proteins. GLP-2 treatment reduced intestinal permeability and increased in vivo glucose absorption, small intestinal weight, surface area, villus height, crypt depth, and microvillus height. Intestinal mucosal DNA and protein content per unit length of the small bowel were increased (P < 0.05 for all comparisons). However, in contrast to previous studies examining GLP-2’s effects on remnant ileum, the jejunal crypt apoptotic index was increased in GLP-2-treated animals, with no increase in SGLT-1 or GLUT 5 expression. These results show that exogenous GLP-2 treatment of animals with jejunal remnant reduces intestinal permeability, increases glucose absorption, and stimulates morphological features of intestinal adaptation including increased micovillus height and surface area. However, the pattern of changes seen is different from that in remnant ileum. This suggests that GLP-2’s effects are specific to different regions of the bowel. Nonetheless, remnant jejunum is responsive to GLP-2 in the absence of enteral nutrition. Further studies are warranted to establish the mechanisms of action and therapeutic potential of GLP-2 in modulating nutrient absorptive capacity.     

Adaptive changes in postprandial motility after intestinal resection and bypass

An electromyographic technique was used to study the changes in postprandial motility induced by jejunal and ileal resection and jejunal bypass (50% reduction of total length of small bowel). Electrodes were implanted in rats throughout the intestine. Compared to control animals, the duration of postprandial interruption of the myoelectric complex (DIMC) was rapidly increased after jejunal resection, more gradually augmented after jejunal bypass, and remained constant after ileal resection. The frequency of occurrence of spike bursts during the postprandial period was significantly decreased in the short remaining proximal segment after jejunal resection and was not changed in the ileum. The jejunal bypass induced no change in the frequency throughout the remaining bowel. Ileal resection was followed by a decrease on the jejunum. The percentage of slow waves superimposed by a spike burst remained constant after jejunal resection and bypass but was significantly decreased after ileal resection on the whole remaining intestine. These results show important modifications in postprandial motor activity of the small bowel, which appear rapidly after jejunal resection, more gradually after jejunal bypass, and which are less pronounced after ileal resection. This electromyographic study emphasizes the role of intestinal motility in the development of adaptation after small bowel resection or bypass.     

Growth hormone plus high protein diet promotes adaptation after massive bowel resection in aged rats

Objective. To determine whether GH improves adaptation following massive bowel resection in the aged rat fed on a high protein-content diet.

Material and methods. Seventy-seven male Wistar rats aged 22±1 months underwent 80% bowel resection or laparotomy (sham-operation). They were randomly placed into one of eight groups, treated with either growth hormone (1 mg/kg/day) or saline, and fed a liquid diet containing either a high or a normal protein content. Intestinal tissue and blood samples were taken seven days after surgery and analysed to measure intestinal mucosal proliferation and mucosal height, as well as plasma levels of IGF-1 and somatostatin.

Results. Resection of the small bowel in aged rats remarkably increased villous height and crypt proliferation. Growth hormone did not potentiate the increase in mucosal height and crypt proliferation observed after intestinal resection in aged rats fed a normal protein content diet, but did in those receiving a high-protein diet. Plasma levels of IGF-1 and somatostatin were not modified by surgery or treatment.

Conclusion. Growth hormone may increase the adaptation of intestinal mucosa in aged rats undergoing massive intestinal resection, but requires an adequate nutritional support with increased amounts of high quality protein.     

Suppression of diamine oxidase activity enhances postresection ileal proliferation in the rat

To assess the influence of diamine oxidase activity on the adaptive process of the small bowel after resection, we administered aminoguanidine, a potent diamine oxidase inhibitor, to rats for 10 days after either small bowel transection (n = 5) or 80% jejunoileal resection (n = 7). Five or more additional animals from each group received saline as controls. Ileal mucosal homogenates from the resection group receiving aminoguanidine, when compared with those from resection controls, showed no diamine oxidase activity with increased putrescine content and ornithine decarboxylase activity. Mucosal proliferation, as measured by mucosal mass, protein content, and deoxyribonucleic acid content, was greater in the resected animals receiving aminoguanidine when compared with that of resection controls. Sucrase activity per gram of mucosa was almost identical in both resection groups. These results show that the suppression of diamine oxidase during the postresection adaptive period results in enhanced mucosal proliferation with no effect on mucosal functional differentiation. Diamine oxidase may play a regulatory role in adaptive intestinal proliferation.     

Essential fatty acid deficiency and postresection mucosal adaptation in the rat

The effect of short-term (biochemical) and long-term (clinical) essential fatty acid (EFA) deficiency on mucosal adaptation was studied in a surgical model of short bowel syndrome. Rats fed an EFA-deficient diet for 4 wk had biochemical evidence of EFA deficiency (hepatic and red blood cell triene to tetraene ratios greater than 0.4). Resected animals (70% proximal jejunoileal resection) receiving an EFA-deficient diet had a significantly impaired intestinal mucosal hyperplasia response in all remaining small bowel segments compared with resected controls. The effect of refeeding a control diet to clinically EFA-deficient resected rats was also evaluated. Short-term refeeding (2 wk) of a control diet resulted in a significant return toward normal tissue triene to tetraene ratios. Concomitantly, refed animals had significantly greater mucosal adaptation in the remaining duodenal/jejunal segment compared with resected animals maintained on an EFA-deficient diet postoperatively. These experiments underscore the dynamic nature of tissue EFA status and the importance of fatty acids in the normal compensatory mechanisms of mucosal adaptation after resection.     

Systemic Short-Chain Fatty Acids Rapidly Alter Gastrointestinal Structure, Function, and Expression of Early Response Genes

Luminal and systemic short chain fatty acids (SCFA) stimulate mucosal proliferation but the mechanism(s) is unclear. This study examined acute effects of systemic SCFAs on gastrointestinal structure and function and signals potentially mediating SCFA-induced mucosal proliferation. Male Sprague-Dawley rats (246 ± 2 g) received nutrients as either standard total parenteral nutrition (TPN) or an isoenergetic, isonitrogenous formulation containing SCFAs (TPN + SCFA). Animals were randomized to one of five treatments: standard TPN for 72 hr, TPN + SCFA for 72 hr, or standard TPN followed by TPN + SCFA for the final 6, 12, and 24 hr. SCFAs reduced (P < 0.003) ileal protein within 6 hr. Jejunal GLUT2 expression was increased (P = 0.0001) in all SCFA groups and ileal GLUT2 protein in the 6-, 12-, and 24-hr SCFA groups (P < 0.05). SCFAs increased (P < 0.003) ileal proglucagon abundance following 6, 12, and 24 hr, and plasma GLP-2 concentration following 12 hr (P < 0.03). Jejunal c-myc expression was increased (P < 0.001) following 6, 12, and 24 hr of SCFAs. SCFAs increased ileal c- myc , c- jun, and c-fos expression following 24 hr (P < 0.02), 12 hr (P < 0.05) and 6, 12, and 24 hr (P = 0.0001), respectively. In conclusion, systemic SCFAs increase plasma GLP-2 and ileal proglucagon mRNA, GLUT2 expression and protein, and c-myc, c-jun, and c-fos expression.     

Effect of bowel rehabilitative therapy on structural adaptation of remnant small intestine: animal experiment

AIM To investigate the individual and thecombined effects of glutamine, dietary fiber,and growth hormone on the structural adaptationof the remnant small bowel.METHODS Forty-two adult male Sprague-Dawley rats underwent 85% mid-small bowelresection and received total parenteral nutrition(TPN) support during the first threepostoperational days. From the 4thpostoperational day, animals were randomlyassigned to receive 7 different treatments for 8days: TPNcon group, receiving TPN and enteral20g·L~1 glycine perfusion; TPN Gin group,receiving TPN and enteral 20 g·L~1 glutamineperfusion; ENcon group, receiving enteralnutrition (EN) fortified with 20 g·L~1 glycine; EN Gin group, enteral nutrition fortified with20g·L~1 glutamine; EN Fib group, enteralnutrition and 2 g·d~1 oral soybean fiber; EN GHgroup, enteral nutrition and subcutaneousgrowth hormone (GH) (0. 3IU) injection twicedaily; and ENint group, glutamine-enriched EN,oral soybean fiber, and subcutaneous GHinjection.RESULTS Enteral glutamine perfusion duringTPN increased the small intestinal villus height(jejunal villus height 250μm 29μm in TPNcon vs 330μm±54μm in TPN Gln, ileal villus height260μm±28μm in TPNcon vs 330μm±22μm inTPN Gln, P<0.05) and mucosa thickness(jejunal mucosa thickness 360μm ± 32μm inTPNcon vs 460μm±65μm in TPN Gln, ilealmucosa thickness 400μm ± 25μm in TPNcon vs490μm ± 11μm in TPN Gin, P<0.05) incomparison with the TPNcon group. Either fibersupplementation or GH administration improvedbody mass gain (end body weight 270 g ± 3.6 g inEN Fib, 265.7 g ± 3.3 g in EN GH, vs 257g±3.3g in ENcon, P<0.05), elevated plasmainsulin-like growth factor (IGF-I) level(880μg·L~1±52μg.L~(-1) in EN Fib, 1200μg·L(-1) 96μg·L~(-1) in EN GH, vs 620μg·L~(-1) ±43μg·L~1 in ENcon, P<0.05), and increased thevillus height (jejunum 560μm ± 44μm in EN ± Fib,530μm ± 30μm in EN±GH, vs 450μm±44μm inENcon, ileum 400μm ± 30μm in EN Fib, 380μm±49μm in EN ± GH, vs 320μm ± 16μm in ENcon,P<0.05) and the mucosa thickness (jejunum740μm ± 66μm in EN ± Fib, 705μm ± 27 μm in EN ±GH, vs 608μm ± 58μm in ENcon, ileum 570μm ±27μm in EN ± Fib, 560μm ± 56μm in EN ± GH, vs480μm ± 40μm in ENcon, P<0.05) in remnantjejunum and ileum. Glutamine-enriched ENproduced little effect in body mass, plasma IGF-I level, and remnant small bowel mucosalstructure. The ENint group had greater bodymass (280g ± 2.2 g), plasma IGF-1 level(1450μg.L~1 ± 137μg.L~1), and villus height(jejunum 620μm ± 56μm, ileum 450μm ± 31μm)and mucosal thickness (jejunum 800μm ± 52μm,ileum 633μm ± 33μm) than those in ENcon, EN Gln (jejunum villus height and mucosa thickness450μm ± 47μm and 610μm ± 63μm, ileum villusheight and mucosa thickness 330μm ± 39μm and500μm±52μm), EN GH groups (P<0.05), andthan those in EN Fib group although nostatistical significance was attained.CONCLUSION Both dietary fiber and GH whenused separately can enhance the postresectionalsmall bowel structural adaptation. Simultaneoususe of these two gut-trophic factors can producesynergistic effects on small bowel structuraladaptation. Enteral glutamine perfusion isbeneficial in preserving small bowel mucosalstructure during TPN, but has little beneficialeffect during EN.     

Injury-induced inhibition of small intestinal protein and nucleic acid synthesis.

Small intestinal mucosal weight and nutrient absorption are significantly diminished early after cutaneous thermal injuries. Because these intestinal properties are highly dependent on rates of nucleic acid and protein synthesis, in vivo incorporation of thymidine, uridine, and leucine into small intestinal deoxyribonucleic acid, ribonucleic acid, and proteins were measured. Deoxyribonucleic acid synthesis was markedly decreased with the lowest thymidine incorporation in the jejunum (p less than 0.01); these findings were confirmed by autoradiographic identification of radiolabeled nuclei in the intestinal crypts. Protein synthesis was decreased by 6 h postinjury (p less than 0.01) but had returned to normal by 48 h. Consistent with a decreased rate of protein synthesis, ribonucleic acid synthesis was also decreased 18 h postinjury (p less than 0.01). These decreased deoxyribonucleic acid, ribonucleic acid, and protein synthesis rates are not likely a result of ischemia because in other studies of this injury model, intestinal blood flow was not significantly changed by the burn injury. Potentially, factors initiating the acute inflammatory reaction may directly inhibit nucleic acid and protein synthesis and lead to alterations in nutrient absorption and intestinal barrier function after injury.     

Relationship between enteral glucose load and adaptive mucosal growth in the small bowel

Infusion of hyperosmolar glucose solutions into small bowel will prevent mucosal atrophy or stimulate mucosal growth in rats otherwise maintained on total parenteral nutrition (TPN). It is not certain whether this growth effect is related to the osmolarity of the solution or its total molecular load. Therefore, various concentrations of glucose and sodium salt solutions were studied for comparative effects on growth of small bowel mucosa. Male Sprague-Dawley rats (240 g) were maintained on TPN and infused continuously with either glucose or sodium chloride (2 and 0.6 ml/hr) or sodium sulfate (0.6 ml/hr) via a catheter placed in the mid-small intestine. Concentrations of infusion solutions ranged in osmotic pressure from 300 to 1500 mosmol/liter. Controls were TPN rats without infusion of any solution. Over a seven-day period, TPN rats receiving mid-gut infusions of 300 mosM saline gained 18.4 g in body weight. In TPN rats receiving mid-gut infusions of progressively greater concentrations of glucose, the additional total kilocalories per day resulted in greater body weight gain compared with the saline controls. After seven days, rats were killed, the small bowel removed, and divided into eight equal segments (segment 1, duodenum; segment 8, terminal ileum). Segment weight, mucosal weight, DNA, and protein concentration per segment were measured. Mid-gut infusions of 900 and 1500 mosM glucose solutions progressively increased mucosal mass in segments downstream from the site of infusion compared with 300 mosM glucose in water or 600 mosM glucose in saline which did not differ from any of the salt solutions or TPN alone.(ABSTRACT TRUNCATED AT 250 WORDS)     

Effect of intestinal resection on human small bowel motility.

BACKGROUND: Few data are available on adaptive changes of human small bowel motility after intestinal resection. AIM: To characterise jejunal motility after extensive and limited distal intestinal resection. METHODS: Seven patients with a short bowel syndrome after total ileal and partial jejunal resection (residual jejunal segments between 60 and 100 cm) and six patients with limited distal ileal resection (resected segment between 30 and 70 cm) underwent ambulatory 24 hour jejunal manometry 15 (6-24) months after the operation. Normal values were obtained from 50 healthy subjects. Fasting motility and the motor response to a 600 kcal solid meal were analysed visually and by a computer program. RESULTS: Limited ileal resection did not result in changed jejunal motility. After extensive distal resection, patients had a significantly shorter migrating motor complex (MMC) cycle and a significantly shorter duration of the postprandial motor response compared with controls (p < 0.005). Intestinal resection had no influence on jejunal contraction frequency and amplitude and did not lead to any abnormal motor pattern. CONCLUSION: Extensive distal resection of the small intestine produces distinct abnormalities of fasting and postprandial motility in the intestinal remnant. The shortening of digestive motility and the increased frequency of MMC cycling could contribute to malabsorption and diarrhoea in the short bowel syndrome.     

Morphological and functional effects of 16,16-dimethyl-prostaglandin-E2 on mucosal adaptation after massive distal small bowel resection in the rat.

The ability of 16,16-dimethyl-prostaglandin-E2 (PGE) to augment mucosal adaptation 14 days after a 70% distal small bowel resection in the rat was evaluated. In resected (R) and sham operated (S) animals, subcutaneous PGE 75 mg/kg, 2 X/day, induced significant (p less than 0.05) increases in mucosal protein, DNA, and disaccharidase concentrations per centimetre of bowel. The respective per cent increases in the residual proximal small intestine compared with their respective untreated controls were: protein, R = 60%, S = 66%; DNA, R = 69%, S = 29%; maltase, R = 57%, S = 5%. The uptake of leucine by intestinal rings was significantly higher (50%) in the PGE treated group at a concentration of 2 mmol/l of substrate, while the uptake of glucose was similar in all groups. The drug appears to be an effective agent in stimulating morphological and functional adaptation after massive distal small bowel resection.     

The value of in vivo electrophysiological measurements for monitoring functional adaptation after massive small bowel resection in the rat.

The process of functional adaptation after extensive small bowel resection is complex and imprecisely understood. In vivo electrophysiological measurements for monitoring the functional adaptive process after massive small bowel resection in Brown-Norway rats were evaluated. Rats underwent either a sham operation (SH) or a 90% small bowel resection (SB). Standard rat chow was fed in unlimited quantities. At three or 10 weeks after operation, jejunal and ileal transepithelial potential differences (PD, mV) were determined. Electrogenic ion transport in the villus was measured after glucose (sodium coupled active glucose absorption; PD-glu) and in the crypt, after theophylline infusion (theophylline stimulated chloride secretion; PD-theo). Biopsies were taken simultaneously. Each experimental group consisted of three to five animals. At three weeks the PD-theo and PD-glu in SB rats were significantly lower than in SH rats in both jejunal and ileal segments. At 10 weeks PD-theo and PD-glu were significantly diminished in the jejunal segment of the SB rats compared with the SH rats. The values of PD-theo and PD-glu in the ileal segments were, however, no longer different between the two groups. Three and 10 weeks after operation the length of the villi in the SB group was increased significantly compared with the SH controls. These results indicate that in the early phase of adaptation in vivo electrophysiological variables do not correlate with histological changes in the SB rats. This might be due to cell immaturity resulting from an increased rate of cell turnover or lack of intercellular tight junctions. This hypothesis is supported by a recovery of PD responses in the ileum 10 weeks after resection.     

Adaptation of jejunal to colonic mucosal autografts in experimentally induced short bowel syndrome

The behavior of jejunal to colonic mucosal autografts was studied in an experimental animal model of short bowel syndrome (SBS). Histological appearances, enterocyte enzyme activities, and in vitro glucose transport were studied at the donor and recipient graft sites in control, short-bowel syndrome, and gastrocolic fistula 5-week-old Sprague-Dawley rats. Small intestinal function was maintained in the jejunocolonic graft after 80% small bowel resection; animals in which small bowel was not resected showed loss of graft function and enzyme activity. This effect is dependent on the presence of jejunal chyme: after gastrocolic fistulae, the jejunum to colon grafts lost jejunal functional activities. Total parenteral nutrition did not alter graft behavior but improved the postoperative mortality of the procedures. The results provide additional information on intestinal adaptation in SBS.     

Adaptation mechanisms to the short intestine. Influence of the biliopancreatic factor: experimental study

Massive small bowel resection that results in short bowel syndrome brings about regulatory mechanisms in the remaining intestine aimed at preventing the ensuing malabsorption. The purpose of the present study was to determine the role of pancreatic and biliary secretions in intestinal adaptation after small bowel resection. To do so, both pancreatic and biliary fluids were prevented from reaching the lumen of most of the small bowel. Four groups of animals were prepared: I) control group; II) eighty percent small bowel resection; III) duodenoileal by-pass; and IV) duodenoileal by-pass plus small bowel resection. After a fifteen days recovery period, the following were recorded: animal weight; plasma protein, BUN, cholesterol, glucose, and Ca++; the length and diameter of the jejunum and ileum, the height of the mucosal layer, and microvilli density. Intestinal adaptation was excellent in animals after small bowel resection. All animals in group IV died due to severe malabsorption. Diversion of pancreatic and biliary juice in animals with duodenoileal by-pass did not prevent intestinal adaptation. We conclude that the effect of pancreatic and biliary juice on intestinal adaptation is additive to that of other putative hormonal mechanisms.