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This was a prospective study performed in a Department of Veterans Affairs Medical Center. The aim of this study was to use endoscopic and histological examinations to determine the potential diagnostic origins of chronic gastrointestinal symptoms among patients who were part of the deployment of troops to the Persian Gulf after August 1990. Twenty-four (8%) male patients (mean age, 42 years) of 308 patients in the Persian Gulf War Registry agreed to undergo endoscopic examination of chronic symptoms, including heartburn (29%), dyspepsia (33%), dysphagia (8%), diarrhea (63%), Hemoccult-positive stool (21%), and rectal bleeding (17%). There were 17 upper endoscopies, 18 colonoscopies, and 4 flexible sigmoidoscopies performed, all with biopsies. Five (33%) of 15 patients had positive serological findings for Helicobacter pylori. With upper endoscopy, major findings included esophagitis (12%), Schatzki's ring (12%), hiatal hernia (47%), antral erythema (59%), and duodenal erythema (29%). With lower endoscopy, major findings included ileitis (5%), lymphoid hyperplasia (9%), polyps (27%), diverticulosis (23%), and hemorrhoids (23%). Major histopathological findings included microscopic esophagitis (24%), gastritis with H. pylori (35%), gastritis without H. pylori (18%), Crohn's disease (5%), tubular adenoma (5%), hyperplastic polyps (18%), and melanosis coli (5%). Most patients with chronic heartburn or dyspepsia have evidence of esophagitis or H. pylori. Individuals with these chronic symptoms should undergo evaluation. [ABSTRACT FROM AUTHOR]

In a recent study, a large proportion of veterans seen for chronic heartburn or dyspepsia after the Persian Gulf War had evidence for Helicobacter pylori. Thomas Jackson was born and raised in an area of West Virginia that has a high prevalence of H. pylori. He suffered chronic dyspeptic symptoms following his service in the Mexican-American War. Therapies that he tried included treatment with a variant of the Sippy diet. Following a bullet wound to the left arm at the battle of Chancellorsville on Saturday, May 2, 1863, Thomas Jackson underwent amputation of the left arm below the left shoulder. He died 1 week later with a diagnosis of pleuropneumonia. The records of the postsurgical course are incomplete. The available clinical information raises the hypothesis that his chronic dyspepsia and his cause of death could have been related to chronic peptic ulcer disease due to gastric H. pylori infection. [ABSTRACT FROM AUTHOR]

Lifestyle intervention programmes often produce insufficient weight loss and poor weight loss maintenance. As a result, an increasing number of patients with obesity and related comorbidities undergo bariatric surgery, which includes approaches such as the adjustable gastric band or the 'divided' Roux-en-Y gastric bypass (RYGB). This Review summarizes the current knowledge on nutrient deficiencies that can develop after bariatric surgery and highlights follow-up and treatment options for bariatric surgery patients who develop a micronutrient deficiency. The major macronutrient deficiency after bariatric surgery is protein malnutrition. Deficiencies in micronutrients, which include trace elements, essential minerals, and water-soluble and fat-soluble vitamins, are common before bariatric surgery and often persist postoperatively, despite universal recommendations on multivitamin and mineral supplements. Other disorders, including small intestinal bacterial overgrowth, can promote micronutrient deficiencies, especially in patients with diabetes mellitus. Recognition of the clinical presentations of micronutrient deficiencies is important, both to enable early intervention and to minimize long-term adverse effects. A major clinical concern is the relationship between vitamin D deficiency and the development of metabolic bone diseases, such as osteoporosis or osteomalacia; metabolic bone diseases may explain the increased risk of hip fracture in patients after RYGB. Further studies are required to determine the optimal levels of nutrient supplementation and whether postoperative laboratory monitoring effectively detects nutrient deficiencies. In the absence of such data, clinicians should inquire about and treat symptoms that suggest nutrient deficiencies. [ABSTRACT FROM AUTHOR]

The emergence of the SARS-CoV-2 Omicron sublineages resulted in increased transmission rates and reduced protection from vaccines. To counteract these effects, multiple booster strategies were used in different countries, although data comparing their efficiency in improving protective immunity remain sparse, especially among vulnerable populations, including older adults. The inactivated CoronaVac vaccine was among the most widely distributed vaccine worldwide and was essential in the early control of SARS-CoV-2-related hospitalizations and deaths. However, it is not well understood whether homologous versus heterologous booster doses in those fully vaccinated with CoronaVac induce distinct humoral responses or whether these responses vary across age groups. We analyzed plasma antibody responses from CoronaVac-vaccinated younger or older individuals who received a homologous CoronaVac or heterologous BNT162b2 or ChAdOx1 booster vaccine. All three evaluated boosters resulted in increased virus-specific IgG titers 28 days after the booster dose. However, we found that both IgG titers against SARS-CoV-2 Spike or RBD and neutralization titers against Omicron sublineages were substantially reduced in participants who received homologous CoronaVac compared with the heterologous BNT162b2 or ChAdOx1 booster. This effect was specifically prominent in recipients >50 years of age. In this group, the CoronaVac booster induced low virus-specific IgG titers and failed to elevate neutralization titers against any Omicron sublineage. Our results point to the notable inefficiency of CoronaVac immunization and boosting in mounting protective antiviral humoral immunity, particularly among older adults, during the Omicron wave. These observations also point to benefits of heterologous regimens in high-risk populations fully vaccinated with CoronaVac.

Obesity is a major factor in the worldwide rise in the prevalence of type 2 diabetes mellitus. The obesity "epidemic" will require novel, effective interventions to permit both the prevention and treatment of diabetes caused by obesity. Laparoscopic vertical sleeve gastrectomy is a newer bariatric surgical procedure with a lower risk of complications (compared to Roux-en-Y gastric bypass surgery). Based in part on restriction of daily caloric intake, sleeve gastrectomy has a major role in inducing significant weight loss and weight loss is maintained for at least 10 years. Prior studies have supported the utility of the vertical sleeve gastrectomy for the treatment and management of subgroups of individuals with diabetes mellitus. There are reports of 11% to 76.9% of obese individuals discontinuing use of diabetic medications in studies lasting up to 8 years after vertical sleeve gastrectomy. Major ongoing issues include the preoperative determination of the suitability of diabetic patients to undergo this bariatric surgical procedure. Understanding how this surgical procedure is performed and the resulting anatomy is important when vertical sleeve gastrectomy is being considered as a treatment option for diabetes. In the postoperative periods, specific macronutrient goals and micronutrient supplements are important for successful and safer clinical results. An understanding of immediate- and long term- potential complications is important for reducing the potential risks of vertical sleeve gastrectomy. This includes the recognition and treatment of postoperative nutritional deficiencies and disorders. Vertical sleeve gastrectomy is a component of a long term, organized program directed at treating diabetes related to obesity. This approach may result in improved patient outcomes when vertical sleeve gastrectomy is performed to treat type 2 diabetes in obese individuals.

We reported that 30% of individuals with medically complicated obesity have bowel symptoms, suggesting irritable bowel syndrome, but this prevalence of bowel symptoms is not related to body mass index or diabetes mellitus. Hypovitaminosis D is common in individuals with obesity and type 2 diabetes mellitus and is associated with depressive symptoms. Because antidepressants improve global symptoms in individuals with bowel symptoms, we hypothesize that the high prevalence of bowel symptoms in medically complicated obesity is associated with hypovitaminosis D. This is a single-institution, retrospective cohort study performed in a large, urban community teaching hospital. Over 2 years, individuals considering bariatric surgery completed a Manning symptom questionnaire to quantify bowel symptoms. Serum 25-hydroxy vitamin D was ordered, and the results were recorded for all individuals. Among 271 subjects, 229 subjects (80% women, 20% men; 67% black, 31% white; age range: 23-73 years; body mass index range: 35-91 kg/m 2 ) completed 25-hydroxy vitamin D testing. Sixty-seven subjects (29%) have 3 to 6 Manning bowel symptoms, suggesting irritable bowel syndrome; 84 (37%) have type 2 diabetes; and 180 (79%) had vitamin D insufficiency. There are significant negative associations between Manning bowel symptoms and vitamin D concentrations in subjects with obesity (P = .01) and with type 2 diabetes mellitus and obesity (P = .007). The results support our hypothesis that the high prevalence of bowel symptoms in people with medically complicated obesity is associated with hypovitaminosis D. A prospective study is required to evaluate vitamin D supplementation and relief of bowel symptoms in people with medically complicated obesity., (Copyright © 2018 Elsevier Inc. All rights reserved.)

Thiamine is a vitamin whose deficient can result in multiorgan symptoms. We described an 18% prevalence of clinical thiamine deficiency after gastric bypass surgery. Our hypotheses are that individuals with medically complicated obesity frequently have clinical thiamine deficiency and that diabetes mellitus is a mechanism for development of clinical thiamine deficiency. This is a single institution, retrospective observational study of consecutive patients with a body mass index of at least 35 kg/m 2 who were evaluated in preoperative gastrointestinal bariatric clinic from 2013 to 2015. Each patient underwent a symptom survey. Clinical thiamine deficiency is defined by both (1) consistent clinical symptom and (2) either a low whole-blood thiamine concentration or significant improvement of or resolution of consistent clinical symptoms after receiving thiamine supplementation. After excluding 101 individuals with prior bariatric surgery or heavy alcohol consumption, 400 patients were included in the study. Sixty-six patients (16.5% of 400) fulfill a diagnosis of clinical thiamine deficiency, with 9 (14% of 66) having consistent gastrointestinal manifestations, 46 (70% of 66) having cardiac manifestations, 39 (59% of 66) having peripheral neurologic manifestations, and 3 (5% of 66) having neuropsychiatric manifestations. Diabetes mellitus is not a risk factor (P=.59). Higher body mass index is a significant risk for clinical thiamine deficiency (P=.007). Clinical thiamine deficiency is common in these individuals and a higher body mass index is an identified risk factor. Mechanisms explaining development of thiamine deficiency in obese individuals remain unclear., (Copyright © 2016 Elsevier Inc. All rights reserved.)

Aim: To evaluate the risks of medical conditions, evaluate gastric sleeve narrowing, and assess hydrostatic balloon dilatation to treat dysphagia after vertical sleeve gastrectomy (VSG)., Methods: VSG is being performed more frequently worldwide as a treatment for medically-complicated obesity, and dysphagia is common post-operatively. We hypothesize that post-operative dysphagia is related to underlying medical conditions or narrowing of the gastric sleeve. This is a retrospective, single institution study of consecutive patients who underwent sleeve gastrectomy from 2013 to 2015. Patients with previous bariatric procedures were excluded. Narrowing of a gastric sleeve includes: inability to pass a 9.6 mm gastroscope due to stenosis or sharp angulation or spiral hindering its passage., Results: Of 400 consecutive patients, 352 are included; the prevalence of dysphagia is 22.7%; 33 patients (9.3%) have narrowing of the sleeve with 25 (7.1%) having sharp angulation or a spiral while 8 (2.3%) have a stenosis. All 33 patients underwent balloon dilatation of the gastric sleeve and dysphagia resolved in 13 patients (39%); 10 patients (30%) noted resolution of dysphagia after two additional dilatations. In a multivariate model, medical conditions associated with post-operative dysphagia include diabetes mellitus, symptoms of esophageal reflux, a low whole blood thiamine level, hypothyroidism, use of non-steroidal anti-inflammatory drugs, and use of opioids., Conclusion: Narrowing of the gastric sleeve and gastric sleeve stenosis are common after VSG. Endoscopic balloon dilatations of the gastric sleeve resolves dysphagia in 69% of patients., Competing Interests: Conflict-of-interest statement: All of the authors have no conflict of interest to report regarding the publication of this paper.

Objective: Abdominal symptoms are common after bariatric surgery, and these individuals commonly have upper gut bacterial overgrowth, a known cause of malabsorption. Breath hydrogen determination after oral glucose is a safe and inexpensive test for malabsorption. This study is designed to investigate breath hydrogen levels after oral glucose in symptomatic individuals who had undergone Roux-en-Y gastric bypass surgery., Methods: This is a retrospective study of individuals (n = 63; 60 females; 3 males; mean age 49 years) who had gastric bypass surgery and then glucose breath testing to evaluate abdominal symptoms., Results: Among 63 postoperative individuals, 51 (81%) had a late rise (≥45 minutes) in breath hydrogen or methane, supporting glucose malabsorption; 46 (90%) of these 51 subjects also had an early rise (≤30 minutes) in breath hydrogen or methane supporting upper gut bacterial overgrowth. Glucose malabsorption was more frequent in subjects with upper gut bacterial overgrowth compared to subjects with no evidence for bacterial overgrowth (P < 0.001)., Conclusion: These data support the presence of intestinal glucose malabsorption associated with upper gut bacterial overgrowth in individuals with abdominal symptoms after gastric bypass surgery. Breath hydrogen testing after oral glucose should be considered to evaluate potential malabsorption in symptomatic, postoperative individuals.

The field of bariatric surgery has been rapidly growing and evolving over the past several decades. During the period that obesity has become a worldwide epidemic, new interventions have been developed to combat this complex disorder. The development of new laparoscopic and minimally invasive treatments for medically-complicated obesity has made it essential that gastrointestinal physicians obtain a thorough understanding of past developments and possible future directions in bariatrics. New laparoscopic advancements provide patients and practitioners with a variety of options that have an improved safety profile and better efficacy without open, invasive surgery. The mechanisms of weight loss after bariatric surgery are complex and may in part be related to altered release of regulatory peptide hormones from the gut. Endoscopic techniques designed to mimic the effects of bariatric surgery and endolumenal interventions performed entirely through the gastrointestinal tract offer potential advantages. Several of these new techniques have demonstrated promising, preliminary results. We outline herein historical and current trends in the development of bariatric surgery and its transition to safer and more minimally invasive procedures designed to induce weight loss.

Background/aims: Roux-en-Y gastric bypass surgery is the most common bariatric surgery worldwide. We have described thiamine deficiency in patients with small intestinal bacterial overgrowth after gastric bypass. We hypothesized that symptoms of thiamine deficiency are common after gastric bypass. The aims of this study were to examine the prevalence of and treatment of symptoms of thiamine deficiency after gastric bypass., Methods: This is a prospective study performed in a large urban, community hospital. Consecutive gastric bypass patients seen from February 1, 2008 to May 1, 2009 are included. Thiamine deficiency in this study included both: consistent clinical symptoms and either (1) low blood thiamine level or (2) resolution of clinical symptoms after receiving thiamine., Results: Of 151 patients, 25 females and 2 males met the criteria for thiamine deficiency (prevalence of 18%). In these 27 patients, 12 had one symptom of thiamine deficiency, while 15 had symptoms consistent with multiple subtypes. Eleven patients reported constipation at 0.33-12 years (mean 4.8) after gastric bypass. Elevated serum folate levels were seen in 6 of 10 tested patients and there was an abnormal glucose-hydrogen breath test in 9 of 10 tested patients, supporting the presence of small intestinal bacterial overgrowth. Frequency of defecation improved after thiamine treatment., Conclusion: Thiamine deficiency resulting from small intestinal bacterial overgrowth should be considered in patients being seen for constipation after gastric bypass surgery., (Copyright © 2013 S. Karger AG, Basel.)

Roux-en-Y gastric bypass surgery remains the major surgical option for individuals with medically complicated obesity. The importance of preoperative evaluation to permit identification of micronutrient deficiencies is being re-evaluated. The risk of complications related to pregnancy after gastric bypass supports careful follow-up. Micronutrient deficiencies are common in postoperative gastric bypass patients, despite the suggested use of routine vitamin and mineral supplements after surgery. Copper deficiency must be considered as an origin for visual disorders after gastric bypass. Vitamin D deficiency with metabolic bone disease remains common after gastric bypass and the results suggest that the present postoperative supplements of calcium and vitamin D are inadequate. Major nutritional complications of bariatric surgery are occurring more than 20 years after surgery. There is no evidence for intestinal adaptation as there remains decreased intestinal absorption of iron up to 18 months after gastric bypass surgery. This article supports ongoing examination of nutritional complications after gastric bypass surgery and supports the notion that the daily doses of micronutrient supplements, such as vitamin D, may need to be revised.

The National Longitudinal Study of Adolescent Health and the National Health and Nutrition Examination Survey reported that over 40% of the US population is overweight. The average weight loss attained by medical management programs is neither sufficient nor durable enough to treat medically complicated obesity. An estimated 220,000 bariatric procedures are performed yearly in the USA and Canada. The divided Roux-en-Y gastric bypass (RYGB) is performed most commonly in these countries and is considered the gold standard bariatric surgical procedure. The complexity of RYGB means that serious and potentially preventable perioperative complications can occur. RYGB alters the normal anatomy and physiology of the upper gut, which has predictable adverse effects and potential complications. Patients seek advice and care for symptoms that develop or persist after RYGB; although some symptoms are expected and predictable, others are complications that may or may not require active medical or surgical intervention. Physicians should be able to predict and manage most postoperative medical and nutritional disorders related to RYGB and should be prepared to assess patients for potential referral for surgical intervention or revision.

Bariatric surgery has become an increasingly important method for management of medically complicated obesity. In patients who have undergone bariatric surgery, up to 87% with type 2 diabetes mellitus develop improvement or resolution of their disease postoperatively. Bariatric surgery can reduce the number of absorbed calories through performance of either a restrictive or a malabsorptive procedure. Patients who have undergone bariatric surgery require indefinite, regular follow-up care by physicians who need to follow laboratory parameters of macronutrient as well as micronutrient malnutrition. Physicians who care for patients after bariatric surgery need to be familiar with common postoperative syndromes that result from specific nutrient deficiencies., (Copyright (c) 2010 Elsevier Inc. All rights reserved.)

It has been proposed that thiamine deficiency after gastric bypass surgery in obese patients results from prolonged nausea and emesis. We hypothesized that thiamine deficiency is induced by altered gut ecology. This report includes 2 retrospective studies of obese patients who underwent Roux-en-Y gastric bypass surgery at our institution from 1999 to 2005. In the first study, 80 patients (52 women and 28 men) had measurement of whole-blood thiamine diphosphate level and serum folate level. In these 80 patients, 39 (49%) had thiamine diphosphate levels less than the lower limit of the reference range, and 28 (72%) of the 39 had folate levels higher than the upper limit of the reference range, an indicator of small intestinal bacterial overgrowth. In 41 patients with normal thiamine levels, only 14 (34%) had folate levels higher than the upper limit of the reference range (chi(2) test, P < .01). In the second study, 21 patients (17 women and 4 men) had thiamine diphosphate levels less than the lower limit of the reference range and abnormal glucose-hydrogen breath tests, consistent with small intestinal bacterial overgrowth. Fifteen patients received oral thiamine supplements, but repeated thiamine levels remained low in all 15. Nine of these patients then received oral antibiotic therapy; repeated thiamine levels were found to be normal in all 9 patients. These results support the hypothesis that small intestinal bacterial overgrowth results from altered gut ecology and induces thiamine deficiency after gastric bypass surgery in obese patients.

The objective of this article is to review the clinical presentation and neurobiology of degeneration of the enteric nervous system with emphasis on human data where available. Constipation, incontinence and evacuation disorders are frequently encountered in the ageing population. Healthy lower gastrointestinal function is essential for successful ageing as it is critical to maintaining independence and autonomy to pursue further activity. One clinical expression of enteric neurodegeneration is constipation. However, the aetiology may be multifactorial as disturbances of epithelial, muscle or neural function may all result from neurodegeneration. There is evidence of loss of excitatory (e.g. cholinergic) enteric neurons and interstitial cells of Cajal, whereas inhibitory (including nitrergic) neurons appear unaffected. Understanding neurodegeneration in the enteric nervous system is key to developing treatments to reverse it. Neurotrophins have been shown to accelerate colonic transit and relieve constipation in the medium term; they are also implicated in maintenance programmes in adult enteric neurons through a role in antioxidant defence. However, their effects in ageing colon require further study. There is evidence that 5-HT(2) and 5-HT(4) mechanisms are involved in development, maintenance and survival of enteric neurons. Further research is needed to understand and potentially reverse enteric neurodegeneration.

It has been proposed that tissue damage induced by nonsteroidal anti-inflammatory drugs is related to increased tissue free radical production with antioxidant depletion. We have shown that esomeprazole increases gastric total antioxidant capacity in mice and, therefore, hypothesized that the protective effect of esomeprazole during treatment with a nonsteroidal anti-inflammatory drug is related to increased gastric antioxidant capacity and decreased tissue free radical production. A/J mice received one of four treatments by daily gavage: saline in vehicle (control), indomethacin, esomeprazole, or indomethacin and esomeprazole. After 10 days, all mice were sacrificed and validated assays were used to measure gastric total antioxidant capacity, lipid peroxide levels, and myeloperoxidase activity. Indomethacin-treated mice developed weight loss and melena. No mice receiving indomethacin and esomeprazole died, but the death rate while receiving indomethacin was 38% (chi2, P = 0.05). Gastric lipid peroxide levels increased in mice receiving indomethacin treatment compared to treatment with esomeprazole and indomethacin (P = 0.03). There was a strong trend (P = 0.08) toward increased gastric total antioxidant capacity in mice receiving esomeprazole and indomethacin compared to mice receiving indomethacin. Gastric myeloperoxidase activities were not different among the four groups. Esomeprazole significantly improved survival in mice that received indomethacin, reduced free radical production, as estimated by lipid peroxide levels, and appeared to increase gastric total antioxidant capacity. The mechanisms for the beneficial effects of esomeprazole in the treatment of gastropathy are more complex than previously thought.

Nonalcoholic fatty liver disease is a common cause of chronic liver disease, a common finding on liver biopsy in those patients with abnormal blood transaminase levels, and a common cause of cryptogenic cirrhosis in the United States. The prevalence of this disorder is expected to rise with the increase in obesity, and the clinical spectrum can range from simple steatosis (fatty liver) to cirrhosis of the liver. Insulin resistance is thought to be pivotal for the development of steatosis, and oxidative stress may be a potential factor that can promote hepatic necroinflammation and fibrosis. Preliminary studies have examined the role of oxidative stress and antioxidants in animal and human studies of this disorder. Efforts to improve the hepatic antioxidant system could be achieved by optimizing the patient's diet, by supplementation with precursors for antioxidants, or by supplementation with essential metals and/or antioxidants. Randomized, controlled trials are required to examine these potential approaches using patients with this disorder.

Antioxidant depletion is believed to be a mechanism involved in the pathophysiology of several upper gastrointestinal disorders, and H, K-ATPase inhibitors can alter free radical production by neutrophils. We hypothesized that the H, K-ATPase inhibitor esomeprazole magnesium would decrease gut free radical production with a concomitant increase in gut total antioxidant capacity. A/J mice (n = 10/group) received either vehicle (control) or one of three concentrations of esomeprazole magnesium in vehicle by once-daily gavage for 10 days. Using tissue extracts from stomach and colon, total antioxidant capacity, lipid peroxide levels, and constitutive Cu/Zn-superoxide dismutase were measured using validated assays. There was a dose-related increase in total antioxidant capacity (analysis of variance, P < 0.001) in stomach, but there was no change in the colon. In the assessment of free radical production, there was a trend toward decreased lipid peroxide levels in stomach from mice receiving esomeprazole. In stomach, Cu/Zn-superoxide dismutase activity was increased (ANOVA: p=.03) in mice receiving esomeprazole. In conclusion, gastric total antioxidant capacity and Cu/Zn-superoxide dismutase activity are increased by esomeprazole, and these changes may result in part from decreased free radical production. The present results support the notion that the pharmacological effects of this agent on upper intestinal tissue are more complex than previously thought, and appear to involve both enzymatic and nonenzymatic tissue antioxidants.

Concern has been expressed about the rapid increase in the incidence of esophageal carcinoma in the United States. This rise is due to an increase in the number of cases of adenocarcinoma of the esophagus. Because of the relatively small number of cases of esophageal carcinoma, the absolute risk of developing this cancer in the United States remains small. Potential origins for this increase in esophageal adenocarcinoma are examined in this review, including the risk induced by obesity, low dietary antioxidants, high dietary fat, family history of breast cancer, smoking, gastroesophageal reflux, and Barrett's esophagus. The risk of esophageal adenocarcinoma is inversely associated with infection by Helicobacter pylori organisms. A better understanding of risk factors involved in the increased incidence of esophageal adenocarcinoma is important for development of new preventive strategies for this serious disorder.

Transplantation of small intestine in a rat model has been shown to affect expression of neurochemicals within enteric inhibitory nerves. However, the mechanism for altered expression of inhibitory neurochemicals is uncertain. Based on our previous studies, we hypothesized that small intestinal transplantation would result in altered intestinal levels of antioxidant capacity. Glutathione, total antioxidant capacity, and lipid peroxide levels were measured at 3 months following (1) transection of rat small intestine, (2) transection and extrinsic denervation of rat intestine, and (3) isotransplantation of rat ileum or (4) allotransplantation of rat ileum with cyclosporine therapy to suppress rejection. Glutathione levels were not significantly different among the four groups. There were trends toward increased lipid peroxide levels following isografting and extrinsic denervation. Total antioxidant capacity was increased following extrinsic denervation (P=0.05). Increased intestinal total antioxidant capacity in response to extrinsic denervation may represent a compensatory mechanism for protection against oxidative stress. This result enhances our understanding of the relationship between tissue antioxidant levels and alteration of enteric nerves.

Increased free radical production with depletion of the antioxidant, glutathione, is a suggested mechanism for the development of ulcer disease in patients with Helicobacter pylori. The effects of ascorbate and omeprazole as potential gut antioxidants are incompletely understood. We hypothesized that as antioxidants, ascorbate and omeprazole protect against glutathione depletion. This study was designed to determine the effects of ascorbate and omeprazole on gastric emptying and gastric antioxidant levels in a mouse model of glutathione depletion. In an acute (10-day) mouse model, glutathione depletion was induced by inhibiting the rate limiting enzyme, gamma-glutamylcysteine synthetase. Enzymatic blockade produced depletion of gastric glutathione (P < 0.05) without increasing gastric lipid hydroperoxides. Glutathione depletion was associated with accelerated liquid gastric emptying. These effects were not prevented by supplementation with ascorbate or omeprazole. Omeprazole induced increased (P < 0.05) gastric and colonic total antioxidant capacity. One of the beneficial effects of omeprazole in patients may involve increased total antioxidant capacity.

Pressures generated by the pharyngeal constrictor muscles and proximal esophagus involve acetylcholine-induced muscle contractions. We hypothesized that the pharyngo-esophageal pressure gradient is related to choline acetyltransferase activity. In nine anesthetized cats, hypopharyngeal pressure and proximal esophageal pressure were recorded with a solid state transducer assembly. Enzymatic activities in the thyropharyngeus, cricopharyngeus, and proximal esophageal muscles were measured. Hypopharyngeal pressure was higher than the proximal esophagus (p < 0.01), and choline acetyltransferase activity was higher in the cricopharyngeus compared to the proximal esophagus ( p < 0.05). The pressure gradient between the hypopharynx and proximal esophagus may be influenced by the activity of choline acetyltransferase.