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Biomedical subjects

R W Sjogren

Publications and source records attributed to R W Sjogren.

9 recordsLinked to original sources
PubMed1997

Role of sensory afferents in the myoelectric response to acute enteric inflammation in the rabbit.

The role of sensory afferents in inflammation-induced alterations in myoelectric activity in vivo was investigated in the rabbit small intestine. Isolated ileal loops were implanted with serosal electrodes and exposed to ricin or vehicle after pretreatment with 125 mg/kg of subcutaneous (125 mg over 3 days) or intraluminal (640 microM) capsaicin. After 5 h of myoelectric recording, the loops were prepared for histology and for ex vivo generation of eicosanoids. Capsaicin exacerbated mucosal damage after exposure to ricin but did not alter neutrophil infiltration. Subcutaneous capsaicin alone elevated slow-wave frequency and spike events and transiently suppressed the myoelectric response to ricin. In contrast, intraluminal capsaicin alone did not alter myoelectric activity but produced a sustained inhibition of the response to ricin. Eicosanoid production was unchanged by capsaicin alone. Intraluminal capsaicin blocked increases in leukotriene C4 and prostaglandin E2 during inflammation, an effect that paralleled its inhibition of myoelectric activity. Thus the contribution of sensory afferents to altered motility during acute ileitis involves the release of mucosal inflammatory mediators that influence neural control of smooth muscle.

Acute Disease↗
PubMed1996

Gastrointestinal features of scleroderma.

Gastrointestinal involvement occurs in most patients with systemic sclerosis and is subclinical in about one third. Early pathology is characterized by vasculopathy, resulting in tissue ischemia and progressive dysfunction. Noninvasive esophageal studies using semisolid bolus scintigraphy are sensitive but lack specificity. Long-term treatment of reflux with high-dose proton pump inhibitors appears safe and effective for symptom relief and may prevent recurrence of esophagitis and stricture. Dyspepsia may result from gastroparesis and antral distension. Gastric antral vascular ectasia is a vascular manifestation, and bleeding may be controlled endoscopically. Prokinetic agents effective in pseudoobstruction include metoclopramide, domperidone, cisapride, octreotide, and erythromycin. Patients with intestinal neuropathy or response to bolus octreotide are more probable long-term responders. The combination of octreotide and erythromycin may be particularly effective in systemic sclerosis. The combination of cisapride and erythromycin may cause serious cardiac arrhythmia and is contraindicated. Omeprazole may predispose to small intestinal bacterial overgrowth. Malabsorption not responding to antibiotic therapy should be investigated with small-bowel biopsy to rule out more unusual causes. Pneumatosis cystoides intestinalis may be due to excessive hydrogen production by intestinal bacteria altering the partial pressure of nitrogen in the intestinal wall. In selected cases, surgery for intestinal failure is an option with resection or bypass of affected segments or placement of enterostomy tubes for feeding or decompression. Careful preoperative characterization of intestinal segments is required.

Esophageal Diseases↗
PubMed1994

Gastrointestinal motility disorders in scleroderma.

After the skin, the gastrointestinal tract is the second most common target of systemic sclerosis. The major clinical manifestations include gastroesophageal reflux, small bowel bacterial overgrowth, malnutrition, and intestinal pseudoobstruction. Treatment is symptomatic and supportive. Gastroesophageal reflux can usually be adequately managed with prokinetic drugs, omeprazole, and judicious use of antireflux surgery. If Barrett's esophagus is present, periodic endoscopic monitoring for development of dysplastic changes or adenocarcinoma is indicated. Bacterial overgrowth usually responds to rotating antibiotics and prokinetic drugs. Malnutrition and intestinal pseudoobstruction remain the major problems and often home total parenteral nutrition is required. Intestinal pseudoobstruction occurs in two phases: an early, neuropathic phase may respond to prokinetic drugs (metoclopramide, cisapride, octreotide, and erythromycin) and dietary modification (low-residue diets, vitamin supplementation). In the late myopathic phase, therapy is usually ineffective. Treatment consists of nutritional support. Careful manometric and radiographic localization of affected segments of stomach and small and large intestines may allow judicious surgical resection or venting procedures to reduce symptoms in this unfortunate group of patients.

Digestive System↗
PubMed1994

Intestinal myoelectric response in two different models of acute enteric inflammation.

The inflammatory responses to intraluminal administration of the cytotoxic lectin ricin or the hapten 2,4,6-trinitrobenzenesulfonic acid in 25% ethanol were compared. Myoelectric activity was recorded from in vivo ileal loops in rabbits after administration of either agent. At the end of a 6-h study the loops were removed and prepared for histological evaluation and for ex vivo generation of leukotriene (LT) C4 and prostaglandin (PG) E2. Both agents induced significant increases in mucosal damage, polymorphonuclear leukocyte infiltration, and edema. These changes tended to be patchy in the hapten model and confluent in the ricin model. Spike burst activity and mucosal LTC4 and PGE2 generation were also enhanced significantly. Intraluminal administration of the specific LTD4 antagonist Wy-48252 1 h before either inflammagen, significantly inhibited the myoelectric response without affecting tissue morphology or eicosanoid synthesis. These data demonstrate that there is a stereotypic spike burst response to acute inflammation, which is mediated in part by LTD4.

Acute Disease↗
PubMed1989

Altered intestinal motility precedes diarrhea during Escherichia coli enteric infection.

Changes in ileal and colonic myoelectric activity during the course of enteric infection of rabbits with the enteropathogenic Escherichia coli strain RDEC-1 were determined and related to microbiological, histological, and clinical parameters of disease. Rabbits were grouped into early, peak, and late stages of infection based on fecal shedding of bacteria. Weight loss and an increase in prolonged spike bursts (both action potential complexes and ileal migrating action potential complexes) developed early in infection, before the onset of diarrhea. Loose stools subsequently developed coincident with maximal numbers of action potential complexes. The myoelectric responses correlated better with mucosal enteroadherence of bacteria than with luminal colonization. These data demonstrate that, in this animal model of enteroadherent bacterial infection of the intestine, changes in intestinal myoelectric activity precede the onset of clinical diarrhea. In addition, bacterial adherence to the intestinal mucosa appears to be important in eliciting the abnormal myoelectric responses.

Action Potentials↗
PubMed1988

Characterization of the plasmid from Escherichia coli RDEC-1 that mediates expression of adhesin AF/R1 and evidence that AF/R1 pili promote but are not essential for enteropathogenic disease.

RDEC-1, an Escherichia coli strain that adheres to rabbit mucosa and causes an attaching, effacing lesion, expresses the pilus adhesin AF/R1 which determines in vitro attachment to rabbit intestinal brush borders. In order to determine the role of AF/R1 pili in the pathogenesis of enteropathogenic diarrhea in rabbits, we localized the genes for AF/R1 expression, constructed an AF/R1- strain, and compared the virulence of the AF/R1+ and AF/R1- strains with particular attention to the development of attaching, effacing lesions. We introduced Tn5 into the 86-megadalton (MDa) conjugative plasmid known to mediate expression of AF/R1 pili and transferred the derivative plasmids into laboratory strain HB101. Transconjugant M5 was found to contain the 86-MDa plasmid from RDEC-1 and to express AF/R1 pili. Pilus expression on M5 was confirmed by reaction with antiserum raised against purified AF/R1 pili and allowed the bacteria to adhere to the rabbit ileum in an in vitro assay. Three Tn5 insertions in the 86-MDa plasmid were obtained which resulted in loss of AF/R1 expression. Part of the plasmid was mapped, including a region necessary for AF/R1 pilus expression. AF/R1- mutant strain M34 was constructed, and its pathogenesis was investigated. M34 produced disease in rabbits but was less virulent than the parent. The characteristic effacing lesions of RDEC-1 and enteropathogenic E. coli developed in the intestine of rabbits infected with either M34 or RDEC-1, although with M34 they were much less frequent and did not involve the small bowel. We conclude that AF/R1 pilus expression is not essential for the attaching, effacing lesion but serves as an accessory virulence factor which promotes an initial interaction of RDEC-1 with normal epithelial cells.

Adhesins, Escherichia coli↗
PubMed1984

Anatomic and physiologic characteristics of transplanted fetal rat intestine.

Avascular segments of fetal rat intestine transplanted to the subcutaneous tissues of host syngeneic rats will become vascularized and grow. This study more fully characterizes this tissue, which we call "neogut," and compares it to normal rat small intestine. Anatomy was studied with light microscopy and scanning and transmission electron microscopy; transport and electrophysiologic parameters were measured in full-thickness pieces of tissue mounted in Ussing chambers; motility patterns, including slow wave and spike activity, were recorded. Subtle anatomic differences (shortened villi and microvilli) were noted in neogut compared to normal small bowel. Both neogut and normal rat ileum demonstrated net mucosal to serosal transport of d-glucose; the magnitudes of the electrophysiologic parameters (PD, Isc, and G) were less in neogut than in ileum. Slow-wave frequency of neogut was slightly less than native small bowel while spike activity was increased. These data show that neogut has structural and physiologic characteristics similar to normal rat small bowel and offers hope that this tissue may provide a nutritionally useful accessory gut for the patient with critical short-gut syndrome.

Animals↗
PubMed1983

Barrett's esophagus: a review.

Barrett's esophagus may be defined as a columnar epithelium-lined distal esophagus. As a frequently recognized complication of gastroesophageal reflux, Barrett's esophagus has become a diagnosis of general clinical concern. Factors governing the development of this complication in patients with gastroesophageal reflux are unknown but may be congenitally determined in part. When symptoms are present, they are due to the complications of reflux, such as esophagitis, stricture, ulcer, or bleeding. Barrett's esophagus may be suspected on the basis of results of a barium meal test, endoscopy, or isotope scanning. Iodine staining at endoscopy or manometrically guided biopsy helps to localize the abnormal mucosal segment. The diagnosis is proved by biopsy. The columnar epithelium of Barrett's esophagus has a malignant predisposition, and, once the diagnosis is made, periodic endoscopy, with biopsy and cytologic study, is indicated. The treatment of Barrett's esophagus is directed toward objective cessation of gastroesophageal reflux. In refractory cases, antireflux surgery improves symptoms and complications from reflux, but the columnar epithelium generally persists along with its malignant potential. It is not known whether effective antireflux treatment will lower the incidence of adenocarcinoma.

Adenocarcinoma↗