Intestinal Stasis Research Articles

Immunoproliferative small intestinal disease: prolonged 30-year course without development of lymphoma

Immunoproliferative small intestinal disease (IPSID) is mostly found in young adults of low socioeconomic class in developing countries. This condition is characterized by a dense lymphoplasmacytic infiltrate beneath the epithelium in the duodenal and proximal jejunal mucosa and in the mesenteric lymph nodes. In two thirds of cases, the involved lymphocytes elaborate an anomalous α-heavy chain protein. The etiology of this disease is unclear, although various parasitic, genetic, and toxic mechanisms have been proposed. Half of all IPSID patients will be found at diagnosis to have a concurrent intestinal B-cell lymphoma, and most of the remaining patients develop frank lymphoma within a few years. Although most reports of IPSID are from developing nations or indigent immigrant populations within Western countries, four cases of an IPSID-like condition have been documented in white women. Furthermore, although many IPSID patients progress to high grade indeterminate-type lymphoma within a few years of initial presentation, there have been occasional reports of long term survival without lymphomatous conversion. Here, we present an atypical case of IPSID—a California native who, though of Mexican heritage, had resided in the United States his entire life and did not belong to an indigent population. This patient had biopsy-proven IPSID that progressed over 30 yr but never exhibited lymphomatous conversion despite end stage intestinal stasis and recurrent obstruction, culminating in death. Our case calls into question some current assumptions about the prelymphomatous nature of this disease.

The comorbid occurrence of other diagnoses in patients with ulcerative colitis and Crohn's disease.

The comorbidity between inflammatory bowel disease (IBD) and other diagnoses may help to shed light on the etiology and pathophysiology of IBD. The US Vital Statistics offer the opportunity to study causes of death broken down by comorbid disease associations. The aim of this study was to analyze the presence of comorbid conditions in persons who died from ulcerative colitis or Crohn's disease. The numbers of deaths from ulcerative colitis and Crohn's disease were retrieved from the computerized 1991-1996 data files of the National Center for Health Statistics. Comorbid associations between other diagnosis and ulcerative colitis or Crohn's disease were expressed as age-, gender-, and race-standardized proportional mortality ratios. Ulcerative colitis and Crohn's disease showed, in general, similar patterns of comorbidity. Both diseases were associated with similar sets of GI complications, such as intestinal obstruction and stasis, mucosal inflammation and infection, vascular complications, and complications related to fistula and abscess formation. Extraintestinal complications of both IBD involved disorders of the hepatobiliary system, urinary system, and various coagulopathies. Ulcerative colitis alone was found to be associated with Hirschsprung's disease and schizophrenia, whereas Crohn's disease alone was found to be related with osteoporosis and amyloidosis. No completely unexplained or hitherto undescribed association was revealed. The numerous intestinal and extraintestinal complications associated with IBD serve as a reminder of the systemic nature and the resultant clinical severity of both ulcerative colitis and Crohn's disease.

The comorbid occurrence of other diagnoses in patients with ulcerative colitis and Crohn’s disease

OBJECTIVES: The comorbidity between inflammatory bowel disease (IBD) and other diagnoses may help to shed light on the etiology and pathophysiology of IBD. The US Vital Statistics offer the opportunity to study causes of death broken down by comorbid disease associations. The aim of this study was to analyze the presence of comorbid conditions in persons who died from ulcerative colitis or Crohn’s disease. METHODS: The numbers of deaths from ulcerative colitis and Crohn’s disease were retrieved from the computerized 1991–1996 data files of the National Center for Health Statistics. Comorbid associations between other diagnosis and ulcerative colitis or Crohn’s disease were expressed as age-, gender-, and race-standardized proportional mortality ratios. RESULTS: Ulcerative colitis and Crohn’s disease showed, in general, similar patterns of comorbidity. Both diseases were associated with similar sets of GI complications, such as intestinal obstruction and stasis, mucosal inflammation and infection, vascular complications, and complications related to fistula and abscess formation. Extraintestinal complications of both IBD involved disorders of the hepatobiliary system, urinary system, and various coagulopathies. Ulcerative colitis alone was found to be associated with Hirschsprung’s disease and schizophrenia, whereas Crohn’s disease alone was found to be related with osteoporosis and amyloidosis. CONCLUSIONS: No completely unexplained or hitherto undescribed association was revealed. The numerous intestinal and extraintestinal complications associated with IBD serve as a reminder of the systemic nature and the resultant clinical severity of both ulcerative colitis and Crohn’s disease.

Notable names in the history of surgery: 2. William Arbuthnot Lane (1856–1943)

Surgery today owes much to the services of early practitioners who made their advances as a result of wide clinical experience and compassion. This two‐part series explores the careers of Percivall Pott and William Arbuthnot Lane. Sir William Arbuthnot Lane was the most brilliant technical surgeon in Britain during the first half of the 20th century. He was one of the many famous physicians and surgeons to train at Guy's Hospital in London since its founding in 1724. Although some of his ideas may be controversial, he had made many original contributions and innovations in a variety of surgical techniques. He introduced mastoid drainage in purulent otitis media with specially designed chisels and gouges; resection of the cervical oesophagus for cancer and reconstruction by skin graft; and the repair of cleft lip and palate in neonates. His greatest contribution must be the introduction of the ‘no‐touch technique’ in open reduction and plating of long bone fractures by Lane's steel plates. In later life, Lane became obsessed with the role of regular bowel motion in health. To combat various real or imagined ailments, he first short‐circuited and later resected the whole large intestine. When surgery failed to resolve the problem, Lane advised regularly taking paraffin oil for the relief of constipation. He was a firm believer as well as a pioneer in alternative or homeopathic medicine. Lane's concept of chronic intestinal stasis is a classic case of a flawless surgical technique subservient to a faulty hypothesis.

Colonisation bactérienne chronique de l’intestin grêle : présentation de six observations et mise au point

Introduction. – Small intestinal bacterial overgrowth syndrome (SIBOS) has various clinical and biological presentations. Six observations are described in this review which is aimed at reporting recent data on SIBOS and proposing diagnosis and therapeutic attitudes. Current knowledge and key points. – Chronic diarrhea, malabsorption syndrome and exsudative enteropathy are the main criteria of diagnosis. Breath hydrogen testing is commonly performed to confirm diagnosis, with a 78% sensitivity and a 89% specificity. The aim of therapy is reparation of malabsorption consequences, reduction of intestinal bacterial overgrowth, and surgical correction of intestinal stasis. In the absence of consensus, norfloxacin or amoxicillin-clavulinic acid (administered for a mean of 7 to 15 days) seem the more appropriate antibiotics. When possible, surgery represents the primary treatment of SIBOS recurrences. Future prospects and projects. – Diagnosis of small intestinal bacterial overgrowth syndrome must be evoked on the basis of either surgical or medical context, i.e., the existence of chronic diarrhea, malabsorption syndrome (complete or not), and exsudative enteropathy. This review reports essential factors for diagnosis and treatment.

Role of stasis and oxidative stress in ileal pouch inflammation.

Although ileal pouch-anal anastomosis has become the operation of choice for patients with chronic ulcerative colitis and familial adenomatous polyposis coli, ileal pouch inflammation or pouchitis remains a significant postoperative complication. Numerous factors such as fecal stasis have been implicated in the etiology of pouchitis; however, pouchitis remains poorly understood due to the lack of a small animal model. One of the primary goals of this study was to surgically create a reservoir or U-pouch in the ileum of a rat in which stasis would occur in a manner that was unimpeded by other complicating factors such as a colectomy. This model would allow investigation of the hypothesis that intestinal stasis leads to biochemical changes that predispose the ileal pouch to inflammation and oxidative stress. A U-pouch was surgically created in the terminal ileum of Lewis rats just proximal to the ileocecal valve without a colectomy. Stasis was assessed by serial barium radiographs over 48 h. Thirty days after surgery, mucosa was obtained from the ileal U-pouches and nonoperated ileum to assess inflammation and neutrophil infiltration histologically and by measuring myeloperoxidase activity. Oxidative stress was assessed by measuring 8-isoprostane levels in urine. Once the model was validated and it was established that stasis and inflammation occurred in the pouch, either vitamin E or allopurinol was administered for 30 days after which myeloperoxidase and 8-isoprostane levels were again measured. In our experimental model, ileal stasis resulted in increases in both mucosal myeloperoxidase activity and urinary 8-isoprostane levels, suggesting that oxidative stress was associated with stasis. Thirty-day treatment with vitamin E or allopurinol reduced ileal myeloperoxidase activity and urinary 8-isoprostane levels. These studies demonstrated that stasis in the ileum occurred and was associated with neutrophil infiltration and oxidative stress. Antioxidant treatment reduced the inflammatory response suggesting a role for antioxidant therapy in the treatment of pouchitis.

In vitro effects of nonsteroidal anti-inflammatory agents and prostaglandins I2, E2, and F2α on contractility of taenia of the large colon of horses

Abstract Objectives To determine the in vitro effect of various prostaglandins (PG) and nonsteroidal anti-inflammatory drugs (NSAID) on contractile activity of the large-colon taenia of horses. Animals 14 healthy horses. Procedure The taenia was collected from the ventral colon, cut into strips (2 × 10 mm), and mounted in a tissue bath system (20-ml capacity) that contained oxygenated Krebs buffer solution warmed to 37.5 ± 0.5 C. After equilibration, incremental doses of PGE2, PGF2α, PGI2, flunixin meglumine, carprofen, ketoprofen, and phenylbutazone were added to the baths, and contractile activity was recorded. Magnitude of the response was calculated by comparing contractile activity before and after administration of the PG or NSAID to the tissue baths. Results PGE2 and PGF2α caused a significant increase in contractile activity, whereas PGL2 induced an inhibitory response. Activity of NSAID on contraction was predominantly inhibitory. At low concentrations, ketoprofen induced an excitatory effect, which then became inhibitory at high concentrations. Compared with the other NSAID, carprofen significantly reduced contractile activity at lower concentrations. Conclusions PGE2 and PGF2α appear to enhance contractility of large-colon taenia of horses, whereas PGL2 was inhibitory in the in vitro model. Administration of NSAID also inhibited contractility, with carprofen having the most potent effect. Clinical Relevance Administration of NSAID in combination with liberation of endogenous PG may predispose horses to development of intestinal stasis and subsequent impaction. (Am J Vet Res 1999;60:1004-1009)

Intestinal stasis associated bowel inflammation.

Anatomical structures that create reservoirs for stagnant intestinal contents are a characteristic feature of common inflammatory disorders such as diverticulitis and appendicitis. Intestinal diverticula, surgically constructed blind loops and pouches, obstructing carcinomas of the colon, and Hirschsprung’s disease are accompanied by chronic inflammatory changes in the intestine, and are occasionally associated with mucosal ulceration followed by massive bleeding. These diseases are etiologically associated with disorders characterized by intestinal stasis and/or an altered fecal stream, resulting from “cul de sac” structures (blind loop or pouch) in the intestinal tract, bowel obstruction or impaired motility. Furthermore, some of these chronic inflammatory conditions appear to exhibit similar pathological features, such as ischemic colitis. Although these inflammatory changes have been described individually, often as case reports, relatively little attention has been devoted to the overall clinical impact of these diseases and to understanding the pathophysiology of disease initiation and progression. Studies in our laboratory and by others have provided novel insights into the molecular and cellular basis for the intense inflammatory responses that are associated with intestinal stasis. This review summarizes the findings of these studies and provides a unifying theory to explain the inflammatory responses that result from intestinal stasis.

The impact of Clostridium difficile on a surgical service: a prospective study of 374 patients.

To evaluate the epidemiology of Clostridium difficile colitis (CDC) in a subset of patients admitted specifically to a surgical service. CDC is an increasingly prevalent nosocomial infection that can prolong hospitalization and adversely affect patient outcome. Although this disease has been investigated extensively in patients admitted to medical services, the incidence and risk factors for the development of this disease in patients admitted to a surgical service have not been studied. Over a 5-month period, 374 patients admitted to the general, vascular, thoracic, and urologic surgery services were monitored for the development of symptomatic CDC (defined as >3 bowel movements per 24 hours and a positive cytotoxin assay or culture). Twenty-one patients developed CDC (incidence, 5.6%). Factors that independently predisposed to infection included admission from a skilled care facility, use of the antibiotic cefoxitin, and an operative procedure for bowel obstruction. Other factors associated with CDC included colectomy, treatment with any antibiotic, nasogastric tube suction, advanced age, and prior antibiotic treatment. Abdominal pain and fever were also more common in patients with CDC. Morbidity included prolonged hospitalization in all patients and urgent colectomy in one. CDC frequently affects surgical patients, producing morbidity ranging from mild diarrhea to life-threatening illness. A variety of factors, many of which are associated with intestinal stasis, predispose to the development of CDC.

Acute blood stasis reduces interstitial uptake of albumin from intestinal microcirculatory networks.

Temporary blood flow stoppage occurs in a greater percentage of the capillaries when blood flow to organs is reduced. Previous studies on the small intestine have suggested that acute blood stasis (< or = 10 min) results in expression of negative charge, not present when blood flow is brisk, on the luminal surface of mucosal capillaries. Negative surface charge would tend to reduce transcapillary passage of albumin from blood to interstitium, since albumin is also negatively charged. Here we test the hypothesis that acute blood stasis reduces the interstitial uptake of albumin from mucosal capillary networks in rat small intestine in situ. Animals were subjected to two treatments, which included intestinal blood flow and acute stasis. After each treatment, fluorescent albumins were perfused into the intestinal circulation, and then interstitial fluorescence was recorded using fluorescence microscopy. Images were later quantified by computer analysis. After brisk blood flow, but not after acute blood stasis, fluorescence rapidly appeared in the interstitium and resulted in higher interstitial fluorescence intensity values. These results may have relevance to the mechanisms by which albumin flux in the small intestine is synchronized with digestion and fasting, which are associated with high and low intestinal blood flow, respectively.

Book Review: Fantasy Surgery, 1880-1930: With Special Reference to Sir William Arbuthnot Lane

Reviewed by: Fantasy Surgery, 1880–1930: With Special Reference to Sir William Arbuthnot Lane. Clio Medica Robert P. Hudson Ann Dally. Fantasy Surgery, 1880–1930: With Special Reference to Sir William Arbuthnot Lane. Clio Medica, vol. 38. Wellcome Institute Series in the History of Medicine. Amsterdam: Editions Rodopi, 1996. viii + 359 pp. $28.00; Hfl. 45.00 (paperbound). The main subject of Fantasy Surgery is Sir Arbuthnot Lane, a turn-of-the-century British surgeon, and his fixation on the concepts of ptosis, intestinal stasis, and autointoxication. My problems with the book began early with Dally’s statement that “medical historians have tended to ignore Lane or to distort his interests, ideas and achievements” (p. 84). Considering his historical weight, Lane has not been neglected: he has had two book-length biographies (W. E. Tanner, Sir W. Arbuthnot Lane: His Life and Work [1946], and T. B. Layton, Sir William Arbuthnot Lane: An Enquiry into the Mind and Influence of a Surgeon [1956]) and a nice clinical assessment by J. L. Smith. 1 There is also my offering, “Theory and Therapy: Ptosis, Stasis, and Autointoxication,” 2 which is listed in Dally’s bibliography but not cited in the text. Modesty aside, my article could serve as a reasonable précis of this book. The two pieces share the same major historical threads and conclusions. As I moved through Dally’s book I was flattered that she found so many of my choice quotations also to her liking. The problem arose when I began finding my own sentences reproduced with scanty alterations; there are far too many copied passages with token paraphrasing and no attribution. 3 I have not attempted to determine if this applied to other authors as well. [End Page 131] Beyond the above, the book presents significant difficulties. In a number of passages, and with no citations, today’s medicine is indicted for the sins of Lane and his contemporaries. These remarks are often not merely judgmental but censorious. There is only lip sympathy for the foibles of humanity and the fact that physicians have always had to practice in relative ignorance. One example can catch the flavor of this. After concluding that Lane’s admirers and critics generally accepted his views on constipation (intestinal stasis), autointoxication, and the uselessness of the human colon, Dally writes: “This may seem odd and their deficiencies may seem ludicrously obvious, but in medicine, as in other areas, there are plenty of things just as illogical that most doctors believe or accept without question today” (p. 154). There are lapses in Dally’s own logic. After stating that “a search of the literature has failed to reveal any writer who offered evidence . . . or even tried to explain why he believed” that ptosis could cause somatic or mental symptoms (p. 47), she lists various physicians for whom the mechanism of ptosis was malnourishment from liver disease, tight corsets, evolutionary changes associated with assuming an upright posture, and irregular bowel habits resulting in excessive ptomaines. As pointed out in the Bulletin article, there were valid new scientific observations that underpinned the theories of ptosis and autointoxication, such as X rays using contrast media that showed the stomach drooping into the pelvis, and the discovery of toxin-producing bacteria in the colon. Dally describes these but has no patience for the fact that, given the science of the time, these discoveries had a reasonable connection to stasis and autointoxication, which led to Lane’s surgical approach. At times she seems to understand that the social nature of science leads to error and correction, but when mistakes are made, she sees them as reprehensible. For Dally, as her title tells us, surgical practices that were later abandoned are better dismissed as fantastic. Robert P. Hudson Kansas University Medical Center Footnotes 1. J. L. Smith, “Sir Arbuthnot Lane, Chronic Intestinal Stasis, and Autointoxication,” Ann. Intern. Med., 1982, 96: 365–69. 2. Robert P. Hudson, “Theory and Therapy: Ptosis, Stasis, and Autointoxication,” Bull. Hist. Med., 1989, 63: 392–413. 3. Editors’ Note: Some examples include the sentence beginning “Between 1885 and 1889” (Hudson, p. 396; Dally, p. 49); the sentence beginning “By 1903 some eight hundred articles” (Hudson...

Liver complications of pediatric parenteral nutrition--epidemiology.

Total parenteral nutrition (TPN)-induced liver disease develops in 40-60% of infants who require long-term TPN for intestinal failure. The clinical spectrum includes cholestasis, cholelithiasis, hepatic fibrosis with progression to biliary cirrhosis, and the development of portal hypertension and liver failure in a significant number of children who are totally parenterally fed. The pathogenesis is multifactorial and is related to prematurity, low birth weight, and duration of TPN. The degree and severity of the liver disease is related to recurrent sepsis including catheter sepsis, bacterial translocation, and cholangitis. Lack of enteral feeding leading to reduced gut hormone secretion, reduction of bile flow, and biliary stasis may be important mechanisms in the development of cholestasis, biliary sludge, and cholelithiasis. Although it is unlikely that modern TPN solutions have a major role in the etiology of TPN liver disease, manganese toxicity recently has been recognized in children with hepatic dysfunction on TPN. Although there is a definite relationship with the degree of manganese toxicity and hepatic decompensation, it is not yet clear whether this is a primary mechanism or whether the high levels are related to reduced biliary excretion of manganese. The management strategies for the prevention of TPN-induced liver disease include early enteral feeding, a multidisciplinary approach to the management of parenteral nutrition, and aseptic catheter techniques to reduce sepsis. The administration of ursodeoxycholic acid may improve bile flow and reduce gall bladder and intestinal stasis. As survival from isolated intestinal transplantation improves, this therapeutic option should be considered before TPN liver disease becomes irreversible and combined liver and small bowel transplantation is required.

Effect of glutamine or glucagon-insulin enriched total parenteral nutrition on liver and gut in 70% hepatectomized rats with colon stenosis

Background: Malnutrition of enterocytes is believed to facilitate the breakdown of the intestinal mucosal barrier, furthering a translocation of enteric bacteria with subsequent severe infection, which has been described after extensive hepatectomy. Glutamine and glucagon insulin are said to attenuate the malnutrition of enterocytes. To determine whether this was true, the effects on the remnant liver and the gut of total parenteral nutrition supplemented by admixtures of glutamine and/or glucagon insulin were investigated in rats subjected to massive hepatectomy and transient intestinal stasis. Study Design: Rats underwent a permanent cannulation of the superior caval vein without restraining their mobility, a 70% hepatectomy, and a 24 hour string-ligation stenosis of the colon. A standard total parenteral nutrition solution was infused without or with 2% glutamine and without or with glucagon-insulin supplementation, respectively. Results: Glutamine and glucagon-insulin supplemented total parenteral nutrition increased ileal mucosal DNA concentrations during and after intestinal stasis. Glutamine or glucagon-insulin alone had less pronounced effects. In the liver, the combined supplementation resulted in reduced adenosine triphosphate concentrations and increased mitochondrial adenosine triphosphate synthesis as well as in an early increase in DNA concentrations. Conclusion: Glutamine and glucagon-insulin enriched total parenteral nutrition attenuates malnutrition of enterocytes after massive abdominal stress and promotes liver regeneration after extensive hepatectomy.

Effect of glutamine or glucagon-insulin enriched total parenteral nutrition on liver and gut in 70% hepatectomized rats with colon stenosis.

Malnutrition of enterocytes is believed to facilitate the breakdown of the intestinal mucosal barrier, furthering a translocation of enteric bacteria with subsequent severe infection, which has been described after extensive hepatectomy. Glutamine and glucagon insulin are said to attenuate the malnutrition of enterocytes. To determine whether this was true, the effects on the remnant liver and the gut of total parenteral nutrition supplemented by admixtures of glutamine and/or glucagon insulin were investigated in rats subjected to massive hepatectomy and transient intestinal stasis. Rats underwent a permanent cannulation of the superior caval vein without restraining their mobility, a 70% hepatectomy, and a 24 hour string-ligation stenosis of the colon. A standard total parenteral nutrition solution was infused without or with 2% glutamine and without or with glucagon-insulin supplementation, respectively. Glutamine and glucagon-insulin supplemented total parenteral nutrition increased ileal mucosal DNA concentrations during and after intestinal stasis. Glutamine or glucagon-insulin alone had less pronounced effects. In the liver, the combined supplementation resulted in reduced adenosine triphosphate concentrations and increased mitochondrial adenosine triphosphate synthesis as well as in an early increase in DNA concentrations. Glutamine and glucagon-insulin enriched total parenteral nutrition attenuates malnutrition of enterocytes after massive abdominal stress and promotes liver regeneration after extensive hepatectomy.

Effects of intestinal stasis on intercellular adhesion molecule 1 expression in the rat: Role of enteric bacteria

BACKGROUND & AIMS: The mechanisms underlying the inflammatory changes associated with intestinal stasis are poorly understood. The objective of this study was to assess whether endothelial expression of intercellular adhesion molecule 1 (ICAM-1) and leukocyte recruitment are altered after intestinal stasis. METHODS: ICAM-1 expression and granulocyte recruitment were quantified in different tissues of Sprague- Dawley rats using the double-radiolabeled monoclonal antibody technique and peroxidase activity, respectively. RESULTS: Both constitutive and endotoxin-induced ICAM-1 expression were significantly higher in the cecum than in distal colon, a finding that cannot be explained by a difference in endothelial surface area between the two organs. Surgical procedures to improve cecal stool flow (cecostomy, ileocecostomy) elicited a significant decrease in constitutive ICAM-1 expression in both cecum and distal colon. Tissue peroxidase activity was normally higher in cecum than in distal colon, and this difference was significantly reduced by ileocecostomy. Oral administration of antibiotics (kanamycin and/or metronidazole for 2 days) significantly reduced constitutive ICAM-1 expression in the cecum, but not in the distal colon. CONCLUSIONS: This study indicates that intestinal stasis is associated with an increased expression of ICAM-1 and granulocyte infiltration, which may be mediated by enteric bacteria. (Gastroenterology 1997 Jun;112(6):1971-8)

Gallstones in a community free of obesity but prone to slow intestinal transit.

To verify anecdotal reports that gallstones were frequent in a remote community where obesity is rare and to look for possible explanations of their occurrence, including slow intestinal transit. Population survey of gallbladder status and stool form. Two villages in Ladakh, a mountainous region of northern India; for comparison, a stratified random sample from general practitioners' lists in East Bristol. Women aged 25-59 years, 437 in Ladakh and 974 in Bristol. Presence of gallstones on ultrasonography and response to questionnaires about parity, the intake of dried legume seeds (pulses) and bowel function including the form or appearance of the stools on a seven-point, transit-sensitive scale. Weight, height and waist circumference were also recorded. Gallstone disease was at least as frequent in Ladakh as in Bristol although Ladakhi women were uniformly slim and their weight, waist size and body mass index failed to rise with age. After adjustment for age, gallstone disease was associated with higher body mass index and waist size in Bristol but not in Ladakh. It was associated with increased parity in Bristol, but not significantly so after adjusting for age and not at all in Ladakh. Gallstone disease was not directly associated with bowel function but Ladakhis often reported their stools to be lumpy (42.4 vs. 26.5% of Bristol women) and seldom as soft or loose (6.4 vs. 42.5%), implying that their intestinal transit tends to be slow. Gallstones can be common in a population free of obesity but prone to intestinal stasis.

Amelioration of intestinal dysmotility and stasis by octreotide early after small-bowel autotransplantation in dogs

Intestinal dysmotility and stasis after intestinal transplantation are considered to promote bacterial overgrowth and translocation. Two prokinetic agents, KW5139 (13-leu-motilin) and the somatostatin analogue octreotide acetate, were studied to determine whether they can ameliorate intestinal dysmotility during the early postoperative period. Motility was recorded by multiple extraluminal strain-gauge transducers in 6 dogs on postoperative days 1, 3, 7, and 14. A barium meal study was performed with a separate group of 8 dogs on postoperative days 3 and 7. The agent KW5139 induced brief, weak contractions in the graft and had little effect on the dilated bowel; however, octreotide induced motor activity that propelled accumulated intestinal contents into the colon and reduced dilation of the transplanted bowel. Octreotide, but not KW5139, ameliorates intestinal dysmotility associated with bowel autotransplantation during the early postoperative period. Short-term administration of octreotide may be useful for the treatment of dysmotility following intestinal transplantation.

ガストログラフィン消化管造影で穿孔を認めないのに尿路が描出された１例

A 85-year-old man was admitted because of gastric cancer and underwent subtotal gastrectomy with regional lymph node dissection. Abdominal pain was experienced on the 37th postoperative day, and signs of peritoneal irritation developed on the 39th day. CT revealed a small amount of ascites and a thickened small bowel wall with a narrow lumen, but no evidence of perforation. On the 40th day, an upper gastrointestinal study with oral Gastrografin showed tubular narrowing of the small bowel and the absence of mucosal folds, while 3-hour follow-up films showed opacification of the renal pelvis, ureter and bladder. The films also showed delayed passage of the Gastrografin. This was interpreted as indicating perforation of the intestine or breakdown of the bowel anastomosis. Laparotomy was performed, but no perforation or breakdown was detected. We think that the Gastrografin was absorbed through the ischemic small bowel as seen in conditions in which there is intestinal stasis and dehydration of the patient.

Intestinal stasis and rupture in rabbits

During one year 23 of 110 New Zealand white, adult male laboratory rabbits died. The pathological findings included intestinal stasis, intestinal blockage, acute intestinal rupture and intestinal rupture with peritonitis. These changes were considered to represent stages in an intestinal stasis and rupture syndrome. Another group of 20 comparable rabbits remained unaffected.

Effect of amitraz and its metabolites on intestinal motility

1. Amitraz was rapidly metabolised to BTS27271 after intravenous administration to sheep. 2. Amitraz and BTS27271 had significant H 1-histamine antagonist activity on isolated guinea-pig ileum. BTS27271 was approximately 3.3 times as potent as amitraz. 3. Intravenous injection of amitraz and its metabolite BTS27271 caused an immediate cessation of caecal motility in sheep, which persisted for 74–245 min. 4. Caecal stasis induced by amitraz was reversed by yohimbine but only partially reversed by 2-pyridylethylamine. 5. The results suggest that despite the significant antihistamine activity of amitraz and BTS27271 in vitro, it is probably the alpha-2-adrenergic agonist activity that is the most important in causing large intestinal stasis in vivo.