Comparison of the Comformation of 20 International Level and the 20 Low Level Jumping Horses Using a 3-D Video Morphometric Measurement Method

The endocannabinoid anandamide may regulate intestinal motility through activation of CB1 receptors. Anandamide is then inactivated by fatty acid amide hydrolase (FAAH), a membrane bound enzyme. Under pathological conditions, inactivation of such enzymatic activity may lead to inhibition of the intestinal motility. Here, preliminary reports on the distribution of Fatty Acid Amide Hydrolase (FAAH) immunoreactivity in the mouse gastrointestinal neurons, and the pharmacological effects of N-arachidonoylserotonin (AA-5HT), a selective inhibitor of FAAH, are reported. FAAH was revealed by an indirect immunofluorescence. Laminar preparations containing the myenteric or the submucous plexus adhered, were peeled off after the whole gut wall had been stretched out and fixed in 4% paraformaldehyde. They were subsequently incubated with a polyclonal anti-serum directed against a region near the N-terminus of the human FAAH and revealed by a FITC-conjugated goat anti-rabbit secondary anti-serum. FAAH-immunoreactive neurons were observed within the myenteric ganglia throughout the GIT. The positive nerve cells varied in size and density of immunoreactivity. Stomach and large intestine showed the highest neuronal density. AA-5HT significantly reduced both gastric emptying and gastrointestinal tract transit. Such inhibitory effect was reduced by the C1 receptor antagonist SR141716A. Both morphological and pharmacological results suggest that FAAH may play a critical role in controlling gut anandamide levels.     

An immunohistochemical study of interstitial cells of Cajal (ICC) in the equine gastrointestinal tract.

The interstitial cells of Cajal (ICC) are c-kit immunoreactive cells of the gastrointestinal tract which are suggested to have a role in the control of intestinal motility. Cells with c-kit immunoreactivity have not been previously described in the gastrointestinal tract of the horse. Immunoreactivity for c-kit was revealed using immunohistochemical labelling with an anti-c-kit polyclonal antibody. Sections of normal gastrointestinal tissue were examined from 13 anatomically defined sites from stomach to small colon taken from horses free from gastrointestinal disease. Three types of c-kit immunoreactive cells were identified: spindle-shaped cells in the region of the myenteric plexus, stellate or bipolar cells in the circular muscle layer, and round cells in the submucosa. The round cells were shown to be mast cells with the use of toluidine blue staining, whereas the other c-kit immunoreactive cells did not exhibit metachromasia and were classified as ICC. This study will serve as a basis for future pathological studies in the horse.     

Evaluation of substance P as a neurotransmitter in equine jejunum

OBJECTIVE: To determine whether substance P (SP) functions as a neurotransmitter in equine jejunum. SAMPLE POPULATION: Samples of jejunum obtained from horses that did not have lesions in the gastrointestinal tract. PROCEDURE: Jejunal smooth muscle strips, oriented in the plane of the circular or longitudinal muscle, were suspended isometrically in muscle baths. Neurotransmitter release was induced by electrical field stimulation (EFS) delivered at 2 intensities (30 and 70 V) and various frequencies on muscle strips that were maintained at low tension or were under contraction. A neurokinin-1 receptor blocker (CP-96,345) was added to baths prior to EFS to interrupt SP neurotransmission. Additionally, direct effects of SP on muscle strips were evaluated, and SP-like immunoreactivity was localized in intestinal tissues, using indirect immunofluorescence testing. RESULTS: Substance P contracted circularly and longitudinally oriented muscle strips. Prior treatment with CP-96,345 altered muscle responses to SP and EFS, suggesting that SP was released from depolarized myenteric neurons. Depending on orientation of muscle strips and stimulation variables used, CP-96,345 increased or decreased the contractile response to EFS. Substance P-like immunoreactivity was detected in the myenteric plexus and circular muscle layers. CONCLUSIONS AND CLINICAL RELEVANCE: Substance P appears to function as a neurotransmitter in equine jejunum. It apparently modulates smooth muscle contractility, depending on preexisting conditions. Effects of SP may be altered in some forms of intestinal dysfunction. Altering SP neurotransmission in the jejunum may provide a therapeutic option for motility disorders of horses that are unresponsive to adrenergic and cholinergic drugs.     

三种不同方法显示仔猪小肠肌间神经元的比较

本研究采用小肠铺片NADPH-d组化法、NADH-d组化法和抗NF免疫组化法分别对0日龄、5日龄、28日龄仔猪的肌间神经元进行了比较研究。结果表明:NADPH-d组化法可以选择性的标记合成NO的神经元亚群,大部分阳性肌间神经元符合DogielI型神经元的形态特征;NADH-d组化法可以非选择性的标记大部分神经元,且采用该法观察到的肌间神经元的密度明显高于NADPH-d组化法,但该法不能清晰的显示肌间神经丛的细微结构,不适合用于神经元类型的观察;抗NF免疫组化法可以清晰的显示肌间神经元的突起,28日龄仔猪体积较大的阳性神经元主要为DogielI型和DogielII型神经元。     

Comparative study of the distribution of NOS-positive neurons in pigeon intestine

Nitric oxide (NO) plays an important role in regulating gut motility, mucosal barrier function and secretions in the enteric nervous system. Nicotinamide adenine dinucleotide phosphate diaphorase (NADPH-d) staining has been used to identify nitrergic neurons of the enteric nervous system in different species. However, NADPH-d staining lacks specificity because it also reflects the presence of enzymes other than nitric oxide synthase (NOS). Therefore, NOS immunohistochemistry techniques are needed to test for nitrergic neurons in the avian gut. In the present work, the morphology, density and size of NOS-positive neurons in the duodenum, jejunum, ileum, caecum and rectum myenteric plexus of adult pigeons were investigated using NOS immunohistochemistry and whole-mount preparations techniques. The density of NOS-positive ganglion was highest in the ileum, similar to the caecum and rectum, and the lowest staining levels were observed in the duodenum. The staining intensity of NOS-positive neurons in the duodenum, jejunum and ileum was dark, followed by the rectal regions, with weak staining in the caecum. These results suggested that NOS immunohistochemistry and whole-mount preparation techniques provide an effective assessment method of the ganglia in the pigeon intestinal myenteric nerve plexus and are more accurate for cell counting compared with conventional sections.     

Histological and immunohistochemical studies of changes in myenteric plexuses and in interstitial cells of Cajal associated with equine colic

In this study we investigated the histological changes of the myenteric plexuses and interstitial cells of Cajal (ICC) in gut samples from horses with colic to try to find results useful in the prognostic evaluation of enteric lesions. A morphologic and quantitative study of myenteric ganglia, ganglion cells and neuronal chromatolytic and necrotic changes of 24 horses with colic was performed. For ganglion cells, enteroglial cells and ICC immunolabeling was also performed to identify cell functional disorders. A significant increase of neuronal chromatolysis and necrosis occurred in horses suffering from colic throughout the gut. The neuron-specific enolase (NSE) and synaptophysin immunoreaction quantified with image analysis showed a significant loss of neuronal activity in all intestinal tracts of the animals under study associated with a significant loss of ICC immunoreactivity. The results supports immunohistochemical evaluation of ENS and ICC as a useful tool along with morphometric investigations in the evaluation of gut lesions produced during colic syndrome.     

Constipation associated with brumation? Intestinal obstruction caused by a fecalith in a wild red diamond rattlesnake (Crotalus ruber)

This report describes the fecalith‐induced intestinal obstruction of a free‐ranging red diamond rattlesnake (Crotalus ruber) and the snake's subsequent history following surgical removal of the fecalith. The captured snake exhibited an abnormally distended abdomen and an extremely hard mass, detected via palpation, near its vent. Coeliotomy yielded a 2.5‐cm, 5‐g fecalith from the large intestine. Microscopic dissection of the fecalith revealed no evidence of gastrointestinal parasitic worms. Subsequently, we implanted a radio‐transmitter that allowed us to track the snake's movements for 7 months (until the radio signal vanished), indicating normal behaviour, complete recovery and good health apart from the obstruction. This observation suggests that fecalith development and intestinal obstruction represent potential risks of long‐term faecal retention, an unusual physiological trait well documented among rattlesnakes and other stout, heavy‐bodied terrestrial viperid snakes. Dehydration and decreased gut motility associated with brumation (≈hibernation) may predispose temperate snakes to fecalith formation. Regional drought and a small mammal diet with indigestible hairs might have also promoted fecalith formation in this specimen.     

Involvement of neuronal nitric oxide synthase (nNOS) in the regulation of migrating motor complex (MMC) in sheep

The objectives of this study were to evaluate the role of nitric oxide (NO) synthase isoforms (nNOS, eNOS, and iNOS) in the regulation of the migrating motor complex (MMC) in sheep using electromyography and their expression in the gastrointestinal (GI) tract by Western blot (WB) and immunohistochemistry. Intravenous administration of L-NAME or the nNOS inhibitor 7-nitroindazole (7-NI) decreased the MMC interval. Myoelectric activity of intestinal phase II was increased, whereas antral activity was reduced. These effects were blocked by L-arginine. Inhibitors of either iNOS (aminoguanidine and S-methylisothiourea) or eNOS (L-NIO) were ineffective. The NO donor sodium nitroprusside decreased GI myoelectric activity, inhibited the MMC pattern, and prevented the effects induced by L-NAME and 7-NI in the intestine. Intracerebroventricular administration of these agents did not modify GI motility. In the rumen, abomasal antrum, duodenum, and jejunum, WB showed three bands at about 155, 145, and 135kDa corresponding to nNOS, and a 140-kDa band (eNOS); however iNOS was not detected. Positive nNOS immunostaining was observed in neurons of the myenteric and submucous plexus of all GI tissues, while eNOS was found in the endothelial cells, ruminal and intestinal epithelium, as well as in some enteric neurons and in endocrine-like cells of the duodenal Brunner's glands. In contrast, only weak iNOS immunoreactivity was found in ruminal epithelium. Taken together, our results suggest that NO, synthesized at a peripheral level by nNOS, is tonically inhibiting the MMC pattern and intestinal motility in sheep.     

Lesions of the enteric nervous system and the possible role of mast cells in the pathogenic mechanisms of migration of schistosome eggs in the small intestine of cattle during Schistosoma bovis infection

The enteric nervous system in the small intestine of cattle during Schistosoma bovis infection was studied by histological stains and immunohistochemical methods. Lesions due to migration of schistosoma eggs were located mainly in the mucous and the submucous layer overlaying the submucous vascular arcades. Granulomas destroyed ganglia, neurons, nerves fibre strands and nerve fibres. Ganglia situated within or near granulomas were infiltrated by mast cells, eosinophils, lymphocytes, globule leukocytes, neutrophils and macrophages. Mast cells were in close contact with degenerating neuronal perikarya. Whereas vasoactive intestinal peptide-like immunoreactivity in the nerves and neurons in the ganglia within and around granulomas was increased, the neurofilament-like immunoreactivity was reduced. Compared to the myenteric and external submucous plexuses, the internal submucous and mucous plexuses were the most damaged. These changes imply reduced functional capacity in the nervous tissue which might cause reduced motility, malabsorption and partly account for the loss of body weight and condition and failure to thrive which occur in schistosomosis.Biotinylated affinity purified swine anti-rabbit and mouse anti-rabbit immunoglobulins reacted nonspecifically with a subset of mast cells. The reaction revealed many mast cells in early forming granulomas and around schistosome egg tracts and infiltration of mast cells into the ganglia of intestinal nerve plexuses. The observation shows a localized, Type I hypersensitivity reaction suggesting for the release of mast cell-derived chemical mediators in the intestinal reaction to trap or evict S. bovis eggs and to cause diarrhoea.     

5-Hydroxytryptamine mediated contractions in isolated preparations of equine ileum and pelvic flexure: pharmacological characterization of a new 5-HT(4) agonist

The effects of 5-hydroxytryptamine (5-HT), HTF 919, a new 5-HT(4) agonist, and the antagonists SB 203-186 (5-HT(4)) and tropisetron (5-HT(3)) on intestinal motility were tested in vitro on isolated preparations of horse ileum and pelvic flexure. Concentration-response curves were created by cumulative application of the agonists with or without preincubation of the antagonists. The 5-HT preparation induced a concentration-dependent contraction in equine ileum and pelvic flexure. The results indicate that 5-HT receptors are present in all parts of equine intestine investigated in this study. Tropisetron was found to act as a noncompetitive antagonist in all locations of the equine intestine. SB 203-106 was confirmed as an antagonist to 5-HT in the equine ileum circular muscle, in pelvic flexure circular and longitudinal muscle. Nevertheless, a discernible increase of smooth muscle contractions caused by HTF 919 could only be observed in pelvic flexure. In accordance with an earlier study in the guinea pig, in the equine gut HTF 919 acted as a partial agonist for the 5-HT(4) receptor with an affinity constant in the nanomolar range. It is concluded that 5-HT receptors, and especially their subtypes, may represent a promising target for the treatment and prevention of gastrointestinal (GI) motility disorders in horses.     

The Distribution and Chemical Coding of Intramural Nerve Structures Supplying the Porcine Stomach

The present study investigated the arrangement and chemical coding of intramural nerve structures supplying the porcine stomach. Tissue samples comprising all layers of the wall of the ventricular fundus were collected from juvenile female pigs (n = 4), which were first deeply anaesthetized and then transcardially perfused with buffered paraformaldehyde. The cryostat sections were processed for double‐labelling immunofluorescence to study the distribution of the intramural nerve structures (visualized with antibodies against protein gene‐product 9.5) and their neurochemical characteristics using antibodies against vesicular acetylcholine transporter (VAChT), nitric oxide synthase (NOS), galanin (GAL), vasoactive intestinal‐polypeptide (VIP), somatostatin (SOM) and substance P (SP). The study confirmed the presence of three distinct nerve plexuses within the wall of the porcine stomach including one myenteric plexus and two, outer and inner, submucous plexuses. The outer and inner submucous plexuses (OSP and ISP, respectively) were similar in respect to the chemical coding of neurons they contained. Most of the neurons expressed immunoreactivity to SP (ISP 58%; OSP 60%) or to VAChT (ISP 56%; OSP 56%), some of them stained for GAL (ISP 18%; OSP 15%) and solitary nerve cells were SOM‐positive (in ISP only). No neurons in the submucous plexuses displayed immunoreactivity to VIP or NOS. In the myenteric plexus, some neurons stained for NOS (20%), VAChT (15%), GAL (10%), VIP (8%) or SP (8%) while no neurons immunoreactive for SOM were encountered. In both submucous and myenteric plexuses, many varicose nerve fibres expressed immunoreactivity to VAChT, GAL or SP, while VIP‐, SOM‐ or NOS‐positive nerve terminals were less numerous. The comparison of the present results with those obtained by other authors has revealed distinct inter‐species differences regarding the arrangement and chemical coding of nerve structures supplying the mammalian stomach.     

The interstitial cells of Cajal of the equine gastrointestinal tract: What we know so far

Gastrointestinal motility disorders are a serious problem in both veterinary and human medicine and may represent a dysfunction of the neural, muscular or pacemaker components (interstitial cells of Cajal) of bowel control. The interstitial cells of Cajal are considered to be the pacemakers and mediators of certain forms of neurotransmission in the gastrointestinal tract. These cells have been implicated, either primarily or secondarily, in the pathogenesis of gastrointestinal disease processes in which there is a prominent element of disturbance to intestinal motility. In the horse, their involvement has been implicated in large intestinal obstructive colic and grass sickness (equine dysautonomia). This review highlights the properties of the interstitial cells of Cajal and the role these cells play in orchestrating gastrointestinal motility patterns. In addition, it examines their role in intestinal motility disorders and summarises our current understanding of their importance in the equine gastrointestinal tract.     

Involvement of PKA signalling in anti‐inflammatory effects of chitosan oligosaccharides in IPEC‐J2 porcine epithelial cells

Weaning is characterized by intestinal inflammation, which is a big challenge in pig industry. Control of intestinal inflammation is important for improvement of growth performance and health. Therefore, the study was focused on the anti‐inflammatory activity of low‐molecular‐weight chitosan oligosaccharide (LCOS) in a porcine small intestinal epithelial cell line (IPEC‐J2). The results showed that TNF‐α, as inflammation inducer, significantly upregulated the mRNA expression of IL‐8 and MCP‐1. Afterwards, LCOS significantly attenuated mRNA expression of IL‐8 and MCP‐1 induced by TNF‐α in the cells. Mannose (MAN), as ligand of mannose receptor, had no effect on the anti‐inflammatory activity of LCOS, which suggested that mannose receptor may not involve in the anti‐inflammatory activity of LCOS in IPEC‐J2 cells. Interestingly, N‐[2‐(p‐bromocinnamylamino)ethyl]‐5‐isoquinolinesulfonamide 2HCl hydrate (H89), as PKA (protein kinase A)‐specific inhibitor, reversed the mRNA expression of IL‐8 when co‐cultured with LCOS. Furthermore, LCOS concentration dependent downregulated the mRNA expression of claudin‐1 compared with TNF‐α treatment. However, the trans‐epithelial electric resistance (TEER) was not affected by LCOS when co‐cultured with TNF‐α in 3 hr. In conclusion, LCOS have a potent anti‐inflammatory activity, and as a feed additives, may be useful for the inhibition of inflammatory process in weaning period of pigs with intestinal inflammation occurring.     

Interstitial cells of Cajal (ICC) in equine colic: an immunohistochemical study of horses with obstructive disorders of the small and large intestines

REASONS FOR PERFORMING STUDY: The gastrointestinal pacemaker cells, the interstitial cells of Cajal (ICC), have been implicated in several human gastrointestinal dysmotility syndromes. Recently, the involvement of these cells in equine gastrointestinal diseases has been investigated in cases of equine grass sickness where a significant reduction in ICC density was observed. OBJECTIVE: To investigate ICC density in equine obstructive gastrointestinal disorders using immunohistochemical labelling methods. METHODS: Intestinal samples were analysed from 44 horses undergoing exploratory surgery for colic and from 11 control animals subjected to euthanasia for conditions not related to the gastrointestinal tract. Immunohistochemical labelling of ICC was carried out using an anti-c-Kit antibody. Two independent observers assessed ICC density using a semiquantitative grading system. RESULTS: There was a significant reduction in ICC density in horses with large colon disorders compared to the controls (P<0.01). Horses with strangulating lesions of the small intestine showed no difference when compared to the controls. CONCLUSIONS: There was a reduction in ICC density in horses with large intestinal disorders. POTENTIAL RELEVANCE: The reduction in ICC density may be associated with the clinical findings as well as recurrent colic episodes observed in a number of these cases. This immunohistochemical study provides a basis for future functional electrophysiological investigations to determine the precise effect of ICC reduction on equine intestinal motility.     

Regulatory peptides

The peptidergic innervation of the gastrointestinal tract was clearly affected in these six cases of Feline Dysautonomia. Most notably there was a striking depletion of VIP-immunoreactivity. However, the lesions in Feline Dysautonomia are not selective for neurons containing this particular peptide, since a reduction in substance P- and Met-enkephalin-immunoreactivity was also found. Depletion of these three neuropeptides does not correlate well with the clinical finding of gastrointestinal atony, since only substance P has excitatory actions on gut smooth muscle (Iversen, 1982). Both VIP and enkephalin have inhibitory actions, acting directly on smooth muscle or via the myenteric plexus respectively (Fahrenkrug and Emson, 1982; North and Egan, 1982). However, as there was no specificity in the distribution of lesions, at least in terms of peptidergic nerves, it is probable that other types of nerves in the intrinsic and extrinsic innervation of the gut are affected, and contribute to the loss of tone. The depletion of neuropeptide immunoreactivity does not distinguish between a loss of peptidergic neurons and a loss of peptide content. However, in routinely stained sections there was little evidence of neuronal loss: only a small number of abnormal, apparently degenerating, nerve cell bodies was seen in the enteric plexuses. Thus, it is possible that levels of immunoreactive materials are reduced in peptidergic nerves. At the ultrastructural level, Griffiths and Sharp (1983) have found disorganized rough endoplasmic reticulum and a depletion of ribosomes in neurons from affected cats, and it is possible that impaired peptide synthesis may contribute to the observed reduction in immunoreactivity. In contrast to the findings in the peptidergic innervation, the peptide-containing endocrine cells appeared to be unaffected. At least, glucagon-and somatostatin-IR cells in the colon were not depleted in number. Thus, in Feline Dysautonomia, while there was little evidence of neuronal lesions in the gastrointestinal tract on routine histological examination, there was a marked loss of neuropeptide immunoreactivity. Neuropeptide immunohistochemistry would appear, therefore, to be more sensitive in detecting neuronal abnormalities in this disease. At present however, it cannot be used as a diagnostic tool for Feline Dysautonomia, as regulatory peptides are known to be involved in several other diseases of the mammalian gastrointestinal tract (Vaillant and others, 1982; Bloom and Polak, 1982). Further studies are required to distinguish the enteric neuropeptide abnormalities in Feline Dysautonomia from those occurring in other disorders affecting the feline gut.     

The transfer of serum IgG1 antibody into the gastrointestinal tract in newborn calves

Transfer of functional blood IgG1 to the gastrointestinal tract was measured in neonatal calves. Radiolabelled immunoglobulin G1 (IgG1) anti-DNP antibody was administered to 2 day old calves by intravenous injection. The serum clearance rate was measured and was compared to the rate of protein-bound 125I excretion in the feces over a 10 day period to determine the importance of transfer to the gastrointestinal tract as a mechanism of serum IgG1 clearance. The amount of protein-bound and DNP-binding 125I present in the gastrointestinal tract of 10 day old calves at necropsy was also measured. Fecal excretion of protein-bound 125I accounted for 32% of the serum 125I-IgG1 clearance. Protein-bound 125I was present in the gastrointestinal tract at necropsy in amounts estimated to account for 68% of the total 125I-IgG1 clearance, and retained 65% of the DNP-binding ability of the original antibody. The discrepancy between the fecal excretion (32% of total IgG1 clearance) and the GI clearance estimated from protein-bound 125I in the gut (68% of total IgG1 clearance) is explained in part by IgG1 proteolysis occurring after transfer to the gastrointestinal tract but before fecal excretion. These results indicate that transfer to the calf gastrointestinal tract accounts for most IgG1 clearance in young calves, and that the intestinal antibody retains antigen binding function and may contribute to intestinal immunity.     

Motility of the equine gastrointestinal tract: Physiology and pharmacotherapy

Normal gastrointestinal (GI) motility patterns are necessary to maintain transit of ingesta and to facilitate digestion and absorption of nutrients. Disorders of the equine GI tract are frequently encountered by the equine practitioner and these disorders are often associated with an interruption in normal intestinal motility patterns, thus complicating treatment of the primary disease. Consequently, numerous treatments have been investigated in horses to facilitate the return of normal intestinal motility. The purpose of this article is to provide a brief review of the anatomy and physiology of the GI tract in the horse and review medications available to the equine veterinarian that may potentially promote intestinal motility.     

First-pass splanchnic metabolism of dietary cysteine in weanling pigs

Cysteine is a semi-indispensable AA in neonates and is synthesized from the indispensable AA, methionine, by transsulfuration. We previously showed that the gastrointestinal tract (GIT) is a metabolically important site of methionine transsulfuration to cysteine, yet the metabolic fate of dietary cysteine in the GIT has not been established. Cysteine use by gut epithelial cells may play an important role for maintenance of glutathione synthesis and cellular redox function. Our aim was to quantify the extent of gastrointestinal first-pass cysteine metabolism in young pigs. Four-week-old weanling pigs (n = 10) were fed a liquid milk-replacer diet and given an intragastric and intravenous [1-(13)C]cysteine infusion on 2 separate days in a crossover design. Arterial and portal blood samples were collected for cysteine isotopic enrichment by gas chromatography-mass spectrometry and for (13)CO(2) enrichment by isotope ratio mass spectrometry. Our results indicated that dietary cysteine is metabolized during its first-pass splanchnic metabolism, accounting for about 40% of dietary cysteine intake. We also showed that intestinal absorption was the major metabolic fate of dietary cysteine, representing about 75% of intake, indicating that the GIT utilizes 25% of the dietary cysteine intake. Thus, utilization by the GIT represents about one-half (approximately 53%) of the first-pass, splanchnic uptake of dietary cysteine. Moreover, a substantial proportion of dietary splanchnic cysteine metabolism was consumed by the GIT via nonoxidative pathways. We conclude that the gut utilizes 25% of the dietary cysteine intake and that synthesis of mucosal epithelial proteins, such as glutathione and mucin, are a major nonoxidative metabolic fate for cysteine.     

Functional intestinal hypomotility in association with neuronal damage in a dog

A young, crossbred dog with a 13-month history of progressively worsening, recurrent episodes of vomiting, anorexia, depression and dehydration was diagnosed as having a functional hypomotility disorder of the small Intestines. During hospitalisation, the dog's condition Improved only when total parenteral nutrition was administered. When fed orally, the dog developed severe gastric dilatation. Intestinal motility was minimal, but was Induced by neostigmine. Post mortem findings Included dilatation of the duodenum and progressive narrowing of the small bowel up to the lleum. Histopathology revealed various grades of neuronal degeneration and necrosis of the myenteric plexuses throughout the small Intestine. Microscopic changes resembled those reported In dysautonomia, but were limited to small intestinal myenteric plexuses. A locallsed congenital neuronal defect causing a lack of parasympathetic tone Is suspected.