Nerve cell density in submucous plexus throughout the gut of cat and opossum

Quantitative differences in submucous plexus density were sought in cat and opossum gut by examining full-thickness whole mounts of the submucosa stained with silver, and counting ganglia per square centimeter and nerve cell bodies per ganglion in order to compute density of innervation (nerve cell bodies per square centimeter). In the cat, the nerve cell bodies per square centimeter in the 12 named regions were as follows: proximal esophagus, 0; mid-esophagus, 0; distal esophagus, 0; fundus, 84; gastric antrum, 18; duodenum, 5831; jejunum, 4632; ileum, 3191; proximal colon, 1275; mid-colon, 689; distal colon, 359; rectum, 144. In the opossum, values were as follows: proximal esophagus, 37; mid-esophagus, 52; distal esophagus, 84; duodenum, 1812; jejunum, 2234; ileum, 1488; proximal colon, 206; mid-colon, 197; distal colon, 121; rectum, 61. Adequate specimens could not be obtained from opossum stomach. Differences were due more to variations in distribution density of ganglia than in ganglionic size. The relatively dense submucous plexus of the intestine probably is related to the capacity of the intestinal mucosa for peptide secretion as well as to its absorptive function.     

Enteric nerves in diabetic rats: increase in vasoactive intestinal polypeptide but not substance P

The distribution of vasoactive intestinal polypeptide (VIP) and substance P-like immunoreactivities was studied by immunohistochemistry in the myenteric plexus and circular muscle layer of the ileum and proximal colon of rats 8 wk after induction of diabetes with streptozotocin. A consistent increase was observed in fluorescence intensity of VIP-like immunoreactivity in the nerve fibers, and intensely stained cell bodies were significantly more frequent in the myenteric plexus of the ileum (p less than 0.001) from diabetic animals. Some varicosities of VIP-like immunoreactive fibers in the myenteric plexus appeared to be enlarged. Vasoactive intestinal polypeptide-like immunoreactivity was increased and VIP-like immunoreactive nerves appeared thicker in the circular muscle layer of both diabetic ileum and proximal colon. The VIP levels were measured biochemically in tissue consisting of the smooth muscle layers and myenteric plexus. A significant increase in the VIP content per centimeter of intestine was found in both the ileum (p less than and proximal colon (p less than 0.01) from diabetic rats. In contrast, no apparent change in substance P innervation was observed immunohistochemically in the myenteric plexus and circular muscle layer of either diabetic ileum or proximal colon when compared with controls. The results are discussed in relation to the symptoms of autonomic neuropathy of the gut in diabetes.     

Calcium-binding activity of rat intestinal mucosa after massive small bowel resection.

Male Sprague-Dawley rats underwent resection of 50 cm of either proximal or distal small intestine or sham-operation. 6-7 weeks after operation mucosal calcium-binding activity was measured in segments of duodenum ileum and remaining 'midgut'. Similar measurements were obtained from weight and age-matched unoperated rats. There was no difference in calcium-binding activity between unoperated and sham-operated animals. After proximal resection the binding activity increased significantly in duodenum and midgut but did not change in ileum. After distal resection the binding activity decreased in duodenum but was unchanged in midgut and ileum. These studies show that mucosal calcium-binding activity undergoes changes but alteration of the binding activity in remaining gut varies with the location of the small bowel resection.     

Glucose transport by rat small intestine after extensive small-bowel resection

In rats 50 cm of proximal or distal small intestine were resected, preserving duodenum and terminal ileum. Glucose transport was studied 5–6 weeks later, using everted gut sacs from duodenum, ileum, and also from a midgut segment consisting of intestine located preresection at mid-small intestine. Sham-operated animals served as controls: The inner (serosal) fluid medium in sacs from duodenum and midgut gained glucose; ileal sac serosal medium lost glucose. Proximal resection resulted in significant growth of duodenal and midgut mucosa. Duodenal transport specific activity (transport per gram dry mucosa) decreased from control values, but mucosal growth compensated so sac transport capacity (transport per centimeter sac length) remained unchanged. Midgut transport specific activity remained unchanged, thus sac transport capacity directly mirrored increased mucosal mass. Ileal sac serosal medium now accumulated glucose; there was no mucosal growth. Transport specific activity and sac transport capacity of ileum increased in parallel. After distal resection there was no alteration of either duodenal and midgut mucosal masses or transport specific activities, hence sac transport capacities remained unchanged. Ileal sac serosal medium also accumulated glucose, but now both transport specific activity and mucosal mass increased. The resultant increased sac transport capacity was identical to that of ileum after proximal resection. In all sacs from control and resected animals uphill [¹⁴C]glucose concentration differences developed between medium and mucosa. Activity of the mucosal uptake process, assessed in terms of a ratio of mucosal intracellular fluid radioactivity to mucosal medium radioactivity, usually mirrored altered transport specific activity. This indicates that the increased undercoats tissue mass that accompanied increased mucosal mass did not critically affect transport. The most striking findings were: (1) decreased duodenal transport specific activity after proximal resection with mucosal growth compensating; and (2) identical adaptations of ileal segment transport capacities after either proximal or distal small-bowel resections, although mechanisms differed. The present study provides a base for further examinations of carrier-mediated hexose transport after extensive loss of small intestine.     

Effect of streptozotocin-induced diabetes mellitus on release of vasoactive intestinal polypeptide from rodent small intestine

Representative longitudinal muscle strips (6 × 10 mm) from proximal and distal small intestine were excised from control and streptozotocin-treated rats after one month of untreated and insulin-treated diabetes. Untreated diabetes significantly reduced tissue concentrations of vasoactive intestinal polypeptide (VIP) at both intestinal loci. Insulin treatment of the diabetic animals restored tissue VIP concentrations to control group levels, although the beneficial effect of insulin treatment was only significant in the duodenum. Spontaneous release of VIP was significantly attenuated by untreated diabetes at both intestinal sites. In the duodenum, insulin treatment of the diabetic animals restored VIP release to levels indistinguishable from control group values. In the ileum, insulin treatment produced levels of VIP release that were not significantly different from those of the control and untreated diabetic groups. Tetrodotoxin (5 × 10^?6 M) significantly—but incompletely—inhibited VIP release from control group animals at both intestinal sites. These observations indicate that diabetes mellitus significantly diminishes VIP tissue concentrations and release from intestinal myenteric nerves. These abnormalities improve with insulin treatment. However, the mechanisms of VIP release from proximal and distal intestine appear to differ not only in their response to the diabetic state, but also in their response to insulin treatment.     

Distribution and density of substance P receptors in the feline gastrointestinal tract using autoradiography.

Autoradiography was used to localize and quantify substance P receptors in the feline gastrointestinal tract. The specific binding of 125I-Bolton Hunter substance P was determined in the esophagus, lower esophageal sphincter, antrum, pylorus, duodenum, jejunum, ileum, ileocecal sphincter, and colon. Competitive binding studies indicated that substance P binding sites or NK-1 receptor sites were demonstrated. The concentration of NK-1 receptors was greatest in the distal half of the gastrointestinal tract, with the highest concentrations in the proximal colon. The circular muscle layer contained the greatest amount of substance P binding. The location and density of binding sites for substance P may be important in understanding the relative importance of both the pharmacological responses to this neuropeptide and the immunohistochemical evidence of the peptide at different sites in the intestine.     

Age related increase of brush border enzyme activities along the small intestine.

Intestinal morphology and brush border hydrolase activities were determined along the small intestine of young adult (three months, n = 10), mature (12 months, n = 10), and senescent (29 months, n = 15) rats. The intestinal segments of the senescent rats contained higher mucosal mass and protein content (p less than 0.05) compared with the young and mature animals. A significant reduction of villus height and crypt depth (p less than 0.05) was found in the proximal intestine during aging. A 35% increase in villus height (p less than 0.05) without changes in crypt depth, was observed in the distal ileum in senescent rats. The activities of sucrase and isomaltase were significantly increased during aging in the duodenum and jejunum (p less than 0.05). Lactase and aminopeptidase activities which showed only minor changes between young and mature animals were significantly enhanced in senescent animals (p less than 0.05) with aminopeptidase exhibiting a three-fold increase in activity in the proximal ileum. The results when combined with those of previous studies suggest that in the aged animal, the increased level of intestinal hydrolase activities may be the consequence of prolonged cellular maturation along the villi in the proximal intestine, and of adaptation to increased concentrations of intraluminal substrates in the distal intestine.     

Regional variation in canine intestinal muscle mass and function

Our aim was to investigate the contribution of variations in intestinal muscle morphology or function to regional differences in motor propertiesin vivo. We quantitated intestinal muscle thickness and surface area along the canine gut and compared thein vitro contractile properties of the jejunum and ileum. The thickness and cross-sectional surface area of both circular and longitudinal muscle demonstrated a parabolic distribution along the intestine, with the greatest values occurring in the proximal and distal regions. The terminal ileum had the greatest circular (885±194 μm) and longitudinal muscle (367±135 μm) thickness. Circular muscle was 2.5–3 times thicker than longitudinal muscle at all points. Passive tension was similar in muscle strips from the mid-jejunum, mid-ileum, and terminal ileum (2.8±0.8, 2.5±0.4, and 2.3±0.8 vs 2.5±0.5, 1.9±0.5, and 2.8±1.0, longitudinal and circular, respectively). Active and total tension, however, were significantly greater in longitudinal than circular muscle in mid-jejunum (active; 8.5±1.4 vs 5.6±1.2,P<0.05 and total 11.3±1.7 vs 8.1±1.2) and in mid-ileum (active 9.5±1.6 vs 5.8±1.2 and total 12.0±1.6 vs 7.7±1.2). Values for each layer were similar in both sites. In contrast, in the terminal ileum, longitudinal and circular muscle strips demonstrated similar active (10.1±1.7 vs 9.0±2.7 NS) and total tension (12.4±2.0 vs 11.9±3.4 NS). Dose-response curves to carbachol (10^?8–10^?2 M) were similar in all these regions. We conclude (1) there are regional variations in muscle mass but contractile properties are similar in jejunum and ileum; and (2) the unique motor properties of the terminal ileum may be related more to differences in muscle morphology and neural input than intrinsic function.     

Effect of chyme on mucosal enzyme levels in small intestine of the rat

Partial jejunectomies, gastrojejunostomies (with closed pylorus), and jejunal Thiry-Vella loops were made in order to elucidate the role of chyme in the control of mucosal mass and the activities of alkaline phosphatase, ATPase, and maltase in the small intestine of the rat. After partial jejunectomy, a partially reversible mucosal hyperplasia was seen in the small intestine with the exception of distal ileum. After gastrojejunostomy a similar hyperplasia took place in the jejunum and proximal ileum. In the jejunal Thiry-Vella loops a mucosal atrophy was found in 4 wk. After partial jejunectomy the activity of alkaline phosphatase decreased slowly in 4 wk in the remaining small intestine with the duodenum as an exception. ATPase activity decreased in the duodenum. Maltase activity remained unchanged during 8 postoperative wk. In gastrojejunostomized rats the activity of alkaline phosphatase and ATPase increased slowly during 12 wk in the jejunum aborally from the gastroenterostomy. A slight depression of maltase activity was observed in the operation area and a slight increase of enzyme activity was found in the middle of the small intestine. In jejunal Thiry-Vella loops the activity of alkaline phosphatase decreased, but no change of maltase activity could be observed during 4 wk. Perfusion of a loop with maltose solution did not cause any changes in the activity of alkaline phosphatase or maltase. The results indicate that after a change in chyme passage the adaptation takes place in the small intestine primarily by the change of mucosal mass, and at least some enzyme levels in the mucosal cells are remarkably stable.     

Immunoreactive secretin in gastrointestinal mucosa of several mammalian species.

Immunoreactive secretin in hydrochloric acid extracts is relatively constant in the duodenum and proximal jejunum of pig and dog (3 microgram per g), but peaks in the distal duodenum of guinea pig (1 microgram per g), no secretin being detectable in the ileum of these species. Secretin is relatively constant throughout the small intestine of the rat and rabbit (0.4 to 0.1 microgram per g). Sephadex gel filtration patterns of all species and throughout the gastrointestinal mucosa revealed primarily a single peak with elution characteristics identical with that of purified or synthetic porcine secretin. The "big" secretin prominent in Boots secretin may be an alteration product perhaps attributable to chemicals used to stabilize the preparation. The "intermediate secretin" described by others has not been detected. It is concluded that in a variety of mammalian species most of the immunoreactive secretin extractable from the intestinal tract lies distal to the proximal duodenum and is not distinguishable from duodenal secretin in terms of molecular size.     

Intestinal morphology and cytokinetics in pancreatic insufficiency

Intraluminal pancreatic enzymes influence intestinal function, adaptation, and susceptibility to injury. These effects may be mediated partly through changes in the rate of epithelial cell turnover. We assessed intestinal morphology and cytokinetics in a rat model of exocrine pancreatic insufficiency that does not alter anatomic relationships or animal growth. Pancreatic duct occlusion was performed by applying metal clips on both sides along the common bile duct. Control animals underwent sham-operation with exposure and manipulation of the pancreas without duct occlusion. Twelve days later, pulse labeling with tritiated thymidine was performed, and mitotic arrest was induced with colcemid. Groups of animals were sacrificed at 0 and 2 hr after colcemid injection. Specimens for histopathology, morphometry, and autoradiography were obtained from duodenum, proximal jejunum, distal jejunum, and ileum. Labeling index, grain counts, mitoses per crypt, cells per crypt, cells per villus, crypt depth, villus height, and number of goblet cells per villus were used as end points. Pancreatic duct occlusion resulted in increased labeling index across intestinal segments relative to sham-operated controls (P<0.01) and increased labeling index and mitotic rate in distal compared to proximal intestine (P<0.05). Grain-count histograms were similar in the two experimental groups. There were no significant morphologic differences between pancreatic duct-occluded animals and controls. Exocrine pancreatic insufficiency increases crypt cell proliferation in distal small intestine but does not alter the duration of S phase. These changes are most likely due to an increase in the size of the proliferative compartment and may be partly responsible for changes in small bowel function and response to injury.Supported by grant 88.616 from The Norwegian Cancer Society.     

Case Report: Fatal Ulcerative Panenteritis Following Colectomy in a Patient with Ulcerative Colitis

A 37-year-old man, previously submitted to colectomy for ulcerative pancolitis unresponsive to medical therapy, presented with nausea, vomiting, epigastric pain, and bloody diarrhea. An upper gastrointestinal endoscopy revealed mucosal friability, petechiae, and erosions throughout the duodenum, whereas prestomal ileum showed large ulcers and pseudopolyps. Histologically, a dense inflammation chiefly composed of lymphocytes and plasma cells with few neutrophils was detected. No bacteria, protozoa, and fungi could be detected. Despite intensive care, intra-1194 venous antibiotics and steroids, the patient died of diffuse intravascular coagulation and multiorgan failure. At post-mortem examination severe ulcerative lesions were observed scattered throughout the duodenum up to the distal ileum. The dramatic clinical presentation with fatal outcome, the widespread ulcers throughout the intestine, and the histological picture are peculiar features in our patient which can not be ascribed to any type of the ulcerative jejunoenteritis so far reported. Patients with pancolitis and diffuse ileal involvement do not necessarily have Crohn's disease but rather may have ulcerative colitis.     

Intestinal regulation of pancreatic enzyme secretion: stimulatory and inhibitory mechanisms]

How exocrine pancreatic secretion is regulated is only partly known. It is assumed that interaction of several neural and hormonal mechanisms is involved. In man, the intestinal component of these control mechanisms is very important while extra-intestinal mechanisms (such as the cephalic and the gastric phase) play lesser roles. Regulation of pancreatic secretion by the intestine is composed of three main mechanisms. 1. The proximal intestinal (duodenal) phase of the secretory response to a meal is elicited by nutrients within the proximal intestinal lumen. It is mediated mainly by interactions between cholinergic reflexes and release of the peptide hormone cholecystokinin (CCK). Recent data suggest that part of the action of CCK is not exerted directly on the acinar cellular level, but rather by modulation of cholinergic inputs. 2. The distal intestinal (ileal) phase is elicited by contact of the distal intestinal mucosa with nutrients that pass through the ileal lumen due to physiological malabsorption. The ileum (in contrast to the duodenum) induces net-inhibition of pancreatic secretion. The mediation is unknown, candidate mediators are PYY and GLP-1. 3. Intestinal feedback-regulation of pancreatic secretion in humans is controlled by intraluminal protease activity; this mechanism is not covered in the present paper.     

Increased smooth muscle contractility of intestine in the genetic null of the endothelin ETB receptor: a rat model for long segment Hirschsprung's disease

BACKGROUND AND AIMS: The endothelin ETB receptor null rat (ETB(-/-)R) has an intestinal segment without ganglia, and this rat is characterised by intestinal obstruction similar to that observed in human Hirschsprung's disease. In the present study, we have examined the myogenic mechanism responsible for obstruction in the ETB(-/-)R. RESULTS: The ETB(-/-)R had an enlarged belly and the average lifespan was 18.1 days. The bowel from the rectum to the lower part of the small ileum was constricted whereas the upper region was dilated with faecal stasis and thus presented as megaileum. The constricted muscle segments without ganglia had a greater increase in absolute force when stimulated by carbachol, high K+, and endothelin-1 compared with that of normal siblings. In contrast, in the dilated part with ganglia, the absolute contractile force due to these stimulants in the ETB(-/-)R was not different from that in the ETB(+/+)R. Such a functional hypertrophy of the musculature was observed in parts of the colon, caecum, and distal ileum without ganglia but not in the part of the proximal ileum and jejunum with ganglia. Morphological study demonstrated that the thickness of the circular and longitudinal muscle layers was greater in the constricted part of the intestine in the ETB(-/-)R, and these changes were associated with an increase in the number of smooth muscle cells. CONCLUSIONS: Our findings suggest that both increased contractility of smooth muscle and increased thickness of the intestinal muscular wall may contribute to the intestinal obstruction in the ETB(-/-)R.     

Expression of iron absorption genes in mouse large intestine

OBJECTIVE: The large intestine has been reported to have a capacity for iron absorption and expresses genes for iron absorption normally found in the duodenum. The importance and function of these genes in the large intestine are not understood. We therefore investigated the cellular localization and regulation of expression of these genes in mouse caecum and colon. MATERIAL AND METHODS: Gene expression was measured by real-time PCR using RNA extracted from iron-deficient and hypoxic mouse large intestine, compared to controls. Protein localization and regulation were measured by immunohistochemistry using frozen sections of the large intestine from the same mice. RESULTS: Dcytb (duodenal ferric reductase) was expressed at very low levels in the large intestine, compared to the duodenum, while Ireg1 and DMT1 were expressed at significant levels in the large intestine and were increased in iron-deficient caecum, proximal and distal colon, with the most significant increases seen in the distal colon. Hypoxia increased Ireg1 expression in the proximal colon. Immunohistochemistry detected significant levels of only IREG1, which was localized to the basolateral membrane of colonic epithelial cells. CONCLUSIONS: Iron absorption genes were expressed at lower levels in mouse caecum and colon than in the duodenum. They are regulated by body iron requirements. Colonic epithelial cells express basolateral IREG1in the same fashion as in the duodenum and this protein could regulate colonic epithelial cell iron levels.     

Nerve Terminals Containing Neuropeptides Decrease in Number After Massive Proximal Small Bowel Resection in the Piglet

The aim of this study was to evaluate possiblechanges in the neuropeptide innervation pattern of theremaining porcine ileum following 75% proximal resectionof the small intestine. Three-month-old piglets were operated on and two months postoperativelyfullthickness specimens of the proximal part of thedistal ileum wall were taken. Age-matched 3- and5-month-old unoperated piglets were used as controls. The number and intensity of VIP-, galanin-,enkephalin-, substance P-, and somatostatin-containingnerve fibers were estimated in sections processed forimmunofluorescence microscopy and subjected toquantitative scoring. The VIP-, galanin-, andenkephalin-immunoreactive fibers of the circular musclelayer and villi were also quantitated bycomputer-assisted morphometry. The number and intensityof VIP-immunoreactive fibers in the mucosa and circular muscle layermarkedly decreased after resection as compared to3-month-old and 5-month-old controls (P < 0.05). Thegalanin immunoreactivity index decreased significantly after resection in the circular muscle layer ascompared to both control groups (P < 0.05). Theincrease in the number of enkephalin-immunoreactivenerve fibers that normally occurred from 3 to 5 monthsof age was inhibited by the resection. We were notable to see any differences in somatostatin or substanceP immunoreactivity between the groups. The resultssuggest that massive resection induces significant changes in the neuropeptide-containinginnervation of the remaining small intestine. Thesefindings are compatible with altered motor activity andmucosa function in the remain intestine.     

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.     

Fractionated irradiation alters enteric neuroendocrine products

Radiation profoundly alters the contractile activity of the small intestine and colon. We hypothesized that some motor changes of the gut might be secondary to impaired neural input to smooth muscle or abnormal release of gut endocrine peptides. The density of products within peptidergic and cholinergic nerves and gut endocrine cells was estimated in six normal controls and six dogs who had received 1500 cGy in six equal fractions of 250 cGy. Choline acetyltransferase, acetylcholinesterase, vasoactive intestinal peptide (VIP), substance P, peptide YY (PYY), and motilin were measured in tissue specimens divided into mucosalsubmucosal (MS) and muscularis externa (ME) layers. Tissue samples were obtained from the duodenum, jejunum, ileum, and proximal and distal colon. In addition, serum levels of motilin and PYY were determined before and during the administration of 1500 cGy in four separate dogs instrumented to record upper gut contractile activity. Intrinsic cholinergic activity as estimated by choline acetyltransferase activity was unchanged, while acetylcholinesterase activity increased in the MS layers of distal small bowel and colon. VIP was increased in the MS layers of jejunum and proximal colon as well as in the ME layers the jejunum and ileum. By contrast, substance P increased in the jejunal and proximal colonic MS layers and in the ME layers of the jejunum and ileum. Duodenal and jejunal motilin levels markedly decreased after radiation exposure, while serum motilin levels continued to cycle at a decreased peak level with migrating motor complexes. Colonic PYY remained unchanged but serum PYY levels decreased after irradiation. Increased neuronal synthesis and inhibition of neurotransmitter release are potential explanations for elevated tissue concentrations of VIP, substance P, and acetylcholinesterase. There appeared to be differences in the sensitivity of gut endocrine cells to irradiation. Changes in gut regulatory peptides and cholinergic enzyme activity occur with fractionated doses of abdominal irradiation, while the same schedule of irradiation produces striking changes in the canine small intestinal and colonic motor activity. It is therefore likely that alterations of contractile events may be produced by changes in gut neuroendocrine products.     

Human myenteric plexus: confirmation of unfamiliar structures in adults and neonates

To define the myenteric plexus along the human gastrointestinal tract, we studied three neonatal and six adult specimens, postmortem, by silver impregnation. There were no clear differences between the neonatal and the adult gastrointestinal tracts. In the body of the esophagus, the plexus was sparse, with few ganglia; 30%-40% of fascicular intersections were devoid of ganglia. In the lower 5 cm, the esophagus had thick bundles of nerve fibers ("shunt fascicles"), which crossed the gastroesophageal junction and radiated to the periphery of the stomach through several branches. The plexus in the stomach was uniform, with intermediate and intrafascicular ganglia. A thick nerve bundle encircled the pylorus and gave branches on either side to the antrum and the duodenum. Shunt fascicles in the stomach did not cross the pylorus but extended to the distal antrum. In the duodenum and proximal jejunum, the plexus was regular, but in the mid-small intestine, the longitudinal interganglionic fascicles were more prominent than the circumferential fascicles. Distally, this pattern was reversed; circumferential fascicles were more prominent and ganglia were dense in the terminal ileum. Thin, short shunt fascicles were scattered along the entire small intestine, becoming more abundant in the terminal ileum. Short, thick shunt fascicles traveled proximally from the ileocecal junction for about 25-30 cm. As in the stomach, shunt fascicles did not cross the ileocecal junction, but a thick nerve bundle encircled it. In the cecum and proximal colon, the plexus was sparse with large intermediate and intrafascicular ganglia. In the rectum and distal colon, the plexus was dense, with parafascicular and intrafascicular ganglia. Long ascending nerves extended from the distal rectum into the midcolon. In addition, there were short, thick nerve bundles in the rectum that traveled proximally.     

Cell-specific immunohistochemical localization of a cellular retinol-binding protein (type two) in the small intestine of rat.

One of us recently has reported the purification of a new retinol-binding protein that is distinctly different from the well-known cellular retinol-binding protein, CRBP. This protein, which we propose to name cellular retinol-binding protein type II [CRBP(II)], was found almost exclusively in the small intestine of the adult rat at levels 1000 times greater than that of CRBP. Here we have determined the cellular location of these two proteins in the small intestine of the rat. By using an immunohistochemical technique, the absorptive cells of the small intestine, from the duodenum to the ileum, were strongly stained when antiserum against CRBP(II) was used. More intense staining was observed in absorptive cells near the tips of the villi than in those located at the base of the villi. However, the proliferative cells in the crypts of Lieberkühn were stained only lightly if at all. In contrast to absorptive cells, goblet cells in the villi did not stain. When tissue sections containing the gastroduodenal junction were examined, no staining was observed in the gastric epithelium, while the epithelium of the most proximal portion of the duodenum showed very strong staining. In tissue sections containing the ileocecal junction, staining terminated abruptly at the end of the distal ileum. No staining was observed in the epithelium of the colon. In contrast, the cellular location of CRBP in the small intestine was quite different from the cellular location of CRBP(II). The epithelial cells of the small intestine showed no staining when affinity-purified anti-CRBP was used. Staining was observed for connective tissue cells in the lamina propria and in cells located within the gut-associated lymphoid tissue. The cell-specific localization pattern determined for these two proteins suggests that CRBP(II), rather than CRBP, is the protein that plays a role in the absorption of retinol.